il 1β  (Millipore)

 
  • Logo
  • About
  • News
  • Press Release
  • Team
  • Advisors
  • Partners
  • Contact
  • Bioz Stars
  • Bioz vStars
  • 97
    Name:
    Interleukin 1beta from mouse
    Description:
    Interleukin 1β IL 1β cytokine is generated by monocytes dendritic cells macrophages and keratinocytes Pro IL 1β an IL 1β precursor undergoes proteolytic cleavage to produce its active form of 17 kDa
    Catalog Number:
    I5271
    Price:
    None
    Applications:
    Interleukin-1β from mouse has been used:. as a proinflammatory agent, to induce inflammatory signaling cascades mediated cellular damage. to study its effect on fetuin A-induced inflammatory response in podocyte. to check its effect on the expression of mitogen-activated protein kinase 4 using 3T3-L1 adipocytes
    Buy from Supplier


    Structured Review

    Millipore il 1β
    Interleukin 1beta from mouse
    Interleukin 1β IL 1β cytokine is generated by monocytes dendritic cells macrophages and keratinocytes Pro IL 1β an IL 1β precursor undergoes proteolytic cleavage to produce its active form of 17 kDa
    https://www.bioz.com/result/il 1β/product/Millipore
    Average 97 stars, based on 1 article reviews
    Price from $9.99 to $1999.99
    il 1β - by Bioz Stars, 2021-05
    97/100 stars

    Images

    1) Product Images from "Tumour necrosis factor alpha promotes secretion of 14-3-3η by inducing necroptosis in macrophages"

    Article Title: Tumour necrosis factor alpha promotes secretion of 14-3-3η by inducing necroptosis in macrophages

    Journal: Arthritis Research & Therapy

    doi: 10.1186/s13075-020-2110-9

    14-3-3η is detectable in culture supernatants of macrophages derived from HD and treated with TNF-α. The culture supernatants of macrophages cultured with or without diamide, TNF-α (100 ng/ml; n = 3), IL-1β (10 ng/ml; n = 3), IL-6/sIL-6R (10 ng/ml; n = 3), or IL-21 (10 ng/ml; n = 3) were subjected to WB. Recombinant 14-3-3η was used as a positive control. BSA was used as a loading control and was stained with CBB-R350. Representative images from three independent experiments are shown
    Figure Legend Snippet: 14-3-3η is detectable in culture supernatants of macrophages derived from HD and treated with TNF-α. The culture supernatants of macrophages cultured with or without diamide, TNF-α (100 ng/ml; n = 3), IL-1β (10 ng/ml; n = 3), IL-6/sIL-6R (10 ng/ml; n = 3), or IL-21 (10 ng/ml; n = 3) were subjected to WB. Recombinant 14-3-3η was used as a positive control. BSA was used as a loading control and was stained with CBB-R350. Representative images from three independent experiments are shown

    Techniques Used: Derivative Assay, Cell Culture, Western Blot, Recombinant, Positive Control, Staining

    2) Product Images from "Glial interleukin-1β upregulates neuronal sodium channel 1.7 in trigeminal ganglion contributing to temporomandibular joint inflammatory hypernociception in rats"

    Article Title: Glial interleukin-1β upregulates neuronal sodium channel 1.7 in trigeminal ganglion contributing to temporomandibular joint inflammatory hypernociception in rats

    Journal: Journal of Neuroinflammation

    doi: 10.1186/s12974-018-1154-0

    Intratrigeminal ganglionic injection of IL-1β resulted in decrease in the head withdrawal threshold and upregulation of Nav1.7, COX-2, and phospho-CREB expressions in both male and female rats. a The head withdrawal threshold in the TMJ region 1 week before or after cannula implantation in male and female rats. Independent samples t test, * P
    Figure Legend Snippet: Intratrigeminal ganglionic injection of IL-1β resulted in decrease in the head withdrawal threshold and upregulation of Nav1.7, COX-2, and phospho-CREB expressions in both male and female rats. a The head withdrawal threshold in the TMJ region 1 week before or after cannula implantation in male and female rats. Independent samples t test, * P

    Techniques Used: Injection

    Diagram of glial IL-1β-induced upregulation of neuronal Nav1.7 contributed to TMJ inflammatory hypernociception through the COX-2/PGE2/EP2-evoked PKA/CREB signaling pathway. TMJ inflammation somehow activates SGCs, which activate the transcriptions of IL-1β and COX-2 leading to increase in PGE2 release from the SGCs to subsequently activate the neuronal EP2/PKA/CREB signaling pathway then leading to upregulation of Nav1.7 in neurons and finally the increase in the neuronal excitability, which amplifies the stimuli in the TMJ contributing to the development of TMJ inflammatory hypernociception. TG, trigeminal ganglion; N, neuron; SGC, satellite glial cells
    Figure Legend Snippet: Diagram of glial IL-1β-induced upregulation of neuronal Nav1.7 contributed to TMJ inflammatory hypernociception through the COX-2/PGE2/EP2-evoked PKA/CREB signaling pathway. TMJ inflammation somehow activates SGCs, which activate the transcriptions of IL-1β and COX-2 leading to increase in PGE2 release from the SGCs to subsequently activate the neuronal EP2/PKA/CREB signaling pathway then leading to upregulation of Nav1.7 in neurons and finally the increase in the neuronal excitability, which amplifies the stimuli in the TMJ contributing to the development of TMJ inflammatory hypernociception. TG, trigeminal ganglion; N, neuron; SGC, satellite glial cells

    Techniques Used:

    Upregulation of trigeminal ganglionic IL-1β, COX-2, phospho-CREB, and Nav1.7 accompanied with decrease in the head withdrawal threshold after induction of TMJ inflammation. a Upregulation of IL-1β, COX-2, and Nav1.7 mRNA expressions in TG after induction of TMJ inflammation for 24 h. Independent samples t test, * P
    Figure Legend Snippet: Upregulation of trigeminal ganglionic IL-1β, COX-2, phospho-CREB, and Nav1.7 accompanied with decrease in the head withdrawal threshold after induction of TMJ inflammation. a Upregulation of IL-1β, COX-2, and Nav1.7 mRNA expressions in TG after induction of TMJ inflammation for 24 h. Independent samples t test, * P

    Techniques Used:

    TMJ inflammation-induced SGCs activation involved in inflammatory hypernociception through communication between glial IL-1β/COX-2 and neuronal phospho-CREB/Nav1.7. a Confocal images of immunofluorescent staining of GFAP, which was not affected in TG explants after treatment with IL-1β for 24 h. b Confocal images of immunofluorescent staining of GFAP, which was increased, specifically surrounding neurons-innervating TMJ (red box), in the TG after TMJ inflammation. The number of GFAP-positive cells was presented with histogram (right panel). V3 represents the mandibular division, and V1 and V2 represent the ophthalmic and maxillary divisions. c TMJ inflammation-induced upregulation of IL-1β, COX-2, and Nav1.7 mRNA expressions in TG were blocked by intratrigeminal injection of SGC activation inhibitor fluorocitrate. One-way ANOVA, * P
    Figure Legend Snippet: TMJ inflammation-induced SGCs activation involved in inflammatory hypernociception through communication between glial IL-1β/COX-2 and neuronal phospho-CREB/Nav1.7. a Confocal images of immunofluorescent staining of GFAP, which was not affected in TG explants after treatment with IL-1β for 24 h. b Confocal images of immunofluorescent staining of GFAP, which was increased, specifically surrounding neurons-innervating TMJ (red box), in the TG after TMJ inflammation. The number of GFAP-positive cells was presented with histogram (right panel). V3 represents the mandibular division, and V1 and V2 represent the ophthalmic and maxillary divisions. c TMJ inflammation-induced upregulation of IL-1β, COX-2, and Nav1.7 mRNA expressions in TG were blocked by intratrigeminal injection of SGC activation inhibitor fluorocitrate. One-way ANOVA, * P

    Techniques Used: Activation Assay, Staining, Injection

    Upregulation of Nav1.7 expression in TG explants after treatment with IL-1β. a Dose-course of Nav1.7 mRNA expression in TG after treatment with IL-1β (0.1 to 10 ng/mL) for 24 h. b Dose-course of Nav1.7 protein expression in TG after treatment with IL-1β (0.1 to 10 ng/mL) for 24 h. c Time-course of Nav1.7 mRNA expression in TG after treatment with IL-1β (10 ng/mL). d Time-course of Nav1.7 protein expression in TG after treatment with IL-1β (10 ng/mL). Quantification of Nav1.7 protein expression was presented as fold change of the control group (lower panel). One-way ANOVA, * P
    Figure Legend Snippet: Upregulation of Nav1.7 expression in TG explants after treatment with IL-1β. a Dose-course of Nav1.7 mRNA expression in TG after treatment with IL-1β (0.1 to 10 ng/mL) for 24 h. b Dose-course of Nav1.7 protein expression in TG after treatment with IL-1β (0.1 to 10 ng/mL) for 24 h. c Time-course of Nav1.7 mRNA expression in TG after treatment with IL-1β (10 ng/mL). d Time-course of Nav1.7 protein expression in TG after treatment with IL-1β (10 ng/mL). Quantification of Nav1.7 protein expression was presented as fold change of the control group (lower panel). One-way ANOVA, * P

    Techniques Used: Expressing

    Upregulation of Nav1.7 expression by IL-1β was dependent on COX-2/PGE2/EP2 in TG explants. a Dose-course of COX-2 mRNA expression in TG after treatment with IL-1β (0.1 to 10 ng/mL) for 24 h. b Dose-course of COX-2 protein expression in TG after treatment with IL-1β (0.1 to 10 ng/mL) for 24 h. c Time-course of COX-2 mRNA expression in TG after treatment with IL-1β (10 ng/mL). d Time-course of COX-2 protein expression in TG after treatment with IL-1β. (E) IL-1β-induced upregulation of Nav1.7 mRNA expression in TG was blocked by COX-2 selective inhibitor NS398. f IL-1β-induced upregulation of Nav1.7 protein expression in TG was blocked by COX-2 selective inhibitor NS398. g EP2 selective antagonist PF-04418948 blocked upregulation of Nav1.7 mRNA expression, but not COX-2 mRNA expression in TG after treatment with IL-1β. h EP2 selective antagonist PF-04418948 blocked upregulation of Nav1.7 protein expression, but not COX-2 protein expression in TG after treatment with IL-1β. Quantification of protein expressions were presented as fold change of the control group (lower panel). One-way ANOVA, * P
    Figure Legend Snippet: Upregulation of Nav1.7 expression by IL-1β was dependent on COX-2/PGE2/EP2 in TG explants. a Dose-course of COX-2 mRNA expression in TG after treatment with IL-1β (0.1 to 10 ng/mL) for 24 h. b Dose-course of COX-2 protein expression in TG after treatment with IL-1β (0.1 to 10 ng/mL) for 24 h. c Time-course of COX-2 mRNA expression in TG after treatment with IL-1β (10 ng/mL). d Time-course of COX-2 protein expression in TG after treatment with IL-1β. (E) IL-1β-induced upregulation of Nav1.7 mRNA expression in TG was blocked by COX-2 selective inhibitor NS398. f IL-1β-induced upregulation of Nav1.7 protein expression in TG was blocked by COX-2 selective inhibitor NS398. g EP2 selective antagonist PF-04418948 blocked upregulation of Nav1.7 mRNA expression, but not COX-2 mRNA expression in TG after treatment with IL-1β. h EP2 selective antagonist PF-04418948 blocked upregulation of Nav1.7 protein expression, but not COX-2 protein expression in TG after treatment with IL-1β. Quantification of protein expressions were presented as fold change of the control group (lower panel). One-way ANOVA, * P

    Techniques Used: Expressing

    IL-1β enhanced CREB binding to the Nav1.7 promoter. The schematic diagram indicates two potential CREs (CRE1 at − 1702/− 1698 and CRE2 at − 1486/− 1482) in the rat Nav1.7 promoter (− 1788/+ 100, translation start site as + 1). ChIP assay showed that CREB could bind to CRE2, and this binding was enhanced by the treatment with IL-1β for 24 h. The densities of the bands were quantified using the NIH ImageJ 1.38 software and expressed as fold change of the control group after normalization to input band. CRE, cAMP response element
    Figure Legend Snippet: IL-1β enhanced CREB binding to the Nav1.7 promoter. The schematic diagram indicates two potential CREs (CRE1 at − 1702/− 1698 and CRE2 at − 1486/− 1482) in the rat Nav1.7 promoter (− 1788/+ 100, translation start site as + 1). ChIP assay showed that CREB could bind to CRE2, and this binding was enhanced by the treatment with IL-1β for 24 h. The densities of the bands were quantified using the NIH ImageJ 1.38 software and expressed as fold change of the control group after normalization to input band. CRE, cAMP response element

    Techniques Used: Binding Assay, Chromatin Immunoprecipitation, Software

    IL-1β upregulated Nav1.7 expression through the EP2-evoked PKA/CREB signaling pathway in TG explants. a Dose-course of phospho-CREB protein expression in TG after treatment with IL-1β (0.1 to 10 ng/mL) for 24 h. b Time-course of phospho-CREB protein expression in TG after treatment with IL-1β. c Upregulation of phospho-CREB protein expression by IL-1β in TG was blocked by COX-2 selective inhibitor NS398. d Upregulation of phospho-CREB protein expression by IL-1β in TG was blocked by EP2 selective antagonist PF-04418948. e PKA inhibitor H89 blocked IL-1β-induced upregulation of Nav1.7 and phospho-CREB protein expressions, but not COX-2 protein expression in TG. f PKA inhibitor H89 blocked IL-1β-induced upregulation of Nav1.7 mRNA expression, but not COX-2 mRNA expression in TG. g PKA inhibitor PKI-(6-22)-amide blocked IL-1β-induced upregulation of Nav1.7 and phospho-CREB protein expression, but not COX-2 protein expression in TG. h PKA inhibitor PKI-(6-22)-amide blocked IL-1β-induced upregulation of Nav1.7 mRNA expression, but not COX-2 mRNA expression in TG. i Forskolin upregulated Nav1.7 mRNA expression in TG for 24 h. j Adenylate cyclase agonist forskolin upregulated Nav1.7 and phospho-CREB protein expressions in TG for 24 h. k PKA inhibitor H89 blocked forskolin-induced upregulation of Nav1.7 and phospho-CREB protein expressions in TG. l PKA inhibitor PKI-(6-22)-amide blocked forskolin-induced upregulation of Nav1.7 and phospho-CREB protein expressions in TG. Quantification of protein expressions were presented as fold change of the control group (lower panel). One-way ANOVA or Independent samples t test, * P
    Figure Legend Snippet: IL-1β upregulated Nav1.7 expression through the EP2-evoked PKA/CREB signaling pathway in TG explants. a Dose-course of phospho-CREB protein expression in TG after treatment with IL-1β (0.1 to 10 ng/mL) for 24 h. b Time-course of phospho-CREB protein expression in TG after treatment with IL-1β. c Upregulation of phospho-CREB protein expression by IL-1β in TG was blocked by COX-2 selective inhibitor NS398. d Upregulation of phospho-CREB protein expression by IL-1β in TG was blocked by EP2 selective antagonist PF-04418948. e PKA inhibitor H89 blocked IL-1β-induced upregulation of Nav1.7 and phospho-CREB protein expressions, but not COX-2 protein expression in TG. f PKA inhibitor H89 blocked IL-1β-induced upregulation of Nav1.7 mRNA expression, but not COX-2 mRNA expression in TG. g PKA inhibitor PKI-(6-22)-amide blocked IL-1β-induced upregulation of Nav1.7 and phospho-CREB protein expression, but not COX-2 protein expression in TG. h PKA inhibitor PKI-(6-22)-amide blocked IL-1β-induced upregulation of Nav1.7 mRNA expression, but not COX-2 mRNA expression in TG. i Forskolin upregulated Nav1.7 mRNA expression in TG for 24 h. j Adenylate cyclase agonist forskolin upregulated Nav1.7 and phospho-CREB protein expressions in TG for 24 h. k PKA inhibitor H89 blocked forskolin-induced upregulation of Nav1.7 and phospho-CREB protein expressions in TG. l PKA inhibitor PKI-(6-22)-amide blocked forskolin-induced upregulation of Nav1.7 and phospho-CREB protein expressions in TG. Quantification of protein expressions were presented as fold change of the control group (lower panel). One-way ANOVA or Independent samples t test, * P

    Techniques Used: Expressing

    3) Product Images from "Astrocyte-shed extracellular vesicles regulate the peripheral leukocyte response to inflammatory brain lesions"

    Article Title: Astrocyte-shed extracellular vesicles regulate the peripheral leukocyte response to inflammatory brain lesions

    Journal: Science signaling

    doi: 10.1126/scisignal.aai7696

    IL-1β stimulation of astrocytes results in the formation of membrane microdomains that are EV release sites
    Figure Legend Snippet: IL-1β stimulation of astrocytes results in the formation of membrane microdomains that are EV release sites

    Techniques Used:

    Brain nSMase regulates the peripheral ACR and leukocyte transmigration after central administration of IL-1β
    Figure Legend Snippet: Brain nSMase regulates the peripheral ACR and leukocyte transmigration after central administration of IL-1β

    Techniques Used: Transmigration Assay

    EVs released from IL-1β–stimulated astrocytes rapidly cross the BBB and localize to peripheral organs
    Figure Legend Snippet: EVs released from IL-1β–stimulated astrocytes rapidly cross the BBB and localize to peripheral organs

    Techniques Used:

    The cargo of EVs shed from astrocytes in response to IL-1β regulates the liver cytokine response through modulation of PPARα
    Figure Legend Snippet: The cargo of EVs shed from astrocytes in response to IL-1β regulates the liver cytokine response through modulation of PPARα

    Techniques Used:

    4) Product Images from "IL-36 promotes myeloid cell infiltration, activation and inflammatory activity in skin"

    Article Title: IL-36 promotes myeloid cell infiltration, activation and inflammatory activity in skin

    Journal: Journal of immunology (Baltimore, Md. : 1950)

    doi: 10.4049/jimmunol.1301481

    IL-36 cytokines induce monocyte expression of inflammatory cytokines Monocytes treated with 100ng/ml IL-36 cytokines for 12h upregulate IL-1A, IL-1B and IL-6, cytokine transcripts (n=9 donors, a-c). Significantly elevated levels of IL-1β and IL-6 were detected in the conditioned culture media after 12h (n=6 donors, e and f). Bars, mean ± SEM. Statistical significance indicated by * p
    Figure Legend Snippet: IL-36 cytokines induce monocyte expression of inflammatory cytokines Monocytes treated with 100ng/ml IL-36 cytokines for 12h upregulate IL-1A, IL-1B and IL-6, cytokine transcripts (n=9 donors, a-c). Significantly elevated levels of IL-1β and IL-6 were detected in the conditioned culture media after 12h (n=6 donors, e and f). Bars, mean ± SEM. Statistical significance indicated by * p

    Techniques Used: Expressing

    Monocyte-derived dendritic cells (MO-DC) have enhanced IL-36R expression and IL-36 cytokines facilitate DC maturation, driving T cell proliferation MO-DC expressed 6-fold more IL-36R mRNA than their monocyte precursors (qRT-PCR, n=6, a). When cultured with 10ng/ml IL-6+0.1μM PGE 2 and either 10ng/ml IL-1β or 100ng/ml IL-36α, MODC significantly increased their surface expression of CD86 (b) and HLA-DR (c), indicative of DC maturation (48hr, bars, mean ± SEM, n=8 donors). MO-DC matured with 10ng/ml IL-6 + 0.1μM PGE 2 and 10ng/ml TNF-α, 10ng/ml IL-1β or 100ng/ml IL-36α drove allogeneic T cell proliferation as determined by CFSE dye dilution (d and e) or DAPI labeling of DNA (f). No DC (T cells only), 1:100 DC:T cell ratio, 1:20 DC:T cell ratio showing mean ± SEM (n=4 donors). Statistical significance indicated by * p
    Figure Legend Snippet: Monocyte-derived dendritic cells (MO-DC) have enhanced IL-36R expression and IL-36 cytokines facilitate DC maturation, driving T cell proliferation MO-DC expressed 6-fold more IL-36R mRNA than their monocyte precursors (qRT-PCR, n=6, a). When cultured with 10ng/ml IL-6+0.1μM PGE 2 and either 10ng/ml IL-1β or 100ng/ml IL-36α, MODC significantly increased their surface expression of CD86 (b) and HLA-DR (c), indicative of DC maturation (48hr, bars, mean ± SEM, n=8 donors). MO-DC matured with 10ng/ml IL-6 + 0.1μM PGE 2 and 10ng/ml TNF-α, 10ng/ml IL-1β or 100ng/ml IL-36α drove allogeneic T cell proliferation as determined by CFSE dye dilution (d and e) or DAPI labeling of DNA (f). No DC (T cells only), 1:100 DC:T cell ratio, 1:20 DC:T cell ratio showing mean ± SEM (n=4 donors). Statistical significance indicated by * p

    Techniques Used: Derivative Assay, Expressing, Quantitative RT-PCR, Cell Culture, Labeling

    IL-36 cytokines induce chemokine expression by keratinocytes 4-day post-confluent normal human keratinocytes (NHK) were stimulated for 24h with recombinant truncated IL-36R ligands or IL-1β. Total RNA was extracted and mRNA transcripts quantified by qRT-PCR relative to the housekeeping gene RPL-P0 and conditioned medium assayed by ELISA. 100ng/ml IL-36α, IL-36β and IL-36γ significantly induced T cell chemokine mRNA expression compared with untreated cells, mean ± S.D. (n=3) (a). IL-36α, IL-36β, IL-36γ and IL-1β but not IL-36Ra dose-dependently induced CXCL1, CCL5, CXCL8 and CCL20 mRNA expression (b-e) and CXCL8 and CCL20 protein secretion (f and g) by keratinocytes. Mean ± S.D. (n=3). Statistical significance indicated by * p
    Figure Legend Snippet: IL-36 cytokines induce chemokine expression by keratinocytes 4-day post-confluent normal human keratinocytes (NHK) were stimulated for 24h with recombinant truncated IL-36R ligands or IL-1β. Total RNA was extracted and mRNA transcripts quantified by qRT-PCR relative to the housekeeping gene RPL-P0 and conditioned medium assayed by ELISA. 100ng/ml IL-36α, IL-36β and IL-36γ significantly induced T cell chemokine mRNA expression compared with untreated cells, mean ± S.D. (n=3) (a). IL-36α, IL-36β, IL-36γ and IL-1β but not IL-36Ra dose-dependently induced CXCL1, CCL5, CXCL8 and CCL20 mRNA expression (b-e) and CXCL8 and CCL20 protein secretion (f and g) by keratinocytes. Mean ± S.D. (n=3). Statistical significance indicated by * p

    Techniques Used: Expressing, Recombinant, Quantitative RT-PCR, Enzyme-linked Immunosorbent Assay

    5) Product Images from "Anti-inflammatory effects of Edaravone and Scutellarin in activated microglia in experimentally induced ischemia injury in rats and in BV-2 microglia"

    Article Title: Anti-inflammatory effects of Edaravone and Scutellarin in activated microglia in experimentally induced ischemia injury in rats and in BV-2 microglia

    Journal: BMC Neuroscience

    doi: 10.1186/s12868-014-0125-3

    Protein expression of inflammatory cytokines and iNOS was decreased in LPS-activated microglial cells following treatment with E, S and E + S. The expression levels of TNF-α, IL-1β and iNOS in LPS-activated microglial cells are depressed significantly following treatment with E, S and E + S. Significant differences in protein levels between LPS and drugs used groups are expressed as *p
    Figure Legend Snippet: Protein expression of inflammatory cytokines and iNOS was decreased in LPS-activated microglial cells following treatment with E, S and E + S. The expression levels of TNF-α, IL-1β and iNOS in LPS-activated microglial cells are depressed significantly following treatment with E, S and E + S. Significant differences in protein levels between LPS and drugs used groups are expressed as *p

    Techniques Used: Expressing

    IL-1β expression was suppressed following treatment of LPS-activated microglia with drugs E, S and E + S in vitro . Confocal images show an upregulation of IL-1β (E) in LPS-activated BV-2 microglia (D) in comparison to control (A-C) . IL-1β was hardly detected (H, K, N) in activated microglia treated with drugs E, S and especially so with E + S (G, J, M) . DAPI – blue. Scale bars in A-O : 50 μm.
    Figure Legend Snippet: IL-1β expression was suppressed following treatment of LPS-activated microglia with drugs E, S and E + S in vitro . Confocal images show an upregulation of IL-1β (E) in LPS-activated BV-2 microglia (D) in comparison to control (A-C) . IL-1β was hardly detected (H, K, N) in activated microglia treated with drugs E, S and especially so with E + S (G, J, M) . DAPI – blue. Scale bars in A-O : 50 μm.

    Techniques Used: Expressing, In Vitro

    Protein expression of inflammatory cytokines and iNOS was decreased in MCAO rat brains following treatment with E, S and E + S. The expression levels of TNF-α, IL-1β and iNOS in MCAO rat brains are depressed significantly at 3 days following treatment with E, S and E + S when compared with the MCAO ( n = 5 for each group). Significant differences in protein levels between MCAO and drugs used rats are expressed as *p
    Figure Legend Snippet: Protein expression of inflammatory cytokines and iNOS was decreased in MCAO rat brains following treatment with E, S and E + S. The expression levels of TNF-α, IL-1β and iNOS in MCAO rat brains are depressed significantly at 3 days following treatment with E, S and E + S when compared with the MCAO ( n = 5 for each group). Significant differences in protein levels between MCAO and drugs used rats are expressed as *p

    Techniques Used: Expressing

    Treatment of MCAO rats with drugs E, SH and E + SH resulted in the reduction of IL-1β expression in activated microglia. Confocal images showing the expression of IL-1β (red) in lectin + microglia (green) in the penumbral zones of MCAO rat brain (D-F) and following treatment with E (G-I) , SH (J-L) and E + SH (M-O) (n = 5 for each group). A noticeable increase in IL-1β expression (E) can be observed in the activated microglia (D) in MCAO rat brain. IL-1β expression (H, K) , however, was depressed in activated microglia (G, J) 3 days following treatment of MCAO rats with drugs E and SH. Also, IL-1β expression (N) was almost totally abolished in activated microglia (M) when MCAO rats were treated with a combination of the two drugs. DAPI – blue. Scale bars in A-O : 50 μm
    Figure Legend Snippet: Treatment of MCAO rats with drugs E, SH and E + SH resulted in the reduction of IL-1β expression in activated microglia. Confocal images showing the expression of IL-1β (red) in lectin + microglia (green) in the penumbral zones of MCAO rat brain (D-F) and following treatment with E (G-I) , SH (J-L) and E + SH (M-O) (n = 5 for each group). A noticeable increase in IL-1β expression (E) can be observed in the activated microglia (D) in MCAO rat brain. IL-1β expression (H, K) , however, was depressed in activated microglia (G, J) 3 days following treatment of MCAO rats with drugs E and SH. Also, IL-1β expression (N) was almost totally abolished in activated microglia (M) when MCAO rats were treated with a combination of the two drugs. DAPI – blue. Scale bars in A-O : 50 μm

    Techniques Used: Expressing

    6) Product Images from "Impaired NFKBIE gene function decreases cellular uptake of methotrexate by down-regulating SLC19A1 expression in a human rheumatoid arthritis cell line"

    Article Title: Impaired NFKBIE gene function decreases cellular uptake of methotrexate by down-regulating SLC19A1 expression in a human rheumatoid arthritis cell line

    Journal: Modern Rheumatology

    doi: 10.3109/14397595.2015.1112481

    Effects of overexpression of Mock, wild-type NFKBIE , and Val194Ala mutant NFKBIE on MTX-metabolizing enzyme expressions. Quantitative gene expressions of FPGS (A), GGH (B), DHFR (C), TYMS (D), MTHFR (E), and ATIC (F) genes in Mock (white), overexpression of wild-type NFKBIE (gray) and Val194Ala mutant NFKBIE (black). Those cells were treated with or without 0.01, 0.1, 1, 5, and 10 μM methotrexate (MTX) application for 24 h in the presence or absence of 20 U/mL IL-1β and 20 U/mL TNF-α. The expression levels of each gene were measured by qRT-PCR. Statistical significance was analyzed using the unpaired t -test (* p
    Figure Legend Snippet: Effects of overexpression of Mock, wild-type NFKBIE , and Val194Ala mutant NFKBIE on MTX-metabolizing enzyme expressions. Quantitative gene expressions of FPGS (A), GGH (B), DHFR (C), TYMS (D), MTHFR (E), and ATIC (F) genes in Mock (white), overexpression of wild-type NFKBIE (gray) and Val194Ala mutant NFKBIE (black). Those cells were treated with or without 0.01, 0.1, 1, 5, and 10 μM methotrexate (MTX) application for 24 h in the presence or absence of 20 U/mL IL-1β and 20 U/mL TNF-α. The expression levels of each gene were measured by qRT-PCR. Statistical significance was analyzed using the unpaired t -test (* p

    Techniques Used: Over Expression, Mutagenesis, Expressing, Quantitative RT-PCR

    Effects of overexpression of Mock, wild-type NFKBIE , and Val194Ala mutant NFKBIE on the expressions of SLC19A1 and the ABC transporters. Quantitative gene expressions of SLC19A1 (A), ABCC1 (B), ABCC5 (C), and ABCG2 (D) genes in Mock (white), overexpression of wild-type NFKBIE (gray), and Val194Ala mutant NFKBIE (black). Those cells were treated with or without 0.01, 0.1, 1, 5, and 10 μM methotrexate (MTX) application for 24 h in the presence or absence of 20 U/mL IL-1β and 20 U/mL TNF-α. The expression levels of each gene were measured by qRT-PCR. Statistical significance was analyzed using the unpaired t -test (* p
    Figure Legend Snippet: Effects of overexpression of Mock, wild-type NFKBIE , and Val194Ala mutant NFKBIE on the expressions of SLC19A1 and the ABC transporters. Quantitative gene expressions of SLC19A1 (A), ABCC1 (B), ABCC5 (C), and ABCG2 (D) genes in Mock (white), overexpression of wild-type NFKBIE (gray), and Val194Ala mutant NFKBIE (black). Those cells were treated with or without 0.01, 0.1, 1, 5, and 10 μM methotrexate (MTX) application for 24 h in the presence or absence of 20 U/mL IL-1β and 20 U/mL TNF-α. The expression levels of each gene were measured by qRT-PCR. Statistical significance was analyzed using the unpaired t -test (* p

    Techniques Used: Over Expression, Mutagenesis, Expressing, Quantitative RT-PCR

    Uptake and efflux of a methotrexate (MTX) derivative under knockdown of NFKBIE by siRNA in MH7A. MH7A cells were cultured for 24 h, and then transfected for 24 h. They were further incubated with 20 U/mL IL-1β and 20 U/mL TNF-α for 24 h. After washing the cells with PBS, the cells were incubated in the presence of 5 μM of MTX derivatives for 5 h. The uptake of MTX derivatives was quantified by measuring the fluorescence emission for each sample. (A) The representative histogram of control (blue) and knockdown of NFKBIE (dark red). The mean fluorescent intensity (MFI) per cell, expressed in arbitrary units, was then determined using a flow cytometer. (B) The summary results. In addition to these experiments, after incubating with MTX derivatives (5 μM) for 5 h and washing cells with PBS, cells were chased for 6 h exclusively in RPMI supplemented with 10% FBS. Subsequently, the MFI per cell was measured at 0 and 6 h. On the basis of these results, differences in the efflux of MTX derivatives between control and NFKBIE knockdown were studied (C). Each column and its corresponding vertical lines represent the mean and the standard error of the mean (SEM) of triplicate cultures. Statistical significance was analyzed with the unpaired t -test (* p
    Figure Legend Snippet: Uptake and efflux of a methotrexate (MTX) derivative under knockdown of NFKBIE by siRNA in MH7A. MH7A cells were cultured for 24 h, and then transfected for 24 h. They were further incubated with 20 U/mL IL-1β and 20 U/mL TNF-α for 24 h. After washing the cells with PBS, the cells were incubated in the presence of 5 μM of MTX derivatives for 5 h. The uptake of MTX derivatives was quantified by measuring the fluorescence emission for each sample. (A) The representative histogram of control (blue) and knockdown of NFKBIE (dark red). The mean fluorescent intensity (MFI) per cell, expressed in arbitrary units, was then determined using a flow cytometer. (B) The summary results. In addition to these experiments, after incubating with MTX derivatives (5 μM) for 5 h and washing cells with PBS, cells were chased for 6 h exclusively in RPMI supplemented with 10% FBS. Subsequently, the MFI per cell was measured at 0 and 6 h. On the basis of these results, differences in the efflux of MTX derivatives between control and NFKBIE knockdown were studied (C). Each column and its corresponding vertical lines represent the mean and the standard error of the mean (SEM) of triplicate cultures. Statistical significance was analyzed with the unpaired t -test (* p

    Techniques Used: Cell Culture, Transfection, Incubation, Fluorescence, Flow Cytometry, Cytometry

    Effects of NFKBIE knockdown on the expression levels of SLC19A1 and ABC transporters. Quantitative gene expressions of NFKBIE (A), SLC19A1 (B), ABCC1 (C), ABCC5 (D), and ABCG2 (E) genes in control (gray) and NFKBIE knockdown (black) MH7A treated with or without 0.01, 0.1, 1, 5, and 10 μM methotrexate (MTX) application for 24 h in the presence or absence of 20 U/mL IL-1β and 20 U/mL TNF-α were measured by qRT-PCR. Statistical significance was analyzed using the unpaired t -test (* p
    Figure Legend Snippet: Effects of NFKBIE knockdown on the expression levels of SLC19A1 and ABC transporters. Quantitative gene expressions of NFKBIE (A), SLC19A1 (B), ABCC1 (C), ABCC5 (D), and ABCG2 (E) genes in control (gray) and NFKBIE knockdown (black) MH7A treated with or without 0.01, 0.1, 1, 5, and 10 μM methotrexate (MTX) application for 24 h in the presence or absence of 20 U/mL IL-1β and 20 U/mL TNF-α were measured by qRT-PCR. Statistical significance was analyzed using the unpaired t -test (* p

    Techniques Used: Expressing, Quantitative RT-PCR

    Effects of NFKBIE knockdown on the expressions of MTX-metabolizing enzymes. Quantitative gene expressions of FPGS (A), GGH (B), DHFR (C), TYMS (D), MTHFR (E), and ATIC (F) genes in control (gray) and NFKBIE knockdown (black) MH7A. Those cells were treated with or without 0.01, 0.1, 1, 5, and 10 μM methotrexate (MTX) application for 24 h in the presence or absence of 20 U/mL IL-1β and 20 U/mL TNF-α. The expression levels of each gene were measured by qRT-PCR. Statistical significance was analyzed by the unpaired t -test (* p
    Figure Legend Snippet: Effects of NFKBIE knockdown on the expressions of MTX-metabolizing enzymes. Quantitative gene expressions of FPGS (A), GGH (B), DHFR (C), TYMS (D), MTHFR (E), and ATIC (F) genes in control (gray) and NFKBIE knockdown (black) MH7A. Those cells were treated with or without 0.01, 0.1, 1, 5, and 10 μM methotrexate (MTX) application for 24 h in the presence or absence of 20 U/mL IL-1β and 20 U/mL TNF-α. The expression levels of each gene were measured by qRT-PCR. Statistical significance was analyzed by the unpaired t -test (* p

    Techniques Used: Expressing, Quantitative RT-PCR

    7) Product Images from "MicroRNAs and histone deacetylase inhibition-mediated protection against inflammatory β-cell damage"

    Article Title: MicroRNAs and histone deacetylase inhibition-mediated protection against inflammatory β-cell damage

    Journal: PLoS ONE

    doi: 10.1371/journal.pone.0203713

    Expression of selected miRs in INS1 cells. INS1 cells were left untreated, treated with 1 μM of the KDACi CI994 or 125 nM Givinostat (Giv) 1 h prior to the addition of 150 pg/ml IL-1β and 0.1 ng/ml IFN-γ (Cyt) or no cytokines for 6 h, 18 h or 24 h. MiR-enriched total RNA was purified, and the expression of specific miRs was measured with qRT-PCR and normalized to the geometric mean of the housekeeping miRs miR-103a and miR-423. Data are presented as mean ± SEM (n = 9–10) of 2 -ΔCT . Statistical significance of a paired t-test is shown in the graphs (*p
    Figure Legend Snippet: Expression of selected miRs in INS1 cells. INS1 cells were left untreated, treated with 1 μM of the KDACi CI994 or 125 nM Givinostat (Giv) 1 h prior to the addition of 150 pg/ml IL-1β and 0.1 ng/ml IFN-γ (Cyt) or no cytokines for 6 h, 18 h or 24 h. MiR-enriched total RNA was purified, and the expression of specific miRs was measured with qRT-PCR and normalized to the geometric mean of the housekeeping miRs miR-103a and miR-423. Data are presented as mean ± SEM (n = 9–10) of 2 -ΔCT . Statistical significance of a paired t-test is shown in the graphs (*p

    Techniques Used: Expressing, Purification, Quantitative RT-PCR

    KDACi reduces cytokine-induced expression of miR-146a-5p in human islets. (A) Human islets from three individual necro-donors were treated with or without 500 nM Givinostat (Giv) 1 h prior to addition of 300 pg/ml IL-1β, 10 ng/ml IFN-γ, and 10 ng/ml TNF-α (Mix) or no cytokines (Ctrl) for 24 h. miR-146a-5p expression was measured with qRT-PCR and normalized to the geometric mean of the housekeeping miRs miR-103a and miR-423. Data are presented as mean ± SEM of 2 -ΔCT . *p
    Figure Legend Snippet: KDACi reduces cytokine-induced expression of miR-146a-5p in human islets. (A) Human islets from three individual necro-donors were treated with or without 500 nM Givinostat (Giv) 1 h prior to addition of 300 pg/ml IL-1β, 10 ng/ml IFN-γ, and 10 ng/ml TNF-α (Mix) or no cytokines (Ctrl) for 24 h. miR-146a-5p expression was measured with qRT-PCR and normalized to the geometric mean of the housekeeping miRs miR-103a and miR-423. Data are presented as mean ± SEM of 2 -ΔCT . *p

    Techniques Used: Expressing, Quantitative RT-PCR

    miR-146a-5p expression in α- and β-cell lines. (A) INS1 cells were exposed to IL-1β (160 pg/ml) for 6 h, 12 h and 24 h. The expression of miR-146a-5p normalized to the internal control let-7c was quantified with qRT-PCR. Mean ± SEM (n = 5). (B) INS1 cells were exposed to IL-1β (160 pg/ml), IFN-γ (5ng/ml) or TNF-α (10 ng/ml) or a mixture of all three cytokines for 8 h. The expression of miR-146a-5p normalized to the internal control let-7c was quantified with qRT-PCR. Mean ± SEM (n = 3). (C) The Luciferase promoter assay was conducted in INS1 cells exposed to IL-1β (160 pg/ml) for 6 h or IL-1β (160 pg/ml) and IFN-γ (5 ng/ml) for 6 h. The cells were pre-treated with transient transfection mix containing both miR-146a-5p promoter construct and a Renilla construct. Mean ± SEM (n = 4). (D) miR-146a-5p expression in the INSrαβ cell line with or without induced Pdx-1 by addition of doxycycline for 24 h prior to cytokine exposure to IL-1β (150 pg/ml) for 2 h, 12 h, or 24 h. The expression of miR-146a-5p and let-7c was quantified using qRT-PCR. Mean ± SEM (n = 4–5). (E) α-TC1 and β-TC3 cells were exposed for 24 h to IL-1β (160 pg/ml) or IL-1β (160 pg/ml) and IFN-γ (5 ng/ml). The expressions of both miR-146a-5p and the internal control let-7c were quantified by qRT-PCR. Mean ± SEM (n = 6–8). *p
    Figure Legend Snippet: miR-146a-5p expression in α- and β-cell lines. (A) INS1 cells were exposed to IL-1β (160 pg/ml) for 6 h, 12 h and 24 h. The expression of miR-146a-5p normalized to the internal control let-7c was quantified with qRT-PCR. Mean ± SEM (n = 5). (B) INS1 cells were exposed to IL-1β (160 pg/ml), IFN-γ (5ng/ml) or TNF-α (10 ng/ml) or a mixture of all three cytokines for 8 h. The expression of miR-146a-5p normalized to the internal control let-7c was quantified with qRT-PCR. Mean ± SEM (n = 3). (C) The Luciferase promoter assay was conducted in INS1 cells exposed to IL-1β (160 pg/ml) for 6 h or IL-1β (160 pg/ml) and IFN-γ (5 ng/ml) for 6 h. The cells were pre-treated with transient transfection mix containing both miR-146a-5p promoter construct and a Renilla construct. Mean ± SEM (n = 4). (D) miR-146a-5p expression in the INSrαβ cell line with or without induced Pdx-1 by addition of doxycycline for 24 h prior to cytokine exposure to IL-1β (150 pg/ml) for 2 h, 12 h, or 24 h. The expression of miR-146a-5p and let-7c was quantified using qRT-PCR. Mean ± SEM (n = 4–5). (E) α-TC1 and β-TC3 cells were exposed for 24 h to IL-1β (160 pg/ml) or IL-1β (160 pg/ml) and IFN-γ (5 ng/ml). The expressions of both miR-146a-5p and the internal control let-7c were quantified by qRT-PCR. Mean ± SEM (n = 6–8). *p

    Techniques Used: Expressing, Quantitative RT-PCR, Luciferase, Promoter Assay, Transfection, Construct

    miR-146a-5p overexpression inhibits NF-κB signaling and blocks iNOS expression. (A) The Luciferase promoter assay was performed in INS1 cells with a NF-κB promoter construct driving Firefly luciferase. The cells were pre-treated with transient transfection mix containing both miR-146a-5p promoter construct and a Renilla construct as internal control. Additionally, the INS1 cells were transiently transfected with a control oligo or a synthetic miR-146a-5p oligo, and exposed to media with or without IL-1β (160 pg/ml) for 6 h. The relative fold change in ratio between Firefly/Renilla luciferase is plotted. Mean ± SEM (n = 4). (B) iNOS activity was measured by luciferase assay as described above. Mean ± SEM (n = 4). (C) NO in medium from INS1 cells transfected with either a control oligo or a synthetic miR-146a-5p 24 h prior to exposure to IL-1β (160 pg/ml) and IFN-γ (5 ng/ml). Mean ± SEM (n = 4). (D) iNOS protein expression was analyzed by Western blotting from INS1 cells transfected with either a control oligo or a synthetic miR-146a-5p 24 h prior to exposure to IL-1β (160 pg/ml) and IFN-γ (5 ng/ml). Mean ± SEM (n = 4). *p
    Figure Legend Snippet: miR-146a-5p overexpression inhibits NF-κB signaling and blocks iNOS expression. (A) The Luciferase promoter assay was performed in INS1 cells with a NF-κB promoter construct driving Firefly luciferase. The cells were pre-treated with transient transfection mix containing both miR-146a-5p promoter construct and a Renilla construct as internal control. Additionally, the INS1 cells were transiently transfected with a control oligo or a synthetic miR-146a-5p oligo, and exposed to media with or without IL-1β (160 pg/ml) for 6 h. The relative fold change in ratio between Firefly/Renilla luciferase is plotted. Mean ± SEM (n = 4). (B) iNOS activity was measured by luciferase assay as described above. Mean ± SEM (n = 4). (C) NO in medium from INS1 cells transfected with either a control oligo or a synthetic miR-146a-5p 24 h prior to exposure to IL-1β (160 pg/ml) and IFN-γ (5 ng/ml). Mean ± SEM (n = 4). (D) iNOS protein expression was analyzed by Western blotting from INS1 cells transfected with either a control oligo or a synthetic miR-146a-5p 24 h prior to exposure to IL-1β (160 pg/ml) and IFN-γ (5 ng/ml). Mean ± SEM (n = 4). *p

    Techniques Used: Over Expression, Expressing, Luciferase, Promoter Assay, Construct, Transfection, Activity Assay, Western Blot

    miR-146a-5p inhibits IL-1β-induced phosphorylation of JNK, p38 and ERK MAPK. Representative Western blot of TRAF6, p-JNK1/2, p-p38, p-ERK1/2, and β-actin (n = 4). INS1 cells were transiently transfected with a negative control oligo or a synthetic miR-146a-5p oligo for 48 h, and exposed to media with or without IL-1β (160 pg/ml) for 30 min.
    Figure Legend Snippet: miR-146a-5p inhibits IL-1β-induced phosphorylation of JNK, p38 and ERK MAPK. Representative Western blot of TRAF6, p-JNK1/2, p-p38, p-ERK1/2, and β-actin (n = 4). INS1 cells were transiently transfected with a negative control oligo or a synthetic miR-146a-5p oligo for 48 h, and exposed to media with or without IL-1β (160 pg/ml) for 30 min.

    Techniques Used: Western Blot, Transfection, Negative Control

    8) Product Images from "MCP-induced protein 1 suppresses TNF?-induced VCAM-1 expression in human endothelial cells"

    Article Title: MCP-induced protein 1 suppresses TNF?-induced VCAM-1 expression in human endothelial cells

    Journal: FEBS letters

    doi: 10.1016/j.febslet.2010.05.040

    TNFα-induced expression of MCPIP1 in HUVECs. (A) Confluent HUVECs were treated with 10 ng/ml TNFα, 10 ng/ml IL-1β, 1 μg/ml LPS or 5 μg/ml OxLDL for 8 h. Total protein was extracted, and the expression of MCPIP1
    Figure Legend Snippet: TNFα-induced expression of MCPIP1 in HUVECs. (A) Confluent HUVECs were treated with 10 ng/ml TNFα, 10 ng/ml IL-1β, 1 μg/ml LPS or 5 μg/ml OxLDL for 8 h. Total protein was extracted, and the expression of MCPIP1

    Techniques Used: Expressing

    9) Product Images from "Plasticity of fibroblasts demonstrated by tissue-specific and function-related proteome profiling"

    Article Title: Plasticity of fibroblasts demonstrated by tissue-specific and function-related proteome profiling

    Journal: Clinical Proteomics

    doi: 10.1186/1559-0275-11-41

    Up - regulation of selected proteins in the cell supernatant of fibroblasts upon IL-1β treatment. Successful inflammatory activation in fibroblasts upon IL-1β treatment was demonstrated by up-regulation of known inflammation-induced proteins. The mean number of distinct peptides identified per protein in the respective cell supernatants, determined from at least three independent experiments, was used. Significant up-regulation was determined using the Chi-squared test (*, p
    Figure Legend Snippet: Up - regulation of selected proteins in the cell supernatant of fibroblasts upon IL-1β treatment. Successful inflammatory activation in fibroblasts upon IL-1β treatment was demonstrated by up-regulation of known inflammation-induced proteins. The mean number of distinct peptides identified per protein in the respective cell supernatants, determined from at least three independent experiments, was used. Significant up-regulation was determined using the Chi-squared test (*, p

    Techniques Used: Activation Assay

    Proteins which are found in all kinds of fibroblasts. Based on the proteome profiles of skin, bone marrow (BM), lung and liver fibroblasts in different functional states, a semi-quantitative assessment of selected proteins in these cells was performed using the corresponding emPAI values (see Methods). The emPAI values for all sub-cellular fractions are visualized by colored cell symbols, increased color intensities corresponding to increased protein abundances. Con, non-activated control cells; +IL-1β, IL-1β treated cells; Cyt, cytoplasmic fraction; SN, cell supernatant; Nuc, nuclear fraction; NHLF, normal human lung fibroblasts; MM, derived from multiple myeloma patients; HCC, derived from hepatocellular carcinoma patients.
    Figure Legend Snippet: Proteins which are found in all kinds of fibroblasts. Based on the proteome profiles of skin, bone marrow (BM), lung and liver fibroblasts in different functional states, a semi-quantitative assessment of selected proteins in these cells was performed using the corresponding emPAI values (see Methods). The emPAI values for all sub-cellular fractions are visualized by colored cell symbols, increased color intensities corresponding to increased protein abundances. Con, non-activated control cells; +IL-1β, IL-1β treated cells; Cyt, cytoplasmic fraction; SN, cell supernatant; Nuc, nuclear fraction; NHLF, normal human lung fibroblasts; MM, derived from multiple myeloma patients; HCC, derived from hepatocellular carcinoma patients.

    Techniques Used: Functional Assay, Derivative Assay

    10) Product Images from "TNF‐α has both stimulatory and inhibitory effects on mouse monocyte‐derived osteoclastogenesis. TNF‐α has both stimulatory and inhibitory effects on mouse monocyte‐derived osteoclastogenesis"

    Article Title: TNF‐α has both stimulatory and inhibitory effects on mouse monocyte‐derived osteoclastogenesis. TNF‐α has both stimulatory and inhibitory effects on mouse monocyte‐derived osteoclastogenesis

    Journal: Journal of Cellular Physiology

    doi: 10.1002/jcp.26024

    The inflammatory cytokines IL‐1β and IL‐6 cannot overcome the inhibitory effect of TNF‐α on monocytes’ osteoclastogenesis. (a) Micrographs of monocyte cultures on plastic with the combination of different cytokines. Cells were visualized with TRAcP staining (purple) and nuclei were counterstained with DAPI (blue). TRAcP + cells with more than two nuclei were counted as osteoclasts. Scale bar = 100 μm. (b) Counting results of these nine different culture conditions. ( n = 6, ** p
    Figure Legend Snippet: The inflammatory cytokines IL‐1β and IL‐6 cannot overcome the inhibitory effect of TNF‐α on monocytes’ osteoclastogenesis. (a) Micrographs of monocyte cultures on plastic with the combination of different cytokines. Cells were visualized with TRAcP staining (purple) and nuclei were counterstained with DAPI (blue). TRAcP + cells with more than two nuclei were counted as osteoclasts. Scale bar = 100 μm. (b) Counting results of these nine different culture conditions. ( n = 6, ** p

    Techniques Used: Staining

    11) Product Images from "Pharmacological Evidences for Curcumin Neuroprotective Effects against Lead-Induced Neurodegeneration: Possible Role of Akt/GSK3 Signaling Pathway"

    Article Title: Pharmacological Evidences for Curcumin Neuroprotective Effects against Lead-Induced Neurodegeneration: Possible Role of Akt/GSK3 Signaling Pathway

    Journal: Iranian Journal of Pharmaceutical Research : IJPR

    doi: 10.22037/ijpr.2020.1101210

    Effects of various doses of Curcumin (10, 20, 40 and 60 mg/kg) on Lead -induced alteration in TNF-α (A) and IL-1β (B) level in rat isolated hippocampus
    Figure Legend Snippet: Effects of various doses of Curcumin (10, 20, 40 and 60 mg/kg) on Lead -induced alteration in TNF-α (A) and IL-1β (B) level in rat isolated hippocampus

    Techniques Used: Isolation

    12) Product Images from "Swine Influenza Virus PA and Neuraminidase Gene Reassortment into Human H1N1 Influenza Virus Is Associated with an Altered Pathogenic Phenotype Linked to Increased MIP-2 Expression"

    Article Title: Swine Influenza Virus PA and Neuraminidase Gene Reassortment into Human H1N1 Influenza Virus Is Associated with an Altered Pathogenic Phenotype Linked to Increased MIP-2 Expression

    Journal: Journal of Virology

    doi: 10.1128/JVI.00087-15

    Early expression of proinflammatory cytokines linked to rILL346 infection. Proinflammatory cytokine expression levels in the BAL fluid of mice infected with rILL346, rILL18, huH1N1, and swH1N2 were evaluated at days 2 and 4 p.i. BALB/c mice ( n = 5) were intranasally infected with 5 × 10 5 PFU of virus. At days 2 and 4 p.i., bronchoalveolar lavage (BAL) fluid was collected from infected mice. The BAL fluid was examined for expression of IL-6 (A), IFN-γ (B), IL-1β (C), and TNF-α (D) by a Luminex Bio-Plex 200. All data are representative of three individual experiments. Asterisks denote significance related to the pH1N1 parental virus while number signs (#) represent P values significant compared to the rILL18 reassortant virus. Results were considered significant with P values of ≤0.05 (*/#), ≤0.01 (**/##), and ≤0.001 (***/###).
    Figure Legend Snippet: Early expression of proinflammatory cytokines linked to rILL346 infection. Proinflammatory cytokine expression levels in the BAL fluid of mice infected with rILL346, rILL18, huH1N1, and swH1N2 were evaluated at days 2 and 4 p.i. BALB/c mice ( n = 5) were intranasally infected with 5 × 10 5 PFU of virus. At days 2 and 4 p.i., bronchoalveolar lavage (BAL) fluid was collected from infected mice. The BAL fluid was examined for expression of IL-6 (A), IFN-γ (B), IL-1β (C), and TNF-α (D) by a Luminex Bio-Plex 200. All data are representative of three individual experiments. Asterisks denote significance related to the pH1N1 parental virus while number signs (#) represent P values significant compared to the rILL18 reassortant virus. Results were considered significant with P values of ≤0.05 (*/#), ≤0.01 (**/##), and ≤0.001 (***/###).

    Techniques Used: Expressing, Infection, Mouse Assay, Luminex

    13) Product Images from "Inflammation-induced Gro1 triggers senescence in neuronal progenitors: effects of estradiol"

    Article Title: Inflammation-induced Gro1 triggers senescence in neuronal progenitors: effects of estradiol

    Journal: Journal of Neuroinflammation

    doi: 10.1186/s12974-018-1298-y

    Proinflammatory cytokines induce Gro1 expression in human and murine hippocampal NPC. a mRNA levels of growth factors in hNPC treated with IL-1β (10 ng/mL) for 10 days. Data are shown as mean ± SEM of three independent experiments. All samples from three experiments were run together in triplicate and normalized against GAPDH. Results are expressed in fold change vs untreated control taken as 1; ** p
    Figure Legend Snippet: Proinflammatory cytokines induce Gro1 expression in human and murine hippocampal NPC. a mRNA levels of growth factors in hNPC treated with IL-1β (10 ng/mL) for 10 days. Data are shown as mean ± SEM of three independent experiments. All samples from three experiments were run together in triplicate and normalized against GAPDH. Results are expressed in fold change vs untreated control taken as 1; ** p

    Techniques Used: Expressing

    14) Product Images from "H3 Relaxin Alleviates Migration, Apoptosis and Pyroptosis Through P2X7R-Mediated Nucleotide Binding Oligomerization Domain-Like Receptor Protein 3 Inflammasome Activation in Retinopathy Induced by Hyperglycemia"

    Article Title: H3 Relaxin Alleviates Migration, Apoptosis and Pyroptosis Through P2X7R-Mediated Nucleotide Binding Oligomerization Domain-Like Receptor Protein 3 Inflammasome Activation in Retinopathy Induced by Hyperglycemia

    Journal: Frontiers in Pharmacology

    doi: 10.3389/fphar.2020.603689

    H3 relaxin alleviated NLRP3 inflammasome activation, apoptosis, pyroptosis and migration in hRMECs. (A) The protein levels of IL-1β and IL-18 in cell culture media. (B) The protein expression of NLRP3 inflammasome and inflammatory cytolines were evaluated by western blot. (C) The protein expression of cleaved caspase-3, cleaved caspase-9, cleaved caspase-8 and GSDMD were evaluated by western blot. (D) The protein expression of VE-cadherin, ZO-1, occludin, MMP2 and MMP9 were evaluated by western blot. (E) The apoptosis in hRMECs were observed by transmission electron microscopy. (original magnification, ×5,000). Ultrastructural evaluation was performed: The majority of hRMECs treated by AGE-BSA showed apoptosis in early and middle phase. After H3 relaxin or/and insulin treatment, hRMECs were noticed improvement in early phase of apoptosis. Medullary corpuscles (arrow) can be noticed. (F,G) Cell apoptosis was measured by flow cytometry. (H,I) Wound-healing assay of hRMECs (Scale bar = 200 µm). (J,K) Transwell assay of hRMECs (Scale bar = 200 µm). Data are the means ± SD, and each measurement was repeated six times. ## p
    Figure Legend Snippet: H3 relaxin alleviated NLRP3 inflammasome activation, apoptosis, pyroptosis and migration in hRMECs. (A) The protein levels of IL-1β and IL-18 in cell culture media. (B) The protein expression of NLRP3 inflammasome and inflammatory cytolines were evaluated by western blot. (C) The protein expression of cleaved caspase-3, cleaved caspase-9, cleaved caspase-8 and GSDMD were evaluated by western blot. (D) The protein expression of VE-cadherin, ZO-1, occludin, MMP2 and MMP9 were evaluated by western blot. (E) The apoptosis in hRMECs were observed by transmission electron microscopy. (original magnification, ×5,000). Ultrastructural evaluation was performed: The majority of hRMECs treated by AGE-BSA showed apoptosis in early and middle phase. After H3 relaxin or/and insulin treatment, hRMECs were noticed improvement in early phase of apoptosis. Medullary corpuscles (arrow) can be noticed. (F,G) Cell apoptosis was measured by flow cytometry. (H,I) Wound-healing assay of hRMECs (Scale bar = 200 µm). (J,K) Transwell assay of hRMECs (Scale bar = 200 µm). Data are the means ± SD, and each measurement was repeated six times. ## p

    Techniques Used: Activation Assay, Migration, Cell Culture, Expressing, Western Blot, Transmission Assay, Electron Microscopy, Flow Cytometry, Wound Healing Assay, Transwell Assay

    Effect of H3 relaxin treatment on inflammation and apoptosis in retinas of diabetic rats. (A) The expression of IL-1β at 4 and 8 weeks in the plasma of diabetic rats. (B) The expression of IL-18 at 4 and 8 weeks in the plasma of diabetic rats. (C) The expression of TNF-α at 4 and 8 weeks in the plasma of diabetic rats. (D) The expression of VEGF at 4 and 8 weeks in the plasma of diabetic rats. (E) The protein expression of NLRP3 inflammasome and inflammatory cytolines at 4 and 8 weeks were evaluated by western blot. (F) The expression of apoptosis-related protein at 4 and 8 weeks were evaluated by western blot. Data are the means ± SD, and each measurement was repeated six times. # p
    Figure Legend Snippet: Effect of H3 relaxin treatment on inflammation and apoptosis in retinas of diabetic rats. (A) The expression of IL-1β at 4 and 8 weeks in the plasma of diabetic rats. (B) The expression of IL-18 at 4 and 8 weeks in the plasma of diabetic rats. (C) The expression of TNF-α at 4 and 8 weeks in the plasma of diabetic rats. (D) The expression of VEGF at 4 and 8 weeks in the plasma of diabetic rats. (E) The protein expression of NLRP3 inflammasome and inflammatory cytolines at 4 and 8 weeks were evaluated by western blot. (F) The expression of apoptosis-related protein at 4 and 8 weeks were evaluated by western blot. Data are the means ± SD, and each measurement was repeated six times. # p

    Techniques Used: Expressing, Western Blot

    15) Product Images from "?-Tocopherol and its major metabolite, in contrast to ?-tocopherol, inhibit cyclooxygenase activity in macrophages and epithelial cells"

    Article Title: ?-Tocopherol and its major metabolite, in contrast to ?-tocopherol, inhibit cyclooxygenase activity in macrophages and epithelial cells

    Journal: Proceedings of the National Academy of Sciences of the United States of America

    doi:

    Inhibition of COX activity by postincubation with γT and γ-CEHC in COX-2-preinduced A549 cells. A549 cells were pretreated with IL-1β (10 ng/ml) for 24 h. ( A ) Cells were washed and incubated with fresh medium containing vehicle or γ-CEHC for 1 h. AA at final concentrations of 5 or 15 μM was added and incubated at 37°C for 10 min. ( B ) For γT, the postincubation period was extended to 24 h. Medium was then removed and replaced with a fresh one containing 10 or 30 μM AA at 37°C for 10 min. ( C ) Cells were postincubated with γT (10 μM) for 1, 8, or 24 h and COX-2 activity was measured as described in B . All reactions were stopped by the addition of 0.5 mM aspirin and PGE 2 in the medium was measured. COX activity (%) is expressed as the ratio of PGE 2 produced in the presence of γT or γ-CEHC to that with vehicle alone. Numbers within brackets indicate the final concentrations of AA. *, P
    Figure Legend Snippet: Inhibition of COX activity by postincubation with γT and γ-CEHC in COX-2-preinduced A549 cells. A549 cells were pretreated with IL-1β (10 ng/ml) for 24 h. ( A ) Cells were washed and incubated with fresh medium containing vehicle or γ-CEHC for 1 h. AA at final concentrations of 5 or 15 μM was added and incubated at 37°C for 10 min. ( B ) For γT, the postincubation period was extended to 24 h. Medium was then removed and replaced with a fresh one containing 10 or 30 μM AA at 37°C for 10 min. ( C ) Cells were postincubated with γT (10 μM) for 1, 8, or 24 h and COX-2 activity was measured as described in B . All reactions were stopped by the addition of 0.5 mM aspirin and PGE 2 in the medium was measured. COX activity (%) is expressed as the ratio of PGE 2 produced in the presence of γT or γ-CEHC to that with vehicle alone. Numbers within brackets indicate the final concentrations of AA. *, P

    Techniques Used: Inhibition, Activity Assay, Incubation, Produced

    16) Product Images from "Long Non-coding RNAs Are Central Regulators of the IL-1β-Induced Inflammatory Response in Normal and Idiopathic Pulmonary Lung Fibroblasts"

    Article Title: Long Non-coding RNAs Are Central Regulators of the IL-1β-Induced Inflammatory Response in Normal and Idiopathic Pulmonary Lung Fibroblasts

    Journal: Frontiers in Immunology

    doi: 10.3389/fimmu.2018.02906

    IL7AS and MIR3142HG regulate the IL-1β-stimulated inflammatory response in control fibroblasts. Control fibroblasts were transfected overnight with LNA antisense sequences against IL7AS (A/C/E/G) and MIR3142HG (B/D/F/H) or scrambled (negative) controls. Cell were then stimulated with IL-1β for 24 h prior to isolation of RNA and measurement of IL7AS (A) or MIR3142HG (B) by qRT-PCR or measurement of supernatant IL-6 (C,D) , IL-8 (E,F) , and CCL2 (G,H) by ELISA. Data represents the mean ± SEM of five control individuals. Following normalization against the IL1β-stimulated cells (100%), statistical significance was assessed (vs. IL1β-stimulated cells) using the repeat measures 1-way analysis of variance (ANOVA) with a Dunnett's test where * p
    Figure Legend Snippet: IL7AS and MIR3142HG regulate the IL-1β-stimulated inflammatory response in control fibroblasts. Control fibroblasts were transfected overnight with LNA antisense sequences against IL7AS (A/C/E/G) and MIR3142HG (B/D/F/H) or scrambled (negative) controls. Cell were then stimulated with IL-1β for 24 h prior to isolation of RNA and measurement of IL7AS (A) or MIR3142HG (B) by qRT-PCR or measurement of supernatant IL-6 (C,D) , IL-8 (E,F) , and CCL2 (G,H) by ELISA. Data represents the mean ± SEM of five control individuals. Following normalization against the IL1β-stimulated cells (100%), statistical significance was assessed (vs. IL1β-stimulated cells) using the repeat measures 1-way analysis of variance (ANOVA) with a Dunnett's test where * p

    Techniques Used: Transfection, Isolation, Quantitative RT-PCR, Enzyme-linked Immunosorbent Assay

    IL-1β-induced expression of IL7AS, MIR3142HG, and the inflammatory mediators is mediated via the NF-κB signaling pathway in control and IPF fibroblasts. Control and IPF fibroblasts were pre-incubated in the stated concentration of TPCA-1 or 0.1% (v/v) DMSO (vehicle) and then incubated in absence or presence of IL-1β for 24 h prior to measurement of IL6, IL8 and CCL2 release (A) and IL7AS and MIR3142HG expression (B) . Data is normalized against IL-1β stimulated cells (100%) and represents the mean ± SEM of five control and IPF patients. The logIC 50 for each individual was determined in GraphPad Prism and comparison between control and IPF groups was performed using an unpaired t -test. The IC 50 was calculated from the mean logIC 50 values.
    Figure Legend Snippet: IL-1β-induced expression of IL7AS, MIR3142HG, and the inflammatory mediators is mediated via the NF-κB signaling pathway in control and IPF fibroblasts. Control and IPF fibroblasts were pre-incubated in the stated concentration of TPCA-1 or 0.1% (v/v) DMSO (vehicle) and then incubated in absence or presence of IL-1β for 24 h prior to measurement of IL6, IL8 and CCL2 release (A) and IL7AS and MIR3142HG expression (B) . Data is normalized against IL-1β stimulated cells (100%) and represents the mean ± SEM of five control and IPF patients. The logIC 50 for each individual was determined in GraphPad Prism and comparison between control and IPF groups was performed using an unpaired t -test. The IC 50 was calculated from the mean logIC 50 values.

    Techniques Used: Expressing, Incubation, Concentration Assay

    Differential expression of mRNAs and lncRNAs following IL-1β-stimulation of control lung fibroblasts . (A) Heat map showing the differential expression of mRNAs in control fibroblasts following IL-1β stimulation for 6 h. (B) Pathway analysis of up-regulated mRNAs. (C) Top 10 most highly expressed lncRNA in non-stimulated control fibroblasts. (D) Heat map showing the differential expression of lncRNAs in control fibroblasts following IL-1β stimulation for 6 h.
    Figure Legend Snippet: Differential expression of mRNAs and lncRNAs following IL-1β-stimulation of control lung fibroblasts . (A) Heat map showing the differential expression of mRNAs in control fibroblasts following IL-1β stimulation for 6 h. (B) Pathway analysis of up-regulated mRNAs. (C) Top 10 most highly expressed lncRNA in non-stimulated control fibroblasts. (D) Heat map showing the differential expression of lncRNAs in control fibroblasts following IL-1β stimulation for 6 h.

    Techniques Used: Expressing

    IL7AS but not MIR3142HG regulates the IL-β-stimulated inflammatory response in IPF fibroblasts. IPF fibroblasts were transfected overnight with LNA antisense sequences against IL7AS (A,C,E,G) and MIR3142HG (B,D,F,H) or scrambled (negative) controls. Cell were then stimulated with IL-1β for 24 h prior to isolation of RNA and measurement of IL7AS (A) or MIR3142HG (B) by qRT-PCR or measurement of supernatant IL-6 (C,D) , IL-8 (E,F) , and CCL2 (G,H) by ELISA. Data represents the mean ± SEM of five IPF individuals. Following normalization against the IL1β-stimulated cells (100%), statistical significance was assessed (vs. IL1β-stimulated cells) using the repeat measures 1-way analysis of variance (ANOVA) with a Dunnett's test where * p
    Figure Legend Snippet: IL7AS but not MIR3142HG regulates the IL-β-stimulated inflammatory response in IPF fibroblasts. IPF fibroblasts were transfected overnight with LNA antisense sequences against IL7AS (A,C,E,G) and MIR3142HG (B,D,F,H) or scrambled (negative) controls. Cell were then stimulated with IL-1β for 24 h prior to isolation of RNA and measurement of IL7AS (A) or MIR3142HG (B) by qRT-PCR or measurement of supernatant IL-6 (C,D) , IL-8 (E,F) , and CCL2 (G,H) by ELISA. Data represents the mean ± SEM of five IPF individuals. Following normalization against the IL1β-stimulated cells (100%), statistical significance was assessed (vs. IL1β-stimulated cells) using the repeat measures 1-way analysis of variance (ANOVA) with a Dunnett's test where * p

    Techniques Used: Transfection, Isolation, Quantitative RT-PCR, Enzyme-linked Immunosorbent Assay

    IL-1β-induced expression of IL7AS, MIR3142HG, miR-146a, miR-3142 and inflammatory mediators in control and IPF fibroblasts . (A) Control and IPF fibroblasts were incubated in the absence of presence of IL-1β for 24 h and the fold-change in the IL7AS and MIR3142 expression determined by qRT-PCR, (B) Aligned sequencing data (merged BAM files) showing MIR3142HG from control and IL-1β-stimulated control fibroblasts was visualized using the IGV genome browser ( https://software.broadinstitute.org/software/igv/ ). Control and IPF fibroblasts were incubated in the absence of presence of IL-1β for 24 h before determination of the fold-change in miR-3142 and miR-146a expression by qRT-PCR (C) and the release of IL-6, IL-8, and CCL2 by ELISA (D) . Values are the mean ± SEM of five control and IPF patients and statistical significance was assessed using 1-way analysis of variance (ANOVA) where * p
    Figure Legend Snippet: IL-1β-induced expression of IL7AS, MIR3142HG, miR-146a, miR-3142 and inflammatory mediators in control and IPF fibroblasts . (A) Control and IPF fibroblasts were incubated in the absence of presence of IL-1β for 24 h and the fold-change in the IL7AS and MIR3142 expression determined by qRT-PCR, (B) Aligned sequencing data (merged BAM files) showing MIR3142HG from control and IL-1β-stimulated control fibroblasts was visualized using the IGV genome browser ( https://software.broadinstitute.org/software/igv/ ). Control and IPF fibroblasts were incubated in the absence of presence of IL-1β for 24 h before determination of the fold-change in miR-3142 and miR-146a expression by qRT-PCR (C) and the release of IL-6, IL-8, and CCL2 by ELISA (D) . Values are the mean ± SEM of five control and IPF patients and statistical significance was assessed using 1-way analysis of variance (ANOVA) where * p

    Techniques Used: Expressing, Incubation, Quantitative RT-PCR, Sequencing, Software, Enzyme-linked Immunosorbent Assay

    Related Articles

    other:

    Article Title: Nicotinamide Phosphoribosyltransferase Is Essential for Interleukin-1?-mediated Dedifferentiation of Articular Chondrocytes via SIRT1 and Extracellular Signal-regulated Kinase (ERK) Complex Signaling *
    Article Snippet: For the experiment, 3-day cell cultures were treated with IL-1β (Calbiochem), lipopolysaccharide (LPS) (Sigma), phorbol 12-myristate 13-acetate (PMA) (Sigma), retinoic acid (RA) (Sigma), epidermal growth factor (EGF) (Invitrogen), transforming growth factor (TGF)-β1 (R & D Systems, Minneapolis, MN), or fibroblast growth factor (FGF) (R & D Systems) as indicated.

    Article Title: Transcription of Liver X Receptor Is Down-Regulated by 15-Deoxy-?12,14-Prostaglandin J2 through Oxidative Stress in Human Neutrophils
    Article Snippet: Chemicals and Reagents Phorbol 12-myristate 13-acetate (PMA), phenylarsine oxide, reduced glutathione (GSH), diethylester maleic acid (DEM), 2,2,6,6-tetramethyl-piperidine-1-oxyl (TEMPO), formyl-Met-Leu-Phe (fMLP), diisopropyl fluorophosphate (DFP), IL-1β, IL-8, TNFα, SP600125, and the vitamin E (Vit E) analog 6-hydroxy-2,5,7,8-tetramethylchroman-2-carboxylic acid were purchased from Sigma-Aldrich (Madrid, Spain).

    Article Title: TLR signaling adaptor protein MyD88 in primary sensory neurons contributes to persistent inflammatory and neuropathic pain and neuroinflammation
    Article Snippet: Reagents We purchased CFA, formalin, IL-1β, paraformaldehyde, DNAse I and Opti MEM culture medium from Sigma-Aldrich Company (St.

    Multiplex Assay:

    Article Title: Differential host response to LPS variants in amniochorion and the TLR4/MD-2 system in Macaca nemestrina
    Article Snippet: Explants were then placed in RNAlater ( Qiagen, Valencia, CA) and incubated at 4°C prior to storing at −80°C. .. Supernatants were tested for IL-1β, TNF-α, IL-6 and IL-8 using a nonhuman primate cytokine multiplex immunoassay (Millipore, Billerica, MA) with Luminex technology (Luminex Corp, Austin, TX). .. Supernatants were also assayed for PGE2 and PGF2α using commercially available ELISA kits (Cayman Chemical, Ann Arbor, MI) known to cross-react with M. nemestrina antigens.

    Article Title: The Probiotic Mixture VSL#3 Alters the Morphology and Secretion Profile of Both Polarized and Unpolarized Human Macrophages in a Polarization-Dependent Manner
    Article Snippet: Stained cells were analyzed with a FACSAria flow cytometer (BD, Franklin Lakes, NJ, USA). .. Cytokine measurement and analysis The levels of IL-1β, IL-4, IL-6, IL-10, IL-12p70, IL-23, and TNF-α in supernatants collected on days 8 and 11 were measured by multiplex assay (HTH17MAG-14K-07, EMD Millipore, Billerica, MA, USA). .. A second multiplex assay (HCYTMAG-60K-PX38, EMD Millipore) was used to measure levels of 38 cytokines and chemokines.

    Staining:

    Article Title: Bax Targeted by miR-29a Regulates Chondrocyte Apoptosis in Osteoarthritis
    Article Snippet: .. Apoptotic Assay Chondrocyte-like ATDC5 cells were stressed with 10 ng/ml IL-1β (Sigma, St. Louis, MO, USA) for 48 h and stained with a permeable dye, Hoechst 33258 (Invitrogen, 5 μ g/ml). .. Then nuclear morphology was revealed, and images were captured by the fluorescence BX51 microscope.

    Plasmid Preparation:

    Article Title: Interleukin-1 beta induces the expression and production of stem cell factor by epithelial cells: crucial involvement of the PI-3K/mTOR pathway and HIF-1 transcription complex
    Article Snippet: Human recombinant IL-1β and SCF were produced by Dr Varani (Bellinzona, Switzerland). .. IL-1β was expressed in Escherichia coli Rosetta-gami cells with a pET21 vector (Novagen, Schaffhausen, Switzerland) and purified by ammonium sulfate precipitation followed by ion exchange and size exclusion chromatography. .. Human SCF protein was produced in E. coli and purified following published protocols.

    Purification:

    Article Title: Interleukin-1 beta induces the expression and production of stem cell factor by epithelial cells: crucial involvement of the PI-3K/mTOR pathway and HIF-1 transcription complex
    Article Snippet: Human recombinant IL-1β and SCF were produced by Dr Varani (Bellinzona, Switzerland). .. IL-1β was expressed in Escherichia coli Rosetta-gami cells with a pET21 vector (Novagen, Schaffhausen, Switzerland) and purified by ammonium sulfate precipitation followed by ion exchange and size exclusion chromatography. .. Human SCF protein was produced in E. coli and purified following published protocols.

    Size-exclusion Chromatography:

    Article Title: Interleukin-1 beta induces the expression and production of stem cell factor by epithelial cells: crucial involvement of the PI-3K/mTOR pathway and HIF-1 transcription complex
    Article Snippet: Human recombinant IL-1β and SCF were produced by Dr Varani (Bellinzona, Switzerland). .. IL-1β was expressed in Escherichia coli Rosetta-gami cells with a pET21 vector (Novagen, Schaffhausen, Switzerland) and purified by ammonium sulfate precipitation followed by ion exchange and size exclusion chromatography. .. Human SCF protein was produced in E. coli and purified following published protocols.

    Similar Products

  • Logo
  • About
  • News
  • Press Release
  • Team
  • Advisors
  • Partners
  • Contact
  • Bioz Stars
  • Bioz vStars
  • 94
    Millipore anti il 1β
    Immunohistochemical localization of IL-1α, <t>IL-1β,</t> TNF-α and IL-6 in the median nerves from normal control rats (C) or from reach limbs of rats that performed a HRNF task for 5 weeks. No immunostaining for these cytokines is visible
    Anti Il 1β, supplied by Millipore, used in various techniques. Bioz Stars score: 94/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/anti il 1β/product/Millipore
    Average 94 stars, based on 1 article reviews
    Price from $9.99 to $1999.99
    anti il 1β - by Bioz Stars, 2021-05
    94/100 stars
      Buy from Supplier

    97
    Millipore il 1β
    Sensory neuron MyD88 contributes to intraplantar <t>IL-1β</t> induced pain hypersensitivity. (A–C ) Intraplantar injection of IL-1β induces sub-acute inflammatory pain, expressed as mechanical hyperalgesia (expresses as 50% paw withdrawal threshold; A ), allodynia (expresses as frequency response to 0.16 von Frey hair stimulation; B ) and heat hyperalgesia ( C ) in WT and MyD88 CKO mice. * P
    Il 1β, supplied by Millipore, used in various techniques. Bioz Stars score: 97/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/il 1β/product/Millipore
    Average 97 stars, based on 1 article reviews
    Price from $9.99 to $1999.99
    il 1β - by Bioz Stars, 2021-05
    97/100 stars
      Buy from Supplier

    Image Search Results


    Immunohistochemical localization of IL-1α, IL-1β, TNF-α and IL-6 in the median nerves from normal control rats (C) or from reach limbs of rats that performed a HRNF task for 5 weeks. No immunostaining for these cytokines is visible

    Journal:

    Article Title: Increase in inflammatory cytokines in median nerves in a rat model of repetitive motion injury

    doi: 10.1016/j.jneuroim.2005.06.013

    Figure Lengend Snippet: Immunohistochemical localization of IL-1α, IL-1β, TNF-α and IL-6 in the median nerves from normal control rats (C) or from reach limbs of rats that performed a HRNF task for 5 weeks. No immunostaining for these cytokines is visible

    Article Snippet: Sections were incubated over-night at room temperature with one of the following primary antibodies from Chemicon diluted with 4% goat serum in phosphate buffered saline (PBS): anti-IL-1α (Chemicon, #AB1415, 1:250), anti-IL-1β (Chemicon, #AB1832P, 1:250), anti-TNF-α (Chemicon, #AB1837P, 1:300), anti-IL-6 (Chemicon, #AB1833P, 1:250), and anti-IL-10 (Chemicon, #AB1492, 1:250).

    Techniques: Immunohistochemistry, Immunostaining

    Sensory neuron MyD88 contributes to intraplantar IL-1β induced pain hypersensitivity. (A–C ) Intraplantar injection of IL-1β induces sub-acute inflammatory pain, expressed as mechanical hyperalgesia (expresses as 50% paw withdrawal threshold; A ), allodynia (expresses as frequency response to 0.16 von Frey hair stimulation; B ) and heat hyperalgesia ( C ) in WT and MyD88 CKO mice. * P

    Journal: Scientific Reports

    Article Title: TLR signaling adaptor protein MyD88 in primary sensory neurons contributes to persistent inflammatory and neuropathic pain and neuroinflammation

    doi: 10.1038/srep28188

    Figure Lengend Snippet: Sensory neuron MyD88 contributes to intraplantar IL-1β induced pain hypersensitivity. (A–C ) Intraplantar injection of IL-1β induces sub-acute inflammatory pain, expressed as mechanical hyperalgesia (expresses as 50% paw withdrawal threshold; A ), allodynia (expresses as frequency response to 0.16 von Frey hair stimulation; B ) and heat hyperalgesia ( C ) in WT and MyD88 CKO mice. * P

    Article Snippet: Reagents We purchased CFA, formalin, IL-1β, paraformaldehyde, DNAse I and Opti MEM culture medium from Sigma-Aldrich Company (St.

    Techniques: Injection, Mouse Assay

    The HIF-1 transcription complex is crucial for IL-1β-induced SCF expression in MCF-7 cells. ( a ) Normal and HIF-1α knockdown MCF-7 cells were exposed to 8 ng/ml IL-1β for 24 h followed by detection of intracellular HIF-1α/SCF levels as well as SCF release. ( b ) Normal and HIF-1α knockdown MCF-7 cells were exposed to 8 ng/ml IL-1β for 6 h followed by analysis of HIF-1α and SCF mRNA levels by qRT-PCR. Each sample was subjected to a contamination control through running qRT-PCR immediately after the decontamination procedure. No response was detected during 55 amplification cycles, indicating that contamination levels were close to zero (and are therefore not shown in the main figure). Western blot data show one representative experiment of 3–7 that gave similar results and were quantitatively analysed. Quantitative data are shown as mean values±s.d. of 3–7 individual experiments; * P

    Journal: Cellular and Molecular Immunology

    Article Title: Interleukin-1 beta induces the expression and production of stem cell factor by epithelial cells: crucial involvement of the PI-3K/mTOR pathway and HIF-1 transcription complex

    doi: 10.1038/cmi.2014.113

    Figure Lengend Snippet: The HIF-1 transcription complex is crucial for IL-1β-induced SCF expression in MCF-7 cells. ( a ) Normal and HIF-1α knockdown MCF-7 cells were exposed to 8 ng/ml IL-1β for 24 h followed by detection of intracellular HIF-1α/SCF levels as well as SCF release. ( b ) Normal and HIF-1α knockdown MCF-7 cells were exposed to 8 ng/ml IL-1β for 6 h followed by analysis of HIF-1α and SCF mRNA levels by qRT-PCR. Each sample was subjected to a contamination control through running qRT-PCR immediately after the decontamination procedure. No response was detected during 55 amplification cycles, indicating that contamination levels were close to zero (and are therefore not shown in the main figure). Western blot data show one representative experiment of 3–7 that gave similar results and were quantitatively analysed. Quantitative data are shown as mean values±s.d. of 3–7 individual experiments; * P

    Article Snippet: IL-1β was expressed in Escherichia coli Rosetta-gami cells with a pET21 vector (Novagen, Schaffhausen, Switzerland) and purified by ammonium sulfate precipitation followed by ion exchange and size exclusion chromatography.

    Techniques: Expressing, Quantitative RT-PCR, Amplification, Western Blot

    The PI-3K/mTOR pathway is crucially involved in IL-1β-induced HIF-1α accumulation in MCF-7 cells. Cells were pre-treated with inhibitors for 1 h (as indicated) and subsequently exposed to 8 ng/ml IL-1β for 4 h. The procedure was followed by Western blot analysis of HIF-1α accumulation ( a ) and detection of PI-3K and HIF-1α PHD activities as well as phospho-S2448 mTOR deposition ( b ). HIF-1α Western blot data show one representative experiment of three similar results and were quantitatively analysed. Quantitative data are shown as mean values±s.d. of at least three individual experiments; results represent percentage values compared to the control. * P

    Journal: Cellular and Molecular Immunology

    Article Title: Interleukin-1 beta induces the expression and production of stem cell factor by epithelial cells: crucial involvement of the PI-3K/mTOR pathway and HIF-1 transcription complex

    doi: 10.1038/cmi.2014.113

    Figure Lengend Snippet: The PI-3K/mTOR pathway is crucially involved in IL-1β-induced HIF-1α accumulation in MCF-7 cells. Cells were pre-treated with inhibitors for 1 h (as indicated) and subsequently exposed to 8 ng/ml IL-1β for 4 h. The procedure was followed by Western blot analysis of HIF-1α accumulation ( a ) and detection of PI-3K and HIF-1α PHD activities as well as phospho-S2448 mTOR deposition ( b ). HIF-1α Western blot data show one representative experiment of three similar results and were quantitatively analysed. Quantitative data are shown as mean values±s.d. of at least three individual experiments; results represent percentage values compared to the control. * P

    Article Snippet: IL-1β was expressed in Escherichia coli Rosetta-gami cells with a pET21 vector (Novagen, Schaffhausen, Switzerland) and purified by ammonium sulfate precipitation followed by ion exchange and size exclusion chromatography.

    Techniques: Western Blot

    IL-1β-induced SCF production by the MCF-7 cells is a time-dependent process. MCF-7 cells were exposed to 8 ng/ml IL-1β for different periods of time followed by analysis of intracellular HIF-1α and SCF accumulation (Western blot) and SCF release (ELISA). Western blot data show one representative experiment of three which demonstrated similar results and were quantitatively analysed. Quantitative data are shown as mean values±s.d. for n =3; * P

    Journal: Cellular and Molecular Immunology

    Article Title: Interleukin-1 beta induces the expression and production of stem cell factor by epithelial cells: crucial involvement of the PI-3K/mTOR pathway and HIF-1 transcription complex

    doi: 10.1038/cmi.2014.113

    Figure Lengend Snippet: IL-1β-induced SCF production by the MCF-7 cells is a time-dependent process. MCF-7 cells were exposed to 8 ng/ml IL-1β for different periods of time followed by analysis of intracellular HIF-1α and SCF accumulation (Western blot) and SCF release (ELISA). Western blot data show one representative experiment of three which demonstrated similar results and were quantitatively analysed. Quantitative data are shown as mean values±s.d. for n =3; * P

    Article Snippet: IL-1β was expressed in Escherichia coli Rosetta-gami cells with a pET21 vector (Novagen, Schaffhausen, Switzerland) and purified by ammonium sulfate precipitation followed by ion exchange and size exclusion chromatography.

    Techniques: Western Blot, Enzyme-linked Immunosorbent Assay

    IL-1β and SCF crosslinks using an in vitro coculture system and human plasma in vivo . ( a ) MCF-7 cells were cocultured with THP-1 cells at a ratio of 3∶1. Cocultures were exposed to 8 ng/ml IL-1β for 24 h in the absence or presence of 2 µg/ml human SCF neutralizing antibody which was added 30 min before IL-1β. ( b ) MTS cell viability and in-cell assay of SCF binding to THP-1 cells and VEGF release as outlined in Materials and Methods. ( c ) IL-1β and SCF levels were analysed in the plasma of ten healthy human donors by ELISA. Correlation analysis was performed using MS Excel software. Imaging data show one representative experiment of three that gave similar results and were quantitatively analysed. Quantitative data are shown as mean values±s.d. of at least three individual experiments; * P

    Journal: Cellular and Molecular Immunology

    Article Title: Interleukin-1 beta induces the expression and production of stem cell factor by epithelial cells: crucial involvement of the PI-3K/mTOR pathway and HIF-1 transcription complex

    doi: 10.1038/cmi.2014.113

    Figure Lengend Snippet: IL-1β and SCF crosslinks using an in vitro coculture system and human plasma in vivo . ( a ) MCF-7 cells were cocultured with THP-1 cells at a ratio of 3∶1. Cocultures were exposed to 8 ng/ml IL-1β for 24 h in the absence or presence of 2 µg/ml human SCF neutralizing antibody which was added 30 min before IL-1β. ( b ) MTS cell viability and in-cell assay of SCF binding to THP-1 cells and VEGF release as outlined in Materials and Methods. ( c ) IL-1β and SCF levels were analysed in the plasma of ten healthy human donors by ELISA. Correlation analysis was performed using MS Excel software. Imaging data show one representative experiment of three that gave similar results and were quantitatively analysed. Quantitative data are shown as mean values±s.d. of at least three individual experiments; * P

    Article Snippet: IL-1β was expressed in Escherichia coli Rosetta-gami cells with a pET21 vector (Novagen, Schaffhausen, Switzerland) and purified by ammonium sulfate precipitation followed by ion exchange and size exclusion chromatography.

    Techniques: In Vitro, In Vivo, Binding Assay, Enzyme-linked Immunosorbent Assay, Mass Spectrometry, Software, Imaging

    Crucial involvement of the PI-3K/mTOR pathway and HIF-1 transcription complex in IL-1β induced SCF production and secretion. eIF4E, eukaryotic translation initiation factor 4E; HIF, hypoxia-inducible factor; mTOR, mammalian target of rapamycin; PDK, phosphatidylinositol (P-3-PI)-dependent kinase; PI-3K, phosphatidylinositol-3 kinase; SCF, stem cell factor; S6K1, ribosomal protein S6 kinase beta-1; TSC, tuberous sclerosis complex.

    Journal: Cellular and Molecular Immunology

    Article Title: Interleukin-1 beta induces the expression and production of stem cell factor by epithelial cells: crucial involvement of the PI-3K/mTOR pathway and HIF-1 transcription complex

    doi: 10.1038/cmi.2014.113

    Figure Lengend Snippet: Crucial involvement of the PI-3K/mTOR pathway and HIF-1 transcription complex in IL-1β induced SCF production and secretion. eIF4E, eukaryotic translation initiation factor 4E; HIF, hypoxia-inducible factor; mTOR, mammalian target of rapamycin; PDK, phosphatidylinositol (P-3-PI)-dependent kinase; PI-3K, phosphatidylinositol-3 kinase; SCF, stem cell factor; S6K1, ribosomal protein S6 kinase beta-1; TSC, tuberous sclerosis complex.

    Article Snippet: IL-1β was expressed in Escherichia coli Rosetta-gami cells with a pET21 vector (Novagen, Schaffhausen, Switzerland) and purified by ammonium sulfate precipitation followed by ion exchange and size exclusion chromatography.

    Techniques:

    The level of IL-1β-induced HIF-1α accumulation in MCF-7 cells is comparable with those observed for classic HIF-1 activators. MCF-7 cells were exposed for 4 h to 8 ng/ml IL-1β, hypoxia (3% oxygen), cobalt chloride (100 µM) or MG132 (5 µM) followed by detection of HIF-1α accumulation and HIF-1 DBA as outlined in the ‘Materials and methods' section. Western blot data show one representative experiment of three that gave similar results and were quantitatively analysed. Quantitative data are shown as mean values±s.d. of n =3; * P

    Journal: Cellular and Molecular Immunology

    Article Title: Interleukin-1 beta induces the expression and production of stem cell factor by epithelial cells: crucial involvement of the PI-3K/mTOR pathway and HIF-1 transcription complex

    doi: 10.1038/cmi.2014.113

    Figure Lengend Snippet: The level of IL-1β-induced HIF-1α accumulation in MCF-7 cells is comparable with those observed for classic HIF-1 activators. MCF-7 cells were exposed for 4 h to 8 ng/ml IL-1β, hypoxia (3% oxygen), cobalt chloride (100 µM) or MG132 (5 µM) followed by detection of HIF-1α accumulation and HIF-1 DBA as outlined in the ‘Materials and methods' section. Western blot data show one representative experiment of three that gave similar results and were quantitatively analysed. Quantitative data are shown as mean values±s.d. of n =3; * P

    Article Snippet: IL-1β was expressed in Escherichia coli Rosetta-gami cells with a pET21 vector (Novagen, Schaffhausen, Switzerland) and purified by ammonium sulfate precipitation followed by ion exchange and size exclusion chromatography.

    Techniques: Western Blot

    IL-1β induces SCF production and HIF-1α accumulation in MCF-7 cells in a concentration-dependent manner. ( a ) MCF-7 cells were exposed to increasing concentrations of IL-1β for 24 h followed by detection of SCF release and HIF-1α accumulation. ( b ) THP-1 human myeloid leukaemia cells were treated in the same way and were used as a negative control cell line which does not produce SCF. Western blot data show one representative experiment of three that produced similar results and were quantitatively analysed. Quantitative data are shown as mean values±s.d. of at least three individual experiments; * P

    Journal: Cellular and Molecular Immunology

    Article Title: Interleukin-1 beta induces the expression and production of stem cell factor by epithelial cells: crucial involvement of the PI-3K/mTOR pathway and HIF-1 transcription complex

    doi: 10.1038/cmi.2014.113

    Figure Lengend Snippet: IL-1β induces SCF production and HIF-1α accumulation in MCF-7 cells in a concentration-dependent manner. ( a ) MCF-7 cells were exposed to increasing concentrations of IL-1β for 24 h followed by detection of SCF release and HIF-1α accumulation. ( b ) THP-1 human myeloid leukaemia cells were treated in the same way and were used as a negative control cell line which does not produce SCF. Western blot data show one representative experiment of three that produced similar results and were quantitatively analysed. Quantitative data are shown as mean values±s.d. of at least three individual experiments; * P

    Article Snippet: IL-1β was expressed in Escherichia coli Rosetta-gami cells with a pET21 vector (Novagen, Schaffhausen, Switzerland) and purified by ammonium sulfate precipitation followed by ion exchange and size exclusion chromatography.

    Techniques: Concentration Assay, Negative Control, Western Blot, Produced

    mTOR is crucially involved in IL-1β-induced SCF production. MCF-7 cells were pre-treated for 1 h with 10 µM rapamycin followed by 4 h exposure to 8 ng/ml IL-1β in the absence or presence of 50 µM CoCl 2 to maintain HIF-1 activity in the case of mTOR inhibition with rapamycin. HIF-1 DNA-binding activity and S2448 mTOR phosphorylation were monitored as described in the ‘Materials and methods' section. Western blot data show one representative experiment of three that gave similar results and were quantitatively analysed. Quantitative data are shown as mean values±s.d. of at least three individual experiments; * P

    Journal: Cellular and Molecular Immunology

    Article Title: Interleukin-1 beta induces the expression and production of stem cell factor by epithelial cells: crucial involvement of the PI-3K/mTOR pathway and HIF-1 transcription complex

    doi: 10.1038/cmi.2014.113

    Figure Lengend Snippet: mTOR is crucially involved in IL-1β-induced SCF production. MCF-7 cells were pre-treated for 1 h with 10 µM rapamycin followed by 4 h exposure to 8 ng/ml IL-1β in the absence or presence of 50 µM CoCl 2 to maintain HIF-1 activity in the case of mTOR inhibition with rapamycin. HIF-1 DNA-binding activity and S2448 mTOR phosphorylation were monitored as described in the ‘Materials and methods' section. Western blot data show one representative experiment of three that gave similar results and were quantitatively analysed. Quantitative data are shown as mean values±s.d. of at least three individual experiments; * P

    Article Snippet: IL-1β was expressed in Escherichia coli Rosetta-gami cells with a pET21 vector (Novagen, Schaffhausen, Switzerland) and purified by ammonium sulfate precipitation followed by ion exchange and size exclusion chromatography.

    Techniques: Activity Assay, Inhibition, Binding Assay, Western Blot

    miR-29a/Bax axis contribute to IL-1β induced chondrocyte-like ATDC5 cell apoptosis . Cells were transfected with dose-dependent of miR-29a mimic (a) or inhibitor (b). The response levels of miR-29a were determined. (c) Representative immunoblots show Bax, PUMA, and cleaved Caspase-3 levels in IL-1 β induced chondrocyte-like ATDC5 cell with or without miR-29a mimic or inhibitor. (d) The relative expression levels of Bax were shown. ∗ donates p

    Journal: BioMed Research International

    Article Title: Bax Targeted by miR-29a Regulates Chondrocyte Apoptosis in Osteoarthritis

    doi: 10.1155/2019/1434538

    Figure Lengend Snippet: miR-29a/Bax axis contribute to IL-1β induced chondrocyte-like ATDC5 cell apoptosis . Cells were transfected with dose-dependent of miR-29a mimic (a) or inhibitor (b). The response levels of miR-29a were determined. (c) Representative immunoblots show Bax, PUMA, and cleaved Caspase-3 levels in IL-1 β induced chondrocyte-like ATDC5 cell with or without miR-29a mimic or inhibitor. (d) The relative expression levels of Bax were shown. ∗ donates p

    Article Snippet: Apoptotic Assay Chondrocyte-like ATDC5 cells were stressed with 10 ng/ml IL-1β (Sigma, St. Louis, MO, USA) for 48 h and stained with a permeable dye, Hoechst 33258 (Invitrogen, 5 μ g/ml).

    Techniques: Transfection, Western Blot, Expressing

    Upregulation of Bax in IL-1β induced chondrocyte-like ATDC5 cell apoptosis . ATDC5 cell was cultured and supplemented with ITS for two weeks. Then cells were treated with 1, 5, 10, and 20 ng/ml IL-1 β for 24 h. Cells were stained with Hoechst 33258 for 10 min and the representative images were shown in (a). The apoptotic rate was counted and shown in (b) and ∗ donates p

    Journal: BioMed Research International

    Article Title: Bax Targeted by miR-29a Regulates Chondrocyte Apoptosis in Osteoarthritis

    doi: 10.1155/2019/1434538

    Figure Lengend Snippet: Upregulation of Bax in IL-1β induced chondrocyte-like ATDC5 cell apoptosis . ATDC5 cell was cultured and supplemented with ITS for two weeks. Then cells were treated with 1, 5, 10, and 20 ng/ml IL-1 β for 24 h. Cells were stained with Hoechst 33258 for 10 min and the representative images were shown in (a). The apoptotic rate was counted and shown in (b) and ∗ donates p

    Article Snippet: Apoptotic Assay Chondrocyte-like ATDC5 cells were stressed with 10 ng/ml IL-1β (Sigma, St. Louis, MO, USA) for 48 h and stained with a permeable dye, Hoechst 33258 (Invitrogen, 5 μ g/ml).

    Techniques: Cell Culture, Staining