cgrp Search Results


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  • 92
    Thermo Fisher gene exp calca hs01100741 m1
    Correlations among <t>CGRP</t> and SP expression in DDD patients. ( a ) Correlation among TAC1 and CGRP gene expression ( r = 0.438; p = 0.042; n = 22; Spearman correlation co-efficient) and, ( b ) Correlation among CGRP and SP ( r = 0.564; p = 0.010; n = 20; Spearman correlation co-efficient) in IVD tissues.
    Gene Exp Calca Hs01100741 M1, supplied by Thermo Fisher, used in various techniques. Bioz Stars score: 92/100, based on 14 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    89
    Millipore anti cgrp antibody
    The colocalization of MORS196A with <t>CGRP</t> or <t>NeuN</t> in the spinal cord of gene-transferred mice. Representative fluorescence micrographs of the spinal cord ( A and C ) and the DRG ( E ) 6 weeks after local injection of dsAAV2-MORS196A-EGFP are shown with a ×20
    Anti Cgrp Antibody, supplied by Millipore, used in various techniques. Bioz Stars score: 89/100, based on 95 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    93
    Tocris mog 35 55 peptide
    The colocalization of MORS196A with <t>CGRP</t> or <t>NeuN</t> in the spinal cord of gene-transferred mice. Representative fluorescence micrographs of the spinal cord ( A and C ) and the DRG ( E ) 6 weeks after local injection of dsAAV2-MORS196A-EGFP are shown with a ×20
    Mog 35 55 Peptide, supplied by Tocris, used in various techniques. Bioz Stars score: 93/100, based on 4 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    cgrp  (Abcam)
    93
    Abcam cgrp
    Immunostaining of <t>YAP</t> with <t>CGRP-</t> or IB4-immunoreactivity in the spinal cord dorsal horn
    Cgrp, supplied by Abcam, used in various techniques. Bioz Stars score: 93/100, based on 228 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    90
    Novus Biologicals anti cgrp antibody
    Distribution of <t>CGRP-immunopositive</t> nerve fibers in gingival tissue. ( a ) Immunofluorescent staining for CGRP and <t>PGP9.5,</t> a neuronal maker (left panel) and TRAP staining (right panel) in consecutive tissue sections of gingival tissues. The arrowhead indicates CGRP-containing nerve fibers that are in the vicinity of osteoclasts on the alveolar bone surface. OC, osteoclasts. AB, alveolar bone. D, dentin. Scale bars represent 50 μm. ( b ) Model of the relative roles of TRPV1 and CGRP on bone remodeling in periodontitis. Activation of TRPV1 on sensory neurons innervating gingival tissues induces afferent input to TG, which results in the synthesis of neuropeptides such as CGRP. Anterograde axonal transportation of CGRP to peripheral tissue and subsequent release of CGRP leads to the inhibition of osteoclast differentiation in alveolar bone.
    Anti Cgrp Antibody, supplied by Novus Biologicals, used in various techniques. Bioz Stars score: 90/100, based on 5 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    cgrp  (Tocris)
    94
    Tocris cgrp
    Role of <t>adrenomedullin</t> in flow-induced eNOS regulation. ( A ) BAECs were treated with adrenomedullin (ADM, 10 nM, 5 minutes), calcitonin gene–related peptide <t>(CGRP;</t> 10 nM, 10 minutes), or adrenomedullin-2 (ADM2, 1 nM, 3 minutes), and phosphorylation of eNOS S635 was determined by immunoblotting. Bar diagram shows the densitometric evaluation ( n = 3). ( B – D and F – H ) BAECs ( B , C , and F – H ) or HAECs ( D ) were transfected with scrambled (control) siRNA or siRNA directed against Gα s , CALCRL, eNOS, or ADM as indicated. In D , eNOS WT or the eNOS phospho-site mutants S1177A and S633A were expressed by lentiviral transduction. Cells were treated with adrenomedullin (ADM, 10 nM, 5 minutes [ B ] or 30 minutes [ D ]) or adrenomedullin-2 (ADM2, 1 nM, 3 minutes, C ) or were exposed to 15 dyn/cm 2 for 30 minutes or for the indicated time periods ( F – H ). Phosphorylation of eNOS at serine 635 and serine 1179 was determined by immunoblotting ( B , C , and F ). Intracellular cAMP concentration ( n = 7, control; n = 6, CALCRL; n = 8, ADM) ( G ) or nitrate and nitrite concentration in the cell culture medium ( n = 6 [ D ]; n = 13, control; n = 4, CALCRL; n = 5, ADM [ H ]) was determined. Bar diagrams in B , C , and F show densitometric evaluation of immunoblots ( n = 3). ( E ) Expression of ADM, CGRP (CALCA), ADM2, and RAMP1–3 RNA in BAECs and HUVECs ( n = 4). Data represent the mean ± SEM; * P ≤ 0.05, ** P ≤ 0.01, *** P ≤ 0.00, 2-way ANOVA with Bonferroni’s post hoc test ( A – D , G , and H ) or 1-way ANOVA with Tukey’s post hoc test ( F ).
    Cgrp, supplied by Tocris, used in various techniques. Bioz Stars score: 94/100, based on 27 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    92
    Peninsula Laboratories cgrp
    The effects of exercise on post fracture gene expression of cutaneous inflammatory mediators Expression of inflammatory mediators in the fracture limb hindpaw skin were measured by real-time PCR. Interleukin-1β (IL-1β, A) and chemokine (C-C motif) ligand 2 (CCL2, E) gene expression were up-regulated at 7 weeks post fracture (FX+No Wheel), compared to nonfractured control mice (Control), and this increase was reversed in FX mice provided with 4 weeks of ad lib access to a running wheel (FX + Wheel), starting at 3 weeks post fracture. There were no changes in the hindpaw skin expression of interleukin-6 (IL-6, B), tumor necrosis factor-α (TNF-α, C), nerve growth factor <t>(NGF,</t> D), substance P (TAC1, F), the substance P NK 1 receptor (TACR1, G), the calcitonin gene-related peptide <t>(CGRP)</t> RAMP1 receptor (RAMP1, H), CGRP (CALCA, I and CALCB, J) and the CGRP receptor (CALCRL, K) at 7 weeks post fracture (FX+No Wheel), compared to control nonfracture mice. Exercise had no effects on the post-fracture expression of IL-6, TNF-α, NGF, TAC1, TACR1, RAMP1, CALCA, CALCB, or CALCRL. Values are means ± SD, n=8. One-way analysis of variance with Bonferroni post hoc testing. *** P
    Cgrp, supplied by Peninsula Laboratories, used in various techniques. Bioz Stars score: 92/100, based on 123 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    91
    Neuromics cgrp
    LSB3i treated hPSCs accelerate via a neural crest intermediate into mature bipolar nociceptors with an action potential To monitor the emergence of neural crest stem cells, a transgenic SOX10∷GFP BAC hESC cell line was treated with (a) LSB, (b) LSB and CHIR99021, or (c) LSB3i. (d) SOX10∷GFP+ expression was accelerated and maximal expression (80% GFP+ by day 12) occurred earlier compared to LSB and CHIR99021 or LSB treatment alone. Sorted SOX10∷GFP+ cells gave rise to (e) ISL1 and (f) BRN3A positive neurons. (g) LSB3i neurons stain for glutamate. (h) Between days 8 and 14 <t>RUNX1</t> expression is extinguished in some of the cells (higher expression in filled arrowhead, lower in empty arrowhead) and RET upregulates. (i) By day 15, mature neurons express peripherin, and after 1 month, (j) neuronal cell bodies arrange as clusters positive for (k) Substance P and (l) <t>CGRP.</t> Scale bars for (a-g, i-m) are 100 μm and 50 μm for (h).
    Cgrp, supplied by Neuromics, used in various techniques. Bioz Stars score: 91/100, based on 49 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    88
    Thermo Fisher gene exp calca rn00569199 m1
    Real-time polymerase chain reaction (RT-PCR) data from the ipsilateral mandibular division (V3) of the trigeminal ganglion 24h following eccentric muscle contraction. Means and SE are plotted, asterisks denote significant fold increases from naive. Note that both EC and rapid stretching increase <t>CGRP</t> mRNA while only EC increases P2X 3 mRNA at 24h.
    Gene Exp Calca Rn00569199 M1, supplied by Thermo Fisher, used in various techniques. Bioz Stars score: 88/100, based on 13 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    94
    Thermo Fisher gene exp calca mm00801463 g1
    Disruption of Jagged-driven Notch signaling has no detectable impact on PNEC and NEB cell fate specification or maintenance. ( A ) qPCR analysis of Ascl1 in E18.5 controls, single and double Jag1 cnull ; Jag2 cnull mutants showing no significant difference in expression. Graph represents mean ± SEM (n = 4 Jag1 control, n = 3 Jag1 cnull ; n = 4 Jag2 control; n = 4 Jag2 cnull ; n = 4 Jag1/Jag2 control; n = 4 Jag1 cnull ; Jag2 cnull ). Student’s t-test was used to analyze data. Side panels: representative <t>Cgrp</t> immunofluorescence (IF) in controls and mutants ( B ) IF of secretory (Scgb3a2), NEB-associated SSEA1 (CC) and Cgrp (PNEC/NEB) in control and Jag mutants. ( C, D ) Preserved NEB microenvironment in E18.5 Jag1 cnull ; Jag2 cnull double mutants: IF showing NEBs (Cgrp) and NEB-associated CCs (SSEA1, N1ICD, CC10 low ) in double null mutants similar to controls (Ex. inset in D). ( E ) qPCR analysis of Upk3a in E18.5 control and double Jag1 cnull ; Jag2 cnull mutants showing nearly abolished Upk3a expression in mutants (n = 3 in each group). Graph: mean ± SEM; ***p
    Gene Exp Calca Mm00801463 G1, supplied by Thermo Fisher, used in various techniques. Bioz Stars score: 94/100, based on 73 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    85
    Thermo Fisher gene exp calca mm00801464 m1
    Serum procalcitonin (PCT) and calcitonin (CT) immunoreactivity in WT and <t>Calca</t> KO mice. ( A ) Combined levels of serum PCT and CT were measured in WT and KO mice (five per group) using a two-site immunoradiometric assay for rat CT, both under baseline (Bsln)
    Gene Exp Calca Mm00801464 M1, supplied by Thermo Fisher, used in various techniques. Bioz Stars score: 85/100, based on 12 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    90
    Biorbyt cgrp
    Serum procalcitonin (PCT) and calcitonin (CT) immunoreactivity in WT and <t>Calca</t> KO mice. ( A ) Combined levels of serum PCT and CT were measured in WT and KO mice (five per group) using a two-site immunoradiometric assay for rat CT, both under baseline (Bsln)
    Cgrp, supplied by Biorbyt, used in various techniques. Bioz Stars score: 90/100, based on 6 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    94
    Thermo Fisher gene exp calcb ss03386432 uh
    Upregulation of pain and inflammatory markers in degenerating IVDs. Quantitative RT-PCR analyses of ( A–C) pain-related genes <t>(CGRP,</t> BDKRB1 and COMT) and ( D , E ) inflammation-related genes (IL-6 and BDNF) harvested from healthy and degenerated IVDs 2, 6, and 10 weeks after intradiscal puncture (n = 3 per group; *p
    Gene Exp Calcb Ss03386432 Uh, supplied by Thermo Fisher, used in various techniques. Bioz Stars score: 94/100, based on 9 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    87
    Thermo Fisher gene exp calca rn01511353 g1
    PC supernatant induced DRG neurons releasing of SP and <t>CGRP</t> in a protease-dependent way After incubation for 2h, the releasing of SP (A) and CGRP (B) form cultured DRG neurons were higher in PC supernatant group than that in NC supernatant group. Similarly, the mRNA levels for SP (C) and CGRP (D) were significantly increased in DRG neurons treated with PC supernatants. Co-incubation with protease inhibitor FUT-175 (50μg/ml) and PC supernatant reduced this neuropeptide release effect in cultured DRG neurons. Ctr: unstimulated DRG. PC: supernatants cultured from pancreatic cancer tissues. NC: supernatants cultured from normal pancreatic tissues. F: a broad-spectrum serine protease inhibitor, FUT-175.*P
    Gene Exp Calca Rn01511353 G1, supplied by Thermo Fisher, used in various techniques. Bioz Stars score: 87/100, based on 2 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    93
    Thermo Fisher cgrp
    Putative mechanisms for the UVB-induced decrease in adiponectin expression in ovarial adipose tissues. The <t>CGRP</t> signal induced by exposure of the skin to UVB can transfer to the brain and then to the liver, possibly via a neural pathway. Increased CGRP in the liver induces the expression and secretion of SAA via the action of IL-6. In an endocrine manner, SAA in the serum downregulates PPARγ, C/EBPα, C/EBPβ, and <t>aP2</t> mRNA levels and upregulates IL-6 and MCP-1 mRNA levels in the ovarial adipose tissues. The downregulation of adiponectin expression in the adipose tissues by these factors contributes to the decrease in serum adiponectin. Reduced levels of adiponectin in the serum may impair skin function (Yamane et al . 2010). Thus, the decrease in adiponectin induced by UVB irradiation can have adverse effects on skin function.
    Cgrp, supplied by Thermo Fisher, used in various techniques. Bioz Stars score: 93/100, based on 127 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    85
    Thermo Fisher cgrp ir
    Putative mechanisms for the UVB-induced decrease in adiponectin expression in ovarial adipose tissues. The <t>CGRP</t> signal induced by exposure of the skin to UVB can transfer to the brain and then to the liver, possibly via a neural pathway. Increased CGRP in the liver induces the expression and secretion of SAA via the action of IL-6. In an endocrine manner, SAA in the serum downregulates PPARγ, C/EBPα, C/EBPβ, and <t>aP2</t> mRNA levels and upregulates IL-6 and MCP-1 mRNA levels in the ovarial adipose tissues. The downregulation of adiponectin expression in the adipose tissues by these factors contributes to the decrease in serum adiponectin. Reduced levels of adiponectin in the serum may impair skin function (Yamane et al . 2010). Thus, the decrease in adiponectin induced by UVB irradiation can have adverse effects on skin function.
    Cgrp Ir, supplied by Thermo Fisher, used in various techniques. Bioz Stars score: 85/100, based on 7 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    Image Search Results


    Correlations among CGRP and SP expression in DDD patients. ( a ) Correlation among TAC1 and CGRP gene expression ( r = 0.438; p = 0.042; n = 22; Spearman correlation co-efficient) and, ( b ) Correlation among CGRP and SP ( r = 0.564; p = 0.010; n = 20; Spearman correlation co-efficient) in IVD tissues.

    Journal: International Journal of Molecular Sciences

    Article Title: NF-κB-Associated Pain-Related Neuropeptide Expression in Patients with Degenerative Disc Disease

    doi: 10.3390/ijms20030658

    Figure Lengend Snippet: Correlations among CGRP and SP expression in DDD patients. ( a ) Correlation among TAC1 and CGRP gene expression ( r = 0.438; p = 0.042; n = 22; Spearman correlation co-efficient) and, ( b ) Correlation among CGRP and SP ( r = 0.564; p = 0.010; n = 20; Spearman correlation co-efficient) in IVD tissues.

    Article Snippet: Predeveloped specific primers for RELA (Hs00153294_m1), NFKB1 (Hs00765730_m1), MMP-3 (Hs00968305_m1), TAC1; gene which encode for SP (Hs00243225_m1), CGRP (Hs01100741_m1), and TRPV1 (Hs00218912_m1) were used to detect targets.

    Techniques: Expressing

    CGRP, SP, and TRPV1 expression. ( a ) Relative gene expression of CGRP ( n = 23 DDD patients and 14 PM control), ( b ) TAC1 ( n = 33 DDD patients and 16 PM control), and ( c ) TRPV1 ( n = 33 DDD patients and 17 PM control) in intervertebral disc (IVD) tissues retrieved from DDD patients and PM controls. Values reported are mean ± SEM. ** p ≤ 0.01, comparison between DDD patients and PM controls calculated by Student’s t -test. ( d ) Protein levels of CGRP ( n = 30 DDD patients and 7 PM control), ( e ) SP (n = 25 DDD patients and 9 PM control), and ( f ) TRPV1 ( n = 28 DDD patients and 9 PM control) in cytosolic extracts retrieved from IVD tissues from DDD patients and PM controls. Values reported are mean ± SEM. * p ≤ 0.05, comparison between DDD patients and PM controls calculated by Student’s t -test.

    Journal: International Journal of Molecular Sciences

    Article Title: NF-κB-Associated Pain-Related Neuropeptide Expression in Patients with Degenerative Disc Disease

    doi: 10.3390/ijms20030658

    Figure Lengend Snippet: CGRP, SP, and TRPV1 expression. ( a ) Relative gene expression of CGRP ( n = 23 DDD patients and 14 PM control), ( b ) TAC1 ( n = 33 DDD patients and 16 PM control), and ( c ) TRPV1 ( n = 33 DDD patients and 17 PM control) in intervertebral disc (IVD) tissues retrieved from DDD patients and PM controls. Values reported are mean ± SEM. ** p ≤ 0.01, comparison between DDD patients and PM controls calculated by Student’s t -test. ( d ) Protein levels of CGRP ( n = 30 DDD patients and 7 PM control), ( e ) SP (n = 25 DDD patients and 9 PM control), and ( f ) TRPV1 ( n = 28 DDD patients and 9 PM control) in cytosolic extracts retrieved from IVD tissues from DDD patients and PM controls. Values reported are mean ± SEM. * p ≤ 0.05, comparison between DDD patients and PM controls calculated by Student’s t -test.

    Article Snippet: Predeveloped specific primers for RELA (Hs00153294_m1), NFKB1 (Hs00765730_m1), MMP-3 (Hs00968305_m1), TAC1; gene which encode for SP (Hs00243225_m1), CGRP (Hs01100741_m1), and TRPV1 (Hs00218912_m1) were used to detect targets.

    Techniques: Expressing

    The colocalization of MORS196A with CGRP or NeuN in the spinal cord of gene-transferred mice. Representative fluorescence micrographs of the spinal cord ( A and C ) and the DRG ( E ) 6 weeks after local injection of dsAAV2-MORS196A-EGFP are shown with a ×20

    Journal:

    Article Title: dsAAV type 2-mediated gene transfer of MORS196A-EGFP into spinal cord as a pain management paradigm

    doi: 10.1073/pnas.0703409104

    Figure Lengend Snippet: The colocalization of MORS196A with CGRP or NeuN in the spinal cord of gene-transferred mice. Representative fluorescence micrographs of the spinal cord ( A and C ) and the DRG ( E ) 6 weeks after local injection of dsAAV2-MORS196A-EGFP are shown with a ×20

    Article Snippet: Anti-NeuN antibody (MAB377; Chemicon) was used at a dilution of 1:500, and anti-CGRP antibody (AB5920; Chemicon) was used at a dilution of 1:2,000.

    Techniques: Mouse Assay, Fluorescence, Injection

    In vivo analysis of axonal growth in Necdin mutant embryos . (A) Whole-mount immunostaining of E13.5 wild type and mutant embryos with TuJ1, a neuronal specific marker illustrating the parameter used for quantification (lcb). (B) Quantitative analysis of the length of the lateral cutaneous branches of the nerves innervating the trunk at E12.5 and E13.5. No significant differences in the length of spinal nerves were observed in mutant embryos compared to wild type. Six peripheral axon bundles, from five mice, for each genotype, were analyzed. Statistical analysis was carried out using the Mann-Whitney test. (C, D) Parvalbumin immunostaining on transverse section at E17.5 showing a decrease of Necdin mutant proprioceptive afferences (D) in spinal cord compared to wild type (C). (E) Representative scheme of defect observed in (C) and (D). (F-I) CGRP immunostaining on coronal section, at adulthood, showing a similar innervation pattern of TrkA fibers in the hindpaw pad (F-G) around an hair follicle or (H-I) in the epidermis under nail of the second toe in NdnKO (G, I) or wild type (F-H) mice. We notice a decrease in the number of fibers in Ndn KO. ab, anterior bud; Ep, epidermis; HF, hair follicle; lcb, lateral cutaneous branch. Scale bar: 500 μm (A); 100 μm (C, D and F-I).

    Journal: BMC Developmental Biology

    Article Title: Sensory defects in Necdin deficient mice result from a loss of sensory neurons correlated within an increase of developmental programmed cell death

    doi: 10.1186/1471-213X-6-56

    Figure Lengend Snippet: In vivo analysis of axonal growth in Necdin mutant embryos . (A) Whole-mount immunostaining of E13.5 wild type and mutant embryos with TuJ1, a neuronal specific marker illustrating the parameter used for quantification (lcb). (B) Quantitative analysis of the length of the lateral cutaneous branches of the nerves innervating the trunk at E12.5 and E13.5. No significant differences in the length of spinal nerves were observed in mutant embryos compared to wild type. Six peripheral axon bundles, from five mice, for each genotype, were analyzed. Statistical analysis was carried out using the Mann-Whitney test. (C, D) Parvalbumin immunostaining on transverse section at E17.5 showing a decrease of Necdin mutant proprioceptive afferences (D) in spinal cord compared to wild type (C). (E) Representative scheme of defect observed in (C) and (D). (F-I) CGRP immunostaining on coronal section, at adulthood, showing a similar innervation pattern of TrkA fibers in the hindpaw pad (F-G) around an hair follicle or (H-I) in the epidermis under nail of the second toe in NdnKO (G, I) or wild type (F-H) mice. We notice a decrease in the number of fibers in Ndn KO. ab, anterior bud; Ep, epidermis; HF, hair follicle; lcb, lateral cutaneous branch. Scale bar: 500 μm (A); 100 μm (C, D and F-I).

    Article Snippet: Antibodies used were: NC243 anti-mouse Necdin (rabbit polyclonal, 1/500, [ ]), anti-Neurofilament (mouse monoclonal, 1:200, Chemicon); anti-TuJ1 (mouse monoclonal to neuron specific class III β-tubulin, 1:200, Berkeley Antibody); anti-Caspase-3-activated (rabbit polyclonal, 1/500, Upstate Biotechnology), anti-Runx3 (rabbit polyclonal, 1:200, a generous gift of Dr Yoran Gruner) anti-Parvalbumin (rabbit polyclonal antibody, 1/200, Swant Swisszerland) and anti-CGRP (Chemicon).

    Techniques: In Vivo, Mutagenesis, Immunostaining, Marker, Mouse Assay, MANN-WHITNEY

    Colocalization of GFRα2 protein with markers of unmyelinated neurons in mouse DRG. Sections of wild-type ( A–C , G–R ) and GFRα2-KO ( D–F ) mouse lumbar L4 DRG are stained for IB4-binding ( B , E ), peripherin ( H ), P2X 3 ( K ), CGRP ( N ), and TRPV1 ( Q ) to estimate colocalization with GFRα2 protein (left; green). The yellow color in the merged images (right) indicates colocalization. No specific GFRα2 staining is seen in the DRG section from the GFRα2-KO mouse ( D ). Note that GFRα2-expressing neurons that are peripherin negative (arrowheads) appear to be similarly sized to neurons that are peripherin positive (arrows). Scale bars, 50 μm.

    Journal: The Journal of Neuroscience

    Article Title: Deficient Nonpeptidergic Epidermis Innervation and Reduced Inflammatory Pain in Glial Cell Line-Derived Neurotrophic Factor Family Receptor α2 Knock-Out Mice

    doi: 10.1523/JNEUROSCI.4065-05.2006

    Figure Lengend Snippet: Colocalization of GFRα2 protein with markers of unmyelinated neurons in mouse DRG. Sections of wild-type ( A–C , G–R ) and GFRα2-KO ( D–F ) mouse lumbar L4 DRG are stained for IB4-binding ( B , E ), peripherin ( H ), P2X 3 ( K ), CGRP ( N ), and TRPV1 ( Q ) to estimate colocalization with GFRα2 protein (left; green). The yellow color in the merged images (right) indicates colocalization. No specific GFRα2 staining is seen in the DRG section from the GFRα2-KO mouse ( D ). Note that GFRα2-expressing neurons that are peripherin negative (arrowheads) appear to be similarly sized to neurons that are peripherin positive (arrows). Scale bars, 50 μm.

    Article Snippet: Primary antibodies were against CGRP (rabbit; Chemicon, Hampshire, UK), GFRα2 (goat; R & D Systems, Abingdon, UK), P2X3 (guinea pig; Chemicon), protein gene product 9.5 (PGP9.5; rabbit; Chemicon), peripherin (rabbit; Chemicon), and transient receptor potential vanilloid 1 (TRPV1) (rabbit; a gift from Dr. Julius, University of California, San Francisco, CA).

    Techniques: Staining, Binding Assay, Expressing

    IB4 binding is unaltered in the GFRα2-KO spinal cord. Cryosections of wild-type ( A ) and GFRα2-KO ( B ) mouse spinal cords were labeled with IB4 (green) and CGRP (red). Scale bar, 100 μm.

    Journal: The Journal of Neuroscience

    Article Title: Deficient Nonpeptidergic Epidermis Innervation and Reduced Inflammatory Pain in Glial Cell Line-Derived Neurotrophic Factor Family Receptor α2 Knock-Out Mice

    doi: 10.1523/JNEUROSCI.4065-05.2006

    Figure Lengend Snippet: IB4 binding is unaltered in the GFRα2-KO spinal cord. Cryosections of wild-type ( A ) and GFRα2-KO ( B ) mouse spinal cords were labeled with IB4 (green) and CGRP (red). Scale bar, 100 μm.

    Article Snippet: Primary antibodies were against CGRP (rabbit; Chemicon, Hampshire, UK), GFRα2 (goat; R & D Systems, Abingdon, UK), P2X3 (guinea pig; Chemicon), protein gene product 9.5 (PGP9.5; rabbit; Chemicon), peripherin (rabbit; Chemicon), and transient receptor potential vanilloid 1 (TRPV1) (rabbit; a gift from Dr. Julius, University of California, San Francisco, CA).

    Techniques: Binding Assay, Labeling

    IB4-lectin binding and P2X 3 -positive neurons are smaller in GFRα2-KO mice. Representative images of IB4-binding ( A , B ), P2X 3 -positive ( D , E ), and CGRP-positive ( G , H ) neurons in adult lumbar DRG from wild-type ( A , D , G ) and GFRα2-KO ( B , E , H ) mice, which were used to count the neurons and to generate the size distribution histograms ( C , F , I ), are shown. Note the atrophy of IB4-binding and P2X 3 -positive but not CGRP-positive neurons in GFRα2-KO mice. Scale bars, 50 μm.

    Journal: The Journal of Neuroscience

    Article Title: Deficient Nonpeptidergic Epidermis Innervation and Reduced Inflammatory Pain in Glial Cell Line-Derived Neurotrophic Factor Family Receptor α2 Knock-Out Mice

    doi: 10.1523/JNEUROSCI.4065-05.2006

    Figure Lengend Snippet: IB4-lectin binding and P2X 3 -positive neurons are smaller in GFRα2-KO mice. Representative images of IB4-binding ( A , B ), P2X 3 -positive ( D , E ), and CGRP-positive ( G , H ) neurons in adult lumbar DRG from wild-type ( A , D , G ) and GFRα2-KO ( B , E , H ) mice, which were used to count the neurons and to generate the size distribution histograms ( C , F , I ), are shown. Note the atrophy of IB4-binding and P2X 3 -positive but not CGRP-positive neurons in GFRα2-KO mice. Scale bars, 50 μm.

    Article Snippet: Primary antibodies were against CGRP (rabbit; Chemicon, Hampshire, UK), GFRα2 (goat; R & D Systems, Abingdon, UK), P2X3 (guinea pig; Chemicon), protein gene product 9.5 (PGP9.5; rabbit; Chemicon), peripherin (rabbit; Chemicon), and transient receptor potential vanilloid 1 (TRPV1) (rabbit; a gift from Dr. Julius, University of California, San Francisco, CA).

    Techniques: Binding Assay, Mouse Assay

    Loss of PGP9.5-positive but not CGRP-positive free nerve endings in the footpad epidermis in GFRα2-KO mice. A , B , Conventional microscopic images of sections through the forepaw footpad skin from wild-type ( A ) and GFRα2-KO ( B ) mice stained for pan-neuronal marker PGP9.5. C , Quantification of PGP9.5- and CGRP-positive nerve fibers per unit length of epidermis indicates profound loss of PGP9.5 fibers (*** p

    Journal: The Journal of Neuroscience

    Article Title: Deficient Nonpeptidergic Epidermis Innervation and Reduced Inflammatory Pain in Glial Cell Line-Derived Neurotrophic Factor Family Receptor α2 Knock-Out Mice

    doi: 10.1523/JNEUROSCI.4065-05.2006

    Figure Lengend Snippet: Loss of PGP9.5-positive but not CGRP-positive free nerve endings in the footpad epidermis in GFRα2-KO mice. A , B , Conventional microscopic images of sections through the forepaw footpad skin from wild-type ( A ) and GFRα2-KO ( B ) mice stained for pan-neuronal marker PGP9.5. C , Quantification of PGP9.5- and CGRP-positive nerve fibers per unit length of epidermis indicates profound loss of PGP9.5 fibers (*** p

    Article Snippet: Primary antibodies were against CGRP (rabbit; Chemicon, Hampshire, UK), GFRα2 (goat; R & D Systems, Abingdon, UK), P2X3 (guinea pig; Chemicon), protein gene product 9.5 (PGP9.5; rabbit; Chemicon), peripherin (rabbit; Chemicon), and transient receptor potential vanilloid 1 (TRPV1) (rabbit; a gift from Dr. Julius, University of California, San Francisco, CA).

    Techniques: Mouse Assay, Staining, Marker

    Immunostaining of YAP with CGRP- or IB4-immunoreactivity in the spinal cord dorsal horn

    Journal: Brain research

    Article Title: Spinal Expression of Hippo Signaling Components YAP and TAZ Following Peripheral Nerve Injury in Rats

    doi: 10.1016/j.brainres.2013.08.049

    Figure Lengend Snippet: Immunostaining of YAP with CGRP- or IB4-immunoreactivity in the spinal cord dorsal horn

    Article Snippet: For double-immunostaining of YAP or TAZ with calcitonin gene-related peptide (CGRP), isolectin B4 Conjugates (IB4), glial fibrillary acidic protein (GFAP), or ionized calcium binding adaptor molecule 1 (Iba1), sections were incubated for 24 hours at 4 °C with first primary antibody YAP (1:2000, Novus, Littleton, CO), TAZ (1:400, Novus, Littleton, CO), CGRP (1:1000, Abcam, Cambridge, MA), IB4 (1:2000, Invitrogen, CA), GFAP (1:400, Santa Cruz, Santa Cruz, CA), or Iba1 (1:100, Abcam, Cambridge, MA).

    Techniques: Immunostaining

    CGRP but not VIP contributes to the generation of Foxp3 + Tregs by SCG-neurons. Neuron cultures were incubated with neutralization antibodies for TGF-β, IL-10, or VIP, and CGRP antagonist for one hour before adding T cells. The co-cultures were incubated for 5 days and T cells were stained for CD3, CD4, CD25 and Foxp3 and were analyzed using flow cytometry. Mean ± SEM percentage of Foxp3 expression among CD3 + CD4 + CD25 + cells in different co-cultures are shown. (n = 6, ** = p

    Journal: PLoS ONE

    Article Title: Superior Cervical Ganglia Neurons Induce Foxp3+ Regulatory T Cells via Calcitonin Gene-Related Peptide

    doi: 10.1371/journal.pone.0152443

    Figure Lengend Snippet: CGRP but not VIP contributes to the generation of Foxp3 + Tregs by SCG-neurons. Neuron cultures were incubated with neutralization antibodies for TGF-β, IL-10, or VIP, and CGRP antagonist for one hour before adding T cells. The co-cultures were incubated for 5 days and T cells were stained for CD3, CD4, CD25 and Foxp3 and were analyzed using flow cytometry. Mean ± SEM percentage of Foxp3 expression among CD3 + CD4 + CD25 + cells in different co-cultures are shown. (n = 6, ** = p

    Article Snippet: One hour before addition of T cells to the neuronal cultures, the neutralization antibodies against NGF (8μg/ml, R & D Systems), TGF-β (1μg/ml, R & D systems), IL-10 (1μg/ml, BD Biosciences) or VIP (1x10-6 M, R & D Systems) or CGRP antagonist (1x10-6 M, Abcam) were incubated with the neurons.

    Techniques: Incubation, Neutralization, Staining, Flow Cytometry, Cytometry, Expressing

    Distribution of CGRP-immunopositive nerve fibers in gingival tissue. ( a ) Immunofluorescent staining for CGRP and PGP9.5, a neuronal maker (left panel) and TRAP staining (right panel) in consecutive tissue sections of gingival tissues. The arrowhead indicates CGRP-containing nerve fibers that are in the vicinity of osteoclasts on the alveolar bone surface. OC, osteoclasts. AB, alveolar bone. D, dentin. Scale bars represent 50 μm. ( b ) Model of the relative roles of TRPV1 and CGRP on bone remodeling in periodontitis. Activation of TRPV1 on sensory neurons innervating gingival tissues induces afferent input to TG, which results in the synthesis of neuropeptides such as CGRP. Anterograde axonal transportation of CGRP to peripheral tissue and subsequent release of CGRP leads to the inhibition of osteoclast differentiation in alveolar bone.

    Journal: Scientific Reports

    Article Title: Neuronal TRPV1 activation regulates alveolar bone resorption by suppressing osteoclastogenesis via CGRP

    doi: 10.1038/srep29294

    Figure Lengend Snippet: Distribution of CGRP-immunopositive nerve fibers in gingival tissue. ( a ) Immunofluorescent staining for CGRP and PGP9.5, a neuronal maker (left panel) and TRAP staining (right panel) in consecutive tissue sections of gingival tissues. The arrowhead indicates CGRP-containing nerve fibers that are in the vicinity of osteoclasts on the alveolar bone surface. OC, osteoclasts. AB, alveolar bone. D, dentin. Scale bars represent 50 μm. ( b ) Model of the relative roles of TRPV1 and CGRP on bone remodeling in periodontitis. Activation of TRPV1 on sensory neurons innervating gingival tissues induces afferent input to TG, which results in the synthesis of neuropeptides such as CGRP. Anterograde axonal transportation of CGRP to peripheral tissue and subsequent release of CGRP leads to the inhibition of osteoclast differentiation in alveolar bone.

    Article Snippet: The slides were then incubated with Alexa Fluor 594 -conjugated anti-rabbit secondary antibody (Abcam) for TRPV1 and Alexa Fluor 488-conjugated anti-goat secondary antibody (Abcam) for CGRP at room temperature for 1 h. For histological analysis of alveolar bone tissues, decalcified and embedded sections were double-stained by anti-CGRP antibody and anti-PGP9.5 antibody (Novus Biologicals, Littleton, CO, USA) with appropriate Alexa Fluor-conjugated secondary antibodies.

    Techniques: Staining, Activation Assay, Inhibition

    Role of adrenomedullin in flow-induced eNOS regulation. ( A ) BAECs were treated with adrenomedullin (ADM, 10 nM, 5 minutes), calcitonin gene–related peptide (CGRP; 10 nM, 10 minutes), or adrenomedullin-2 (ADM2, 1 nM, 3 minutes), and phosphorylation of eNOS S635 was determined by immunoblotting. Bar diagram shows the densitometric evaluation ( n = 3). ( B – D and F – H ) BAECs ( B , C , and F – H ) or HAECs ( D ) were transfected with scrambled (control) siRNA or siRNA directed against Gα s , CALCRL, eNOS, or ADM as indicated. In D , eNOS WT or the eNOS phospho-site mutants S1177A and S633A were expressed by lentiviral transduction. Cells were treated with adrenomedullin (ADM, 10 nM, 5 minutes [ B ] or 30 minutes [ D ]) or adrenomedullin-2 (ADM2, 1 nM, 3 minutes, C ) or were exposed to 15 dyn/cm 2 for 30 minutes or for the indicated time periods ( F – H ). Phosphorylation of eNOS at serine 635 and serine 1179 was determined by immunoblotting ( B , C , and F ). Intracellular cAMP concentration ( n = 7, control; n = 6, CALCRL; n = 8, ADM) ( G ) or nitrate and nitrite concentration in the cell culture medium ( n = 6 [ D ]; n = 13, control; n = 4, CALCRL; n = 5, ADM [ H ]) was determined. Bar diagrams in B , C , and F show densitometric evaluation of immunoblots ( n = 3). ( E ) Expression of ADM, CGRP (CALCA), ADM2, and RAMP1–3 RNA in BAECs and HUVECs ( n = 4). Data represent the mean ± SEM; * P ≤ 0.05, ** P ≤ 0.01, *** P ≤ 0.00, 2-way ANOVA with Bonferroni’s post hoc test ( A – D , G , and H ) or 1-way ANOVA with Tukey’s post hoc test ( F ).

    Journal: The Journal of Clinical Investigation

    Article Title: Shear stress–induced endothelial adrenomedullin signaling regulates vascular tone and blood pressure

    doi: 10.1172/JCI123825

    Figure Lengend Snippet: Role of adrenomedullin in flow-induced eNOS regulation. ( A ) BAECs were treated with adrenomedullin (ADM, 10 nM, 5 minutes), calcitonin gene–related peptide (CGRP; 10 nM, 10 minutes), or adrenomedullin-2 (ADM2, 1 nM, 3 minutes), and phosphorylation of eNOS S635 was determined by immunoblotting. Bar diagram shows the densitometric evaluation ( n = 3). ( B – D and F – H ) BAECs ( B , C , and F – H ) or HAECs ( D ) were transfected with scrambled (control) siRNA or siRNA directed against Gα s , CALCRL, eNOS, or ADM as indicated. In D , eNOS WT or the eNOS phospho-site mutants S1177A and S633A were expressed by lentiviral transduction. Cells were treated with adrenomedullin (ADM, 10 nM, 5 minutes [ B ] or 30 minutes [ D ]) or adrenomedullin-2 (ADM2, 1 nM, 3 minutes, C ) or were exposed to 15 dyn/cm 2 for 30 minutes or for the indicated time periods ( F – H ). Phosphorylation of eNOS at serine 635 and serine 1179 was determined by immunoblotting ( B , C , and F ). Intracellular cAMP concentration ( n = 7, control; n = 6, CALCRL; n = 8, ADM) ( G ) or nitrate and nitrite concentration in the cell culture medium ( n = 6 [ D ]; n = 13, control; n = 4, CALCRL; n = 5, ADM [ H ]) was determined. Bar diagrams in B , C , and F show densitometric evaluation of immunoblots ( n = 3). ( E ) Expression of ADM, CGRP (CALCA), ADM2, and RAMP1–3 RNA in BAECs and HUVECs ( n = 4). Data represent the mean ± SEM; * P ≤ 0.05, ** P ≤ 0.01, *** P ≤ 0.00, 2-way ANOVA with Bonferroni’s post hoc test ( A – D , G , and H ) or 1-way ANOVA with Tukey’s post hoc test ( F ).

    Article Snippet: Adrenomedullin-2 (intermedin) was obtained from Phoenix Europe GmbH (catalog 010-48); CGRP was from Tocris Bio (catalog 1161).

    Techniques: Flow Cytometry, Transfection, Transduction, Concentration Assay, Cell Culture, Western Blot, Expressing

    CGRP induces [Ca 2+ ] i increases selectively in SGCs, but not in TG neurons. Representative temporal plot of [Ca 2+ ] i changes recorded from a SGC (black line) and a neuron (gray line) upon a 1 μ m CGRP challenge, followed by 50 m m KCl application.

    Journal: The Journal of Neuroscience

    Article Title: Calcitonin Gene-Related Peptide-Mediated Enhancement of Purinergic Neuron/Glia Communication by the Algogenic Factor Bradykinin in Mouse Trigeminal Ganglia from Wild-Type and R192Q Cav2.1 Knock-In Mice: Implications for Basic Mechanisms of Migraine Pain

    doi: 10.1523/JNEUROSCI.6440-10.2011

    Figure Lengend Snippet: CGRP induces [Ca 2+ ] i increases selectively in SGCs, but not in TG neurons. Representative temporal plot of [Ca 2+ ] i changes recorded from a SGC (black line) and a neuron (gray line) upon a 1 μ m CGRP challenge, followed by 50 m m KCl application.

    Article Snippet: The culture medium was replaced 24 h later, and experiments were performed after additional 24 h. Both primary mixed and purified SGC cultures were exposed to 100 n m BK (Sigma-Aldrich), or 1 μ m CGRP (Tocris Bioscience) for the indicated time periods (see Results and figures).

    Techniques:

    CGRP-induced P2Y receptor upregulation involves the ERK1/2 MAP kinase pathway. A , Representative Western blotting experiment showing the time-dependent activation of ERK1/2 induced by application of 1 μ m CGRP for 10, 20 and 40 min, 6 h and overnight

    Journal: The Journal of Neuroscience

    Article Title: Calcitonin Gene-Related Peptide-Mediated Enhancement of Purinergic Neuron/Glia Communication by the Algogenic Factor Bradykinin in Mouse Trigeminal Ganglia from Wild-Type and R192Q Cav2.1 Knock-In Mice: Implications for Basic Mechanisms of Migraine Pain

    doi: 10.1523/JNEUROSCI.6440-10.2011

    Figure Lengend Snippet: CGRP-induced P2Y receptor upregulation involves the ERK1/2 MAP kinase pathway. A , Representative Western blotting experiment showing the time-dependent activation of ERK1/2 induced by application of 1 μ m CGRP for 10, 20 and 40 min, 6 h and overnight

    Article Snippet: The culture medium was replaced 24 h later, and experiments were performed after additional 24 h. Both primary mixed and purified SGC cultures were exposed to 100 n m BK (Sigma-Aldrich), or 1 μ m CGRP (Tocris Bioscience) for the indicated time periods (see Results and figures).

    Techniques: Western Blot, Activation Assay

    The effects of exercise on post fracture gene expression of cutaneous inflammatory mediators Expression of inflammatory mediators in the fracture limb hindpaw skin were measured by real-time PCR. Interleukin-1β (IL-1β, A) and chemokine (C-C motif) ligand 2 (CCL2, E) gene expression were up-regulated at 7 weeks post fracture (FX+No Wheel), compared to nonfractured control mice (Control), and this increase was reversed in FX mice provided with 4 weeks of ad lib access to a running wheel (FX + Wheel), starting at 3 weeks post fracture. There were no changes in the hindpaw skin expression of interleukin-6 (IL-6, B), tumor necrosis factor-α (TNF-α, C), nerve growth factor (NGF, D), substance P (TAC1, F), the substance P NK 1 receptor (TACR1, G), the calcitonin gene-related peptide (CGRP) RAMP1 receptor (RAMP1, H), CGRP (CALCA, I and CALCB, J) and the CGRP receptor (CALCRL, K) at 7 weeks post fracture (FX+No Wheel), compared to control nonfracture mice. Exercise had no effects on the post-fracture expression of IL-6, TNF-α, NGF, TAC1, TACR1, RAMP1, CALCA, CALCB, or CALCRL. Values are means ± SD, n=8. One-way analysis of variance with Bonferroni post hoc testing. *** P

    Journal: Anesthesiology

    Article Title: Exercise reverses nociceptive sensitization, up-regulated neuropeptide signaling, inflammatory changes, anxiety, and memory impairment in the mouse tibia fracture model

    doi: 10.1097/ALN.0000000000002332

    Figure Lengend Snippet: The effects of exercise on post fracture gene expression of cutaneous inflammatory mediators Expression of inflammatory mediators in the fracture limb hindpaw skin were measured by real-time PCR. Interleukin-1β (IL-1β, A) and chemokine (C-C motif) ligand 2 (CCL2, E) gene expression were up-regulated at 7 weeks post fracture (FX+No Wheel), compared to nonfractured control mice (Control), and this increase was reversed in FX mice provided with 4 weeks of ad lib access to a running wheel (FX + Wheel), starting at 3 weeks post fracture. There were no changes in the hindpaw skin expression of interleukin-6 (IL-6, B), tumor necrosis factor-α (TNF-α, C), nerve growth factor (NGF, D), substance P (TAC1, F), the substance P NK 1 receptor (TACR1, G), the calcitonin gene-related peptide (CGRP) RAMP1 receptor (RAMP1, H), CGRP (CALCA, I and CALCB, J) and the CGRP receptor (CALCRL, K) at 7 weeks post fracture (FX+No Wheel), compared to control nonfracture mice. Exercise had no effects on the post-fracture expression of IL-6, TNF-α, NGF, TAC1, TACR1, RAMP1, CALCA, CALCB, or CALCRL. Values are means ± SD, n=8. One-way analysis of variance with Bonferroni post hoc testing. *** P

    Article Snippet: Mouse interleukin 1 beta (IL-1), interleukin 6 (IL-6), tumor necrosis factor-alpha (TNF), nerve growth factor (NGF), chemokine (C-C motif) ligand 2 (CCL2), substance P (SP), and calcitonin gene-related peptide (CGRP) protein levels were measured in duplicate by using mouse IL-1, IL-6, TNF, and CCL2 (R & D Systems, Minneapolis, MN), NGF (Millipore Merck, Darmstadt, Germany), SP (MyBioSource, San Diego, CA), and CGRP (Peninsula Laboratories, San Carlos, CA) ELISA kits following the manufacturer’s instructions.

    Techniques: Expressing, Real-time Polymerase Chain Reaction, Mouse Assay

    The effects of exercise on post fracture gene expression of spinal cord inflammatory mediators Inflammatory mediator expression in the lumbar cord innervating the fracture limb was measured by real-time PCR. IL-1β, IL-6, TNF-α, CCL2, TAC1, RAMP1, CALCA and CALCB (A–C, E–F, H–J) gene expression were up-regulated at 7 weeks post fracture (FX+No Wheel), compared to nonfractured control mice (Control). All these increases were reversed by voluntary wheel running for 4 weeks starting at day 21 after fracture (FX + Wheel). There were no changes in the hindpaw skin expression of NGF (D), TACR1 (G) and CALCRL (K) at 7 weeks post fracture, compared to nonfracture control mice, and exercise had no effects on the post fracture expression of NGF, TACR1, or CALCRL. Values are means ± SD, n=8 per cohort. One-way analysis of variance with Bonferroni post hoc testing. * P

    Journal: Anesthesiology

    Article Title: Exercise reverses nociceptive sensitization, up-regulated neuropeptide signaling, inflammatory changes, anxiety, and memory impairment in the mouse tibia fracture model

    doi: 10.1097/ALN.0000000000002332

    Figure Lengend Snippet: The effects of exercise on post fracture gene expression of spinal cord inflammatory mediators Inflammatory mediator expression in the lumbar cord innervating the fracture limb was measured by real-time PCR. IL-1β, IL-6, TNF-α, CCL2, TAC1, RAMP1, CALCA and CALCB (A–C, E–F, H–J) gene expression were up-regulated at 7 weeks post fracture (FX+No Wheel), compared to nonfractured control mice (Control). All these increases were reversed by voluntary wheel running for 4 weeks starting at day 21 after fracture (FX + Wheel). There were no changes in the hindpaw skin expression of NGF (D), TACR1 (G) and CALCRL (K) at 7 weeks post fracture, compared to nonfracture control mice, and exercise had no effects on the post fracture expression of NGF, TACR1, or CALCRL. Values are means ± SD, n=8 per cohort. One-way analysis of variance with Bonferroni post hoc testing. * P

    Article Snippet: Mouse interleukin 1 beta (IL-1), interleukin 6 (IL-6), tumor necrosis factor-alpha (TNF), nerve growth factor (NGF), chemokine (C-C motif) ligand 2 (CCL2), substance P (SP), and calcitonin gene-related peptide (CGRP) protein levels were measured in duplicate by using mouse IL-1, IL-6, TNF, and CCL2 (R & D Systems, Minneapolis, MN), NGF (Millipore Merck, Darmstadt, Germany), SP (MyBioSource, San Diego, CA), and CGRP (Peninsula Laboratories, San Carlos, CA) ELISA kits following the manufacturer’s instructions.

    Techniques: Expressing, Real-time Polymerase Chain Reaction, Mouse Assay

    LSB3i treated hPSCs accelerate via a neural crest intermediate into mature bipolar nociceptors with an action potential To monitor the emergence of neural crest stem cells, a transgenic SOX10∷GFP BAC hESC cell line was treated with (a) LSB, (b) LSB and CHIR99021, or (c) LSB3i. (d) SOX10∷GFP+ expression was accelerated and maximal expression (80% GFP+ by day 12) occurred earlier compared to LSB and CHIR99021 or LSB treatment alone. Sorted SOX10∷GFP+ cells gave rise to (e) ISL1 and (f) BRN3A positive neurons. (g) LSB3i neurons stain for glutamate. (h) Between days 8 and 14 RUNX1 expression is extinguished in some of the cells (higher expression in filled arrowhead, lower in empty arrowhead) and RET upregulates. (i) By day 15, mature neurons express peripherin, and after 1 month, (j) neuronal cell bodies arrange as clusters positive for (k) Substance P and (l) CGRP. Scale bars for (a-g, i-m) are 100 μm and 50 μm for (h).

    Journal: Nature biotechnology

    Article Title: Combined small molecule inhibition accelerates developmental timing and converts human pluripotent stem cells into nociceptors

    doi: 10.1038/nbt.2249

    Figure Lengend Snippet: LSB3i treated hPSCs accelerate via a neural crest intermediate into mature bipolar nociceptors with an action potential To monitor the emergence of neural crest stem cells, a transgenic SOX10∷GFP BAC hESC cell line was treated with (a) LSB, (b) LSB and CHIR99021, or (c) LSB3i. (d) SOX10∷GFP+ expression was accelerated and maximal expression (80% GFP+ by day 12) occurred earlier compared to LSB and CHIR99021 or LSB treatment alone. Sorted SOX10∷GFP+ cells gave rise to (e) ISL1 and (f) BRN3A positive neurons. (g) LSB3i neurons stain for glutamate. (h) Between days 8 and 14 RUNX1 expression is extinguished in some of the cells (higher expression in filled arrowhead, lower in empty arrowhead) and RET upregulates. (i) By day 15, mature neurons express peripherin, and after 1 month, (j) neuronal cell bodies arrange as clusters positive for (k) Substance P and (l) CGRP. Scale bars for (a-g, i-m) are 100 μm and 50 μm for (h).

    Article Snippet: Primary antibodies used for microscopy included PAX6 (Covance), TUJ1 (Covance), Ki67 (Sigma), ISL1 (DSHB, Abcam), BRN3A (Millipore), RET (R & D), RUNX1 (Sigma), glutamate (Sigma), peripherin (Santa Cruz), TRPV1 (Neuromics), Substance P (Neuromics), CGRP (Neuromics), SOX10 (Santa Cruz).

    Techniques: Transgenic Assay, BAC Assay, Expressing, Staining

    Real-time polymerase chain reaction (RT-PCR) data from the ipsilateral mandibular division (V3) of the trigeminal ganglion 24h following eccentric muscle contraction. Means and SE are plotted, asterisks denote significant fold increases from naive. Note that both EC and rapid stretching increase CGRP mRNA while only EC increases P2X 3 mRNA at 24h.

    Journal: Pain

    Article Title: Eccentric Muscle Contraction and Stretching Evoke Mechanical Hyperalgesia and Modulate CGRP and P2X3 Expression in a Functionally Relevant Manner

    doi: 10.1016/j.pain.2010.02.022

    Figure Lengend Snippet: Real-time polymerase chain reaction (RT-PCR) data from the ipsilateral mandibular division (V3) of the trigeminal ganglion 24h following eccentric muscle contraction. Means and SE are plotted, asterisks denote significant fold increases from naive. Note that both EC and rapid stretching increase CGRP mRNA while only EC increases P2X 3 mRNA at 24h.

    Article Snippet: All TaqMan primers and probes with high efficiency were obtained from ABI (cat. no. Rn00569199 for rat CGRP; Rn00579301 for rat P2X3 ; 4352338E for rat GAPDH).

    Techniques: Real-time Polymerase Chain Reaction, Reverse Transcription Polymerase Chain Reaction

    Percentage of immuno-positive muscle afferent neurons following eccentric muscle contraction and stretching. A. Percentage of CGRP and P2X 3 positive muscle afferent neurons following EC. Note the increase in P2X 3 muscle afferent neurons 2d and 12d following EC. B. Percentage of CGRP and P2X 3 muscle afferent neurons following stretching. Note the increase in P2X 3 muscle afferent neurons 2d and 12d following stretching. Means and SE are plotted, asterisks denote significant differences from naive.

    Journal: Pain

    Article Title: Eccentric Muscle Contraction and Stretching Evoke Mechanical Hyperalgesia and Modulate CGRP and P2X3 Expression in a Functionally Relevant Manner

    doi: 10.1016/j.pain.2010.02.022

    Figure Lengend Snippet: Percentage of immuno-positive muscle afferent neurons following eccentric muscle contraction and stretching. A. Percentage of CGRP and P2X 3 positive muscle afferent neurons following EC. Note the increase in P2X 3 muscle afferent neurons 2d and 12d following EC. B. Percentage of CGRP and P2X 3 muscle afferent neurons following stretching. Note the increase in P2X 3 muscle afferent neurons 2d and 12d following stretching. Means and SE are plotted, asterisks denote significant differences from naive.

    Article Snippet: All TaqMan primers and probes with high efficiency were obtained from ABI (cat. no. Rn00569199 for rat CGRP; Rn00579301 for rat P2X3 ; 4352338E for rat GAPDH).

    Techniques:

    Disruption of Jagged-driven Notch signaling has no detectable impact on PNEC and NEB cell fate specification or maintenance. ( A ) qPCR analysis of Ascl1 in E18.5 controls, single and double Jag1 cnull ; Jag2 cnull mutants showing no significant difference in expression. Graph represents mean ± SEM (n = 4 Jag1 control, n = 3 Jag1 cnull ; n = 4 Jag2 control; n = 4 Jag2 cnull ; n = 4 Jag1/Jag2 control; n = 4 Jag1 cnull ; Jag2 cnull ). Student’s t-test was used to analyze data. Side panels: representative Cgrp immunofluorescence (IF) in controls and mutants ( B ) IF of secretory (Scgb3a2), NEB-associated SSEA1 (CC) and Cgrp (PNEC/NEB) in control and Jag mutants. ( C, D ) Preserved NEB microenvironment in E18.5 Jag1 cnull ; Jag2 cnull double mutants: IF showing NEBs (Cgrp) and NEB-associated CCs (SSEA1, N1ICD, CC10 low ) in double null mutants similar to controls (Ex. inset in D). ( E ) qPCR analysis of Upk3a in E18.5 control and double Jag1 cnull ; Jag2 cnull mutants showing nearly abolished Upk3a expression in mutants (n = 3 in each group). Graph: mean ± SEM; ***p

    Journal: eLife

    Article Title: Jagged and Delta-like ligands control distinct events during airway progenitor cell differentiation

    doi: 10.7554/eLife.50487

    Figure Lengend Snippet: Disruption of Jagged-driven Notch signaling has no detectable impact on PNEC and NEB cell fate specification or maintenance. ( A ) qPCR analysis of Ascl1 in E18.5 controls, single and double Jag1 cnull ; Jag2 cnull mutants showing no significant difference in expression. Graph represents mean ± SEM (n = 4 Jag1 control, n = 3 Jag1 cnull ; n = 4 Jag2 control; n = 4 Jag2 cnull ; n = 4 Jag1/Jag2 control; n = 4 Jag1 cnull ; Jag2 cnull ). Student’s t-test was used to analyze data. Side panels: representative Cgrp immunofluorescence (IF) in controls and mutants ( B ) IF of secretory (Scgb3a2), NEB-associated SSEA1 (CC) and Cgrp (PNEC/NEB) in control and Jag mutants. ( C, D ) Preserved NEB microenvironment in E18.5 Jag1 cnull ; Jag2 cnull double mutants: IF showing NEBs (Cgrp) and NEB-associated CCs (SSEA1, N1ICD, CC10 low ) in double null mutants similar to controls (Ex. inset in D). ( E ) qPCR analysis of Upk3a in E18.5 control and double Jag1 cnull ; Jag2 cnull mutants showing nearly abolished Upk3a expression in mutants (n = 3 in each group). Graph: mean ± SEM; ***p

    Article Snippet: The following primers (Thermo Fisher) were used: Ascl1 (Mm03058063_m1), Cgrp (Mm00801463_g1), Foxj1 (Mm01267279_m1), Scgb1a1/CC10 (Mm00442046_m1), Scgb3a2 (Mm00504412_m1), Upk3a (Mm00452321_m1).

    Techniques: Real-time Polymerase Chain Reaction, Expressing, Immunofluorescence

    Loss of Dll-driven Notch signaling results in expansion of the NEBs. ( A–B ) Ascl1 immunofluorescence (IF) in E14.5 control lungs ( A ) showing discrete clusters of Ascl1+ NEBs in large intrapulmonary airways (bronchi: br) in contrast to the aberrant NEB expansion in Dll1 cnull ; Dll4 cnull lungs. At E18.5 ( B ) NEBs at branchpoints are also enlarged in mutants compared to controls and express Cgrp (bottom panel). ( C ) Double Ki67; Ascl1 IF shows no evidence that NEB expansion results from increased proliferation at E18.5 (top) or E14.5 (bottom panel). ( D ) qPCR analysis of NE markers at E18.5: significant increase in Ascl1 and Cgrp expression in double null mutants compared to controls; single mutant Dll1 cnull but not Dll4 cnull showed increased expression of Ascl1 (n = 3 Dll1 control, n = 5 Dll1 cnull for Ascl1 and n = 4 Dll1 control, n = 5 Dll1 cnull for Cgrp ; n = 3 Dll4 control n = 6 Dll4 cnull for Ascl1 and Cgrp ; n = 3 Dll1/Dll4 control; n = 3 Dll1 cnull ; Dll4 cnull for Ascl1 and Cgrp ). Graphs: mean ± SEM. ***p

    Journal: eLife

    Article Title: Jagged and Delta-like ligands control distinct events during airway progenitor cell differentiation

    doi: 10.7554/eLife.50487

    Figure Lengend Snippet: Loss of Dll-driven Notch signaling results in expansion of the NEBs. ( A–B ) Ascl1 immunofluorescence (IF) in E14.5 control lungs ( A ) showing discrete clusters of Ascl1+ NEBs in large intrapulmonary airways (bronchi: br) in contrast to the aberrant NEB expansion in Dll1 cnull ; Dll4 cnull lungs. At E18.5 ( B ) NEBs at branchpoints are also enlarged in mutants compared to controls and express Cgrp (bottom panel). ( C ) Double Ki67; Ascl1 IF shows no evidence that NEB expansion results from increased proliferation at E18.5 (top) or E14.5 (bottom panel). ( D ) qPCR analysis of NE markers at E18.5: significant increase in Ascl1 and Cgrp expression in double null mutants compared to controls; single mutant Dll1 cnull but not Dll4 cnull showed increased expression of Ascl1 (n = 3 Dll1 control, n = 5 Dll1 cnull for Ascl1 and n = 4 Dll1 control, n = 5 Dll1 cnull for Cgrp ; n = 3 Dll4 control n = 6 Dll4 cnull for Ascl1 and Cgrp ; n = 3 Dll1/Dll4 control; n = 3 Dll1 cnull ; Dll4 cnull for Ascl1 and Cgrp ). Graphs: mean ± SEM. ***p

    Article Snippet: The following primers (Thermo Fisher) were used: Ascl1 (Mm03058063_m1), Cgrp (Mm00801463_g1), Foxj1 (Mm01267279_m1), Scgb1a1/CC10 (Mm00442046_m1), Scgb3a2 (Mm00504412_m1), Upk3a (Mm00452321_m1).

    Techniques: Immunofluorescence, Real-time Polymerase Chain Reaction, Expressing, Mutagenesis

    Expansion of the NEB-associated Club cells (CC) in the absence Delta ligands. ( A ) Double immunofluorescence of E18.5 control and Dll1 cnull ; Dll4 cnull lungs: Ascl1 and Cgrp expression in control and in the abnormally expanded NEBs (dotted areas) of mutants; robust N1ICD and SSEA1 expression in NEB-associated CCs (arrowheads and brackets). ( B ) Double ISH ( Cyp2f2) /immunohistochemistry (Ascl1) showing strong Cyp2f2 expression (arrowheads) in cells flanking the NE microenvironment but only low signals in the NEB-associated CCs (asterisks) of both control and Dll1 cnull ; Dll4 cnull mutants. Note reciprocal high (arrowhead) and low (*) intensity of signals in areas inside and outside the NEB microenvironment. Scale bars in A = 20 μm.

    Journal: eLife

    Article Title: Jagged and Delta-like ligands control distinct events during airway progenitor cell differentiation

    doi: 10.7554/eLife.50487

    Figure Lengend Snippet: Expansion of the NEB-associated Club cells (CC) in the absence Delta ligands. ( A ) Double immunofluorescence of E18.5 control and Dll1 cnull ; Dll4 cnull lungs: Ascl1 and Cgrp expression in control and in the abnormally expanded NEBs (dotted areas) of mutants; robust N1ICD and SSEA1 expression in NEB-associated CCs (arrowheads and brackets). ( B ) Double ISH ( Cyp2f2) /immunohistochemistry (Ascl1) showing strong Cyp2f2 expression (arrowheads) in cells flanking the NE microenvironment but only low signals in the NEB-associated CCs (asterisks) of both control and Dll1 cnull ; Dll4 cnull mutants. Note reciprocal high (arrowhead) and low (*) intensity of signals in areas inside and outside the NEB microenvironment. Scale bars in A = 20 μm.

    Article Snippet: The following primers (Thermo Fisher) were used: Ascl1 (Mm03058063_m1), Cgrp (Mm00801463_g1), Foxj1 (Mm01267279_m1), Scgb1a1/CC10 (Mm00442046_m1), Scgb3a2 (Mm00504412_m1), Upk3a (Mm00452321_m1).

    Techniques: Immunofluorescence, Expressing, In Situ Hybridization, Immunohistochemistry

    Serum procalcitonin (PCT) and calcitonin (CT) immunoreactivity in WT and Calca KO mice. ( A ) Combined levels of serum PCT and CT were measured in WT and KO mice (five per group) using a two-site immunoradiometric assay for rat CT, both under baseline (Bsln)

    Journal: American Journal of Respiratory Cell and Molecular Biology

    Article Title: Deletion of the Gene Encoding Calcitonin and Calcitonin Gene-Related Peptide ? Does Not Affect the Outcome of Severe Infection in Mice

    doi: 10.1165/rcmb.2012-0489OC

    Figure Lengend Snippet: Serum procalcitonin (PCT) and calcitonin (CT) immunoreactivity in WT and Calca KO mice. ( A ) Combined levels of serum PCT and CT were measured in WT and KO mice (five per group) using a two-site immunoradiometric assay for rat CT, both under baseline (Bsln)

    Article Snippet: The qRT-PCR reactions were performed in a 20-μl reaction mix that included 8 ng of cDNA, FAM-labeled PCT exon 3–4 assay primers (assay ID: Mm00801464_m1; Life Technologies, Carlsbad, CA), VIC-labeled glyceraldehyde 3-phosphate dehydrogenase endogenous control assay primers (catalog no. 4352339E; Life Technologies), PerfeCta qRT-PCR FastMix (Quanta Biosciences), and uracil-N-glycolase (Quanta Biosciences).

    Techniques: Mouse Assay, Immunoradiometric Assay

    Responses of wild-type (WT) and Calca knockout (KO) mice to pneumonic challenges. ( A ) WT ( n = 13) and KO ( n = 14) mice were exposed to aerosolized Streptococcus pneumoniae (6.0 × 10 10 CFU/ml for 60 min), and survival was measured after 7 days.

    Journal: American Journal of Respiratory Cell and Molecular Biology

    Article Title: Deletion of the Gene Encoding Calcitonin and Calcitonin Gene-Related Peptide ? Does Not Affect the Outcome of Severe Infection in Mice

    doi: 10.1165/rcmb.2012-0489OC

    Figure Lengend Snippet: Responses of wild-type (WT) and Calca knockout (KO) mice to pneumonic challenges. ( A ) WT ( n = 13) and KO ( n = 14) mice were exposed to aerosolized Streptococcus pneumoniae (6.0 × 10 10 CFU/ml for 60 min), and survival was measured after 7 days.

    Article Snippet: The qRT-PCR reactions were performed in a 20-μl reaction mix that included 8 ng of cDNA, FAM-labeled PCT exon 3–4 assay primers (assay ID: Mm00801464_m1; Life Technologies, Carlsbad, CA), VIC-labeled glyceraldehyde 3-phosphate dehydrogenase endogenous control assay primers (catalog no. 4352339E; Life Technologies), PerfeCta qRT-PCR FastMix (Quanta Biosciences), and uracil-N-glycolase (Quanta Biosciences).

    Techniques: Knock-Out, Mouse Assay

    Responses of WT and Calca KO mice to septic peritoneal challenge. WT and KO mice (five per group) were injected intraperitoneally with 100 μl of an S. pneumonia suspension (50–100 CFU), then killed and evaluated after 24 hours. ( A ) Weight

    Journal: American Journal of Respiratory Cell and Molecular Biology

    Article Title: Deletion of the Gene Encoding Calcitonin and Calcitonin Gene-Related Peptide ? Does Not Affect the Outcome of Severe Infection in Mice

    doi: 10.1165/rcmb.2012-0489OC

    Figure Lengend Snippet: Responses of WT and Calca KO mice to septic peritoneal challenge. WT and KO mice (five per group) were injected intraperitoneally with 100 μl of an S. pneumonia suspension (50–100 CFU), then killed and evaluated after 24 hours. ( A ) Weight

    Article Snippet: The qRT-PCR reactions were performed in a 20-μl reaction mix that included 8 ng of cDNA, FAM-labeled PCT exon 3–4 assay primers (assay ID: Mm00801464_m1; Life Technologies, Carlsbad, CA), VIC-labeled glyceraldehyde 3-phosphate dehydrogenase endogenous control assay primers (catalog no. 4352339E; Life Technologies), PerfeCta qRT-PCR FastMix (Quanta Biosciences), and uracil-N-glycolase (Quanta Biosciences).

    Techniques: Mouse Assay, Injection

    Upregulation of pain and inflammatory markers in degenerating IVDs. Quantitative RT-PCR analyses of ( A–C) pain-related genes (CGRP, BDKRB1 and COMT) and ( D , E ) inflammation-related genes (IL-6 and BDNF) harvested from healthy and degenerated IVDs 2, 6, and 10 weeks after intradiscal puncture (n = 3 per group; *p

    Journal: Scientific Reports

    Article Title: Molecular pain markers correlate with pH-sensitive MRI signal in a pig model of disc degeneration

    doi: 10.1038/s41598-018-34582-6

    Figure Lengend Snippet: Upregulation of pain and inflammatory markers in degenerating IVDs. Quantitative RT-PCR analyses of ( A–C) pain-related genes (CGRP, BDKRB1 and COMT) and ( D , E ) inflammation-related genes (IL-6 and BDNF) harvested from healthy and degenerated IVDs 2, 6, and 10 weeks after intradiscal puncture (n = 3 per group; *p

    Article Snippet: The expression of the following porcine genes was quantified: Bradykinin receptor B1 (BDKRB1; Ss03389804_s1, Thermo Fisher Scientific, Waltham, MA, USA), calcitonin gene–related peptide (CGRP; Ss03386432_uH) and catechol-O -methyltransferase (COMT; Ss04247881_g1), interleukin-6 (IL-6; Ss03384604_u1), and brain-derived neurotrophic factor (BDNF; Ss03822335_s1).

    Techniques: Quantitative RT-PCR

    Immunofluorescence of pain-related marker upregulation. Microphotographs showing IVD tissue samples after immunostaining against COMT, CGRP, and BDKRB1, and counterstaining with DAPI; the samples were examined 2, 6, and 10 weeks after intradiscal puncture. Merged panels of the various stains are presented in the right column (NP = nucleus pulposus, CGRP = calcitonin gene-related peptide, BDKRB1 = bradykinin receptor B1, COMT = catechol- O -methyltransferase).

    Journal: Scientific Reports

    Article Title: Molecular pain markers correlate with pH-sensitive MRI signal in a pig model of disc degeneration

    doi: 10.1038/s41598-018-34582-6

    Figure Lengend Snippet: Immunofluorescence of pain-related marker upregulation. Microphotographs showing IVD tissue samples after immunostaining against COMT, CGRP, and BDKRB1, and counterstaining with DAPI; the samples were examined 2, 6, and 10 weeks after intradiscal puncture. Merged panels of the various stains are presented in the right column (NP = nucleus pulposus, CGRP = calcitonin gene-related peptide, BDKRB1 = bradykinin receptor B1, COMT = catechol- O -methyltransferase).

    Article Snippet: The expression of the following porcine genes was quantified: Bradykinin receptor B1 (BDKRB1; Ss03389804_s1, Thermo Fisher Scientific, Waltham, MA, USA), calcitonin gene–related peptide (CGRP; Ss03386432_uH) and catechol-O -methyltransferase (COMT; Ss04247881_g1), interleukin-6 (IL-6; Ss03384604_u1), and brain-derived neurotrophic factor (BDNF; Ss03822335_s1).

    Techniques: Immunofluorescence, Marker, Immunostaining

    Linear correlation between qCEST and biomarkers in degenerating IVDs. Correlation plots between qCEST signal and expression levels of ( A ) CGRP, ( B ) BDKRB1, ( C ) COMT, ( D ) IL-6, and ( E ) BDNF extracted from degenerated and healthy annulus fibrosus and nucleus pulposus (RQ, relative quantification).

    Journal: Scientific Reports

    Article Title: Molecular pain markers correlate with pH-sensitive MRI signal in a pig model of disc degeneration

    doi: 10.1038/s41598-018-34582-6

    Figure Lengend Snippet: Linear correlation between qCEST and biomarkers in degenerating IVDs. Correlation plots between qCEST signal and expression levels of ( A ) CGRP, ( B ) BDKRB1, ( C ) COMT, ( D ) IL-6, and ( E ) BDNF extracted from degenerated and healthy annulus fibrosus and nucleus pulposus (RQ, relative quantification).

    Article Snippet: The expression of the following porcine genes was quantified: Bradykinin receptor B1 (BDKRB1; Ss03389804_s1, Thermo Fisher Scientific, Waltham, MA, USA), calcitonin gene–related peptide (CGRP; Ss03386432_uH) and catechol-O -methyltransferase (COMT; Ss04247881_g1), interleukin-6 (IL-6; Ss03384604_u1), and brain-derived neurotrophic factor (BDNF; Ss03822335_s1).

    Techniques: Expressing

    PC supernatant induced DRG neurons releasing of SP and CGRP in a protease-dependent way After incubation for 2h, the releasing of SP (A) and CGRP (B) form cultured DRG neurons were higher in PC supernatant group than that in NC supernatant group. Similarly, the mRNA levels for SP (C) and CGRP (D) were significantly increased in DRG neurons treated with PC supernatants. Co-incubation with protease inhibitor FUT-175 (50μg/ml) and PC supernatant reduced this neuropeptide release effect in cultured DRG neurons. Ctr: unstimulated DRG. PC: supernatants cultured from pancreatic cancer tissues. NC: supernatants cultured from normal pancreatic tissues. F: a broad-spectrum serine protease inhibitor, FUT-175.*P

    Journal: Oncotarget

    Article Title: Trypsin-protease activated receptor-2 signaling contributes to pancreatic cancer pain

    doi: 10.18632/oncotarget.18696

    Figure Lengend Snippet: PC supernatant induced DRG neurons releasing of SP and CGRP in a protease-dependent way After incubation for 2h, the releasing of SP (A) and CGRP (B) form cultured DRG neurons were higher in PC supernatant group than that in NC supernatant group. Similarly, the mRNA levels for SP (C) and CGRP (D) were significantly increased in DRG neurons treated with PC supernatants. Co-incubation with protease inhibitor FUT-175 (50μg/ml) and PC supernatant reduced this neuropeptide release effect in cultured DRG neurons. Ctr: unstimulated DRG. PC: supernatants cultured from pancreatic cancer tissues. NC: supernatants cultured from normal pancreatic tissues. F: a broad-spectrum serine protease inhibitor, FUT-175.*P

    Article Snippet: Gene expression probes used in this study were 4352340E, Rn01500392-m1, and Rn01511353-g1 for measuring β-actin, substance P precursor pre-protachykinin (PPT), and CGRP, respectively.

    Techniques: Incubation, Cell Culture, Protease Inhibitor

    PAR-2 antagonist reversed PC supernatant induced releasing of SP and CGRP in cultured DRG neurons (A and B) FS-NH 2 (100μM), a selective antagonist peptide of PAR-2, caused a marked decrease in SP and CGRP releasing in the medium of cultured DRG neurons in contrast to the control peptide LR-NH 2 (100μM). (C and D) Similarly, FS-NH 2 decreased the SP and CGRP mRNA levels in DRG neurons. FS: FSLLRY-NH 2 , PAR-2 antagonist peptide; LR: LRGILS-NH 2, control peptide. *P

    Journal: Oncotarget

    Article Title: Trypsin-protease activated receptor-2 signaling contributes to pancreatic cancer pain

    doi: 10.18632/oncotarget.18696

    Figure Lengend Snippet: PAR-2 antagonist reversed PC supernatant induced releasing of SP and CGRP in cultured DRG neurons (A and B) FS-NH 2 (100μM), a selective antagonist peptide of PAR-2, caused a marked decrease in SP and CGRP releasing in the medium of cultured DRG neurons in contrast to the control peptide LR-NH 2 (100μM). (C and D) Similarly, FS-NH 2 decreased the SP and CGRP mRNA levels in DRG neurons. FS: FSLLRY-NH 2 , PAR-2 antagonist peptide; LR: LRGILS-NH 2, control peptide. *P

    Article Snippet: Gene expression probes used in this study were 4352340E, Rn01500392-m1, and Rn01511353-g1 for measuring β-actin, substance P precursor pre-protachykinin (PPT), and CGRP, respectively.

    Techniques: Cell Culture

    Putative mechanisms for the UVB-induced decrease in adiponectin expression in ovarial adipose tissues. The CGRP signal induced by exposure of the skin to UVB can transfer to the brain and then to the liver, possibly via a neural pathway. Increased CGRP in the liver induces the expression and secretion of SAA via the action of IL-6. In an endocrine manner, SAA in the serum downregulates PPARγ, C/EBPα, C/EBPβ, and aP2 mRNA levels and upregulates IL-6 and MCP-1 mRNA levels in the ovarial adipose tissues. The downregulation of adiponectin expression in the adipose tissues by these factors contributes to the decrease in serum adiponectin. Reduced levels of adiponectin in the serum may impair skin function (Yamane et al . 2010). Thus, the decrease in adiponectin induced by UVB irradiation can have adverse effects on skin function.

    Journal: PLoS ONE

    Article Title: Ultraviolet B Irradiation Reduces the Expression of Adiponectin in Ovarial Adipose Tissues through Endocrine Actions of Calcitonin Gene-Related Peptide-Induced Serum Amyloid A

    doi: 10.1371/journal.pone.0098040

    Figure Lengend Snippet: Putative mechanisms for the UVB-induced decrease in adiponectin expression in ovarial adipose tissues. The CGRP signal induced by exposure of the skin to UVB can transfer to the brain and then to the liver, possibly via a neural pathway. Increased CGRP in the liver induces the expression and secretion of SAA via the action of IL-6. In an endocrine manner, SAA in the serum downregulates PPARγ, C/EBPα, C/EBPβ, and aP2 mRNA levels and upregulates IL-6 and MCP-1 mRNA levels in the ovarial adipose tissues. The downregulation of adiponectin expression in the adipose tissues by these factors contributes to the decrease in serum adiponectin. Reduced levels of adiponectin in the serum may impair skin function (Yamane et al . 2010). Thus, the decrease in adiponectin induced by UVB irradiation can have adverse effects on skin function.

    Article Snippet: The primers and probes for mouse β-actin , adiponectin , PPARγ , C/EBPα , C/EBPβ , aP2, IL-6 , MCP-1 , SAA , IL-1β , TNFα , and CGRP were obtained from Applied Biosystems as Assays-on-Demand primer/probe gene expression products.

    Techniques: Expressing, Irradiation