Journal: Genes & Nutrition

Article Title: Preventive effects of protopanaxadiol and protopanaxatriol ginsenosides on liver inflammation and apoptosis in hyperlipidemic apoE KO mice

doi: 10.1007/s12263-011-0245-7

Figure Lengend Snippet: Alterations of lipid profiles and atherogenic indices in plasma and liver tissues of apoE KO mice administrated with the R1 and R2 ginseng extracts

Article Snippet: Animals and treatment Male apoE KO mice with wild-type C57BL/6 were purchased from Japan SLC Incorporation (Tokyo, Japan), which were kept both for 12 weeks on a high-cholesterol diet (1.25% cholesterol, 7.5% cocoa butter, 0.5% sodium cholate, DYET#102068; Dyets Inc., Bethelehem, PA, USA) (Guo et al. 2005 ).

Techniques: Clinical Proteomics

Journal: Genes & Nutrition

Article Title: Preventive effects of protopanaxadiol and protopanaxatriol ginsenosides on liver inflammation and apoptosis in hyperlipidemic apoE KO mice

doi: 10.1007/s12263-011-0245-7

Figure Lengend Snippet: The changes in production of lipid peroxides, LPO, and MDA in apoE KO mice treated with R1 and R2 ginseng extracts

Article Snippet: Animals and treatment Male apoE KO mice with wild-type C57BL/6 were purchased from Japan SLC Incorporation (Tokyo, Japan), which were kept both for 12 weeks on a high-cholesterol diet (1.25% cholesterol, 7.5% cocoa butter, 0.5% sodium cholate, DYET#102068; Dyets Inc., Bethelehem, PA, USA) (Guo et al. 2005 ).

Techniques: Clinical Proteomics

Journal: Genes & Nutrition

Article Title: Preventive effects of protopanaxadiol and protopanaxatriol ginsenosides on liver inflammation and apoptosis in hyperlipidemic apoE KO mice

doi: 10.1007/s12263-011-0245-7

Figure Lengend Snippet: Alterations of lipid profiles and atherogenic indices in plasma and liver tissues of apoE KO mice administrated with the R1 and R2 ginseng extracts

Article Snippet: Male apoE KO mice with wild-type C57BL/6 were purchased from Japan SLC Incorporation (Tokyo, Japan), which were kept both for 12 weeks on a high-cholesterol diet (1.25% cholesterol, 7.5% cocoa butter, 0.5% sodium cholate, DYET#102068; Dyets Inc., Bethelehem, PA, USA) (Guo et al. 2005 ).

Techniques:

Journal: Genes & Nutrition

Article Title: Preventive effects of protopanaxadiol and protopanaxatriol ginsenosides on liver inflammation and apoptosis in hyperlipidemic apoE KO mice

doi: 10.1007/s12263-011-0245-7

Figure Lengend Snippet: The changes in production of lipid peroxides, LPO, and MDA in apoE KO mice treated with R1 and R2 ginseng extracts

Article Snippet: Male apoE KO mice with wild-type C57BL/6 were purchased from Japan SLC Incorporation (Tokyo, Japan), which were kept both for 12 weeks on a high-cholesterol diet (1.25% cholesterol, 7.5% cocoa butter, 0.5% sodium cholate, DYET#102068; Dyets Inc., Bethelehem, PA, USA) (Guo et al. 2005 ).

Techniques:

Journal: Journal of Virology

Article Title: STING agonist diABZI confers protection against swine acute diarrhea syndrome coronavirus in neonatal mice by activating antiviral immunity

doi: 10.1128/jvi.01703-25

Figure Lengend Snippet: SADS-CoV infection has high lethality in C57BL/6J mice. Three-day-old, 7-day-old, and 3-week-old mice were infected with SADS-CoV, and 3-day-old infected mice were used as a control group ( n = 6). ( A ) Newborn C57BL/6J mice were inoculated with SADS-CoV via intraperitoneal injection. ( B ) Daily monitoring of survival rate. ( C ) Clinical scores were monitored daily, with clinical scoring based on . ( D ) Viral RNA in tissues collected from infected mice at 3 and 7 dpi was quantified using RT-qPCR. Data (mean ± SD) are from three independent triplicate experiments. ns, not significant; * P < 0.05; ** P < 0.01; *** P < 0.001; **** P < 0.0001.

Article Snippet: WT C57BL/6J mice of different ages and C57BL/6J Smoc-STING KO mice were procured from Shanghai Model Organisms Center, Inc.

Techniques: Infection, Control, Injection, Quantitative RT-PCR

Journal: Journal of Virology

Article Title: STING agonist diABZI confers protection against swine acute diarrhea syndrome coronavirus in neonatal mice by activating antiviral immunity

doi: 10.1128/jvi.01703-25

Figure Lengend Snippet: The antiviral activity of diABZI against SADS-CoV is STING dependent. SADS-CoV or mock infection of neonatal C57BL/6J wild-type (WT) and C57BL/6J Smoc-STING KO (STING KO ) 3-day-old neonatal mice ( n = 6) was performed, followed by intraperitoneal injection (12 h post-viral infection) of corn oil containing 2.5 mg/kg diABZI (an agonist of the STING pathway) or DMSO dissolved in corn oil once per day for 3 days. The mice were euthanized after 3 days, and spleen tissues were collected for real-time PCR analysis, with a focus on the expression levels of the cytokines IFN-β ( A ), IFN-λ3 ( B ), IFIT1 ( C ), MX1 ( D ), IL-1β ( E ), and IFN-γ ( F ). Scale bar: 100 μm. Data (mean ± SD) are from three independent triplicate experiments. ns, not significant; * P < 0.05; ** P < 0.01; *** P < 0.001; **** P < 0.0001. ( G ) Western blotting was used to evaluate STING and SADS-CoV N protein levels and the phosphorylation status of the STING protein in the spleen. ( H ) Immunofluorescence was used to detect the expression of STING and SADS-CoV N protein in the spleen. ( I ) Mouse mortality rates were recorded daily. ( J ) The expression of SADS-CoV genome copies in spleen tissues was assessed using RT-qPCR. Scale bar: 100 μm. Data (mean ± SD) are from three independent triplicate experiments. ns, not significant; * P < 0.05; ** P < 0.01; *** P < 0.001; **** P < 0.0001. ( K ) Pathological examinations of the brain and spleen were performed via H&E staining. Scale bar: 100 μm.

Article Snippet: WT C57BL/6J mice of different ages and C57BL/6J Smoc-STING KO mice were procured from Shanghai Model Organisms Center, Inc.

Techniques: Activity Assay, Infection, Injection, Real-time Polymerase Chain Reaction, Expressing, Western Blot, Phospho-proteomics, Immunofluorescence, Quantitative RT-PCR, Staining

Journal: Journal of Virology

Article Title: STING agonist diABZI confers protection against swine acute diarrhea syndrome coronavirus in neonatal mice by activating antiviral immunity

doi: 10.1128/jvi.01703-25

Figure Lengend Snippet: The diABZI protects mice from SADS-CoV-induced damage by promoting IFN production. Neonatal C57BL/6J wild-type (WT) mice were intraperitoneally administered IgG1 + diABZI ( n = 6) or anti-IFNAR (1 mg) + diABZI ( n = 6). Spleen tissues were collected for qPCR analysis to assess the mRNA expression levels of the interferon-stimulated genes MX1 ( A ), CXCL10 ( B ), and ISG15 ( C ). Data (mean ± SD) are from three independent triplicate experiments. ns, not significant; * P < 0.05; ** P < 0.01; *** P < 0.001; **** P < 0.0001. Additional neonatal WT mice received the same treatments followed by infection or mock infection with SADS-CoV. Immunohistochemistry was performed to detect SADS-CoV nucleocapsid (N) protein expression in tissues ( D ). Mouse body weight loss ( E ) and survival ( F ) were monitored daily. Scale bar: 100 μm.

Article Snippet: WT C57BL/6J mice of different ages and C57BL/6J Smoc-STING KO mice were procured from Shanghai Model Organisms Center, Inc.

Techniques: Expressing, Infection, Immunohistochemistry

Journal: Respiratory research

Article Title: Lsm2 is critical to club cell proliferation and its inhibition aggravates COPD progression.

doi: 10.1186/s12931-025-03126-8

Figure Lengend Snippet: Fig. 1 Cigarette smoke enhances the expression of Lsm2. A The expression of LSM2 in nonsmokers (Control) and patients with COPD was obtained from the Gene Expression Omnibus (GEO) database, using datasets GSE5058 and GSE8545. B Schematic of COPD modeling. C Immunohistochemistry (IHC) of LSM2 (n = 3 biological replicates). Black arrows indicate LSM2+ cells. D Lsm2 gene expression in mice (n = 6 biological replicates). E Schematic diagram of CSE stimulation in 16HBE cells. F Expression of LSM2 in 16HBE cells stimulated with 1.5% CSE at different time points. G Expression of LSM2 in 16HBE cells stimulated with different concentrations of CSE for 72 h. H Lentivirus-containing short hairpin RNA (shRNA) targeting Lsm2 inhibited Lsm2 expression in 16HBE cells (n = 4 biological replicates). I Reduction in cell viability following Lsm2 knockdown (n = 4 biological replicates). J Cell cycle in NC and shLSM2 group (n = 3 biological replicates). **p < 0.01; ****p < 0.0001

Article Snippet: Construction of COPD model with club cell‐specific Lsm2 knockout mice To generate Club cell-specific Lsm2 knockout mice (Lsm2ΔScgb1a1), C57BL/6J-Lsm2em#1(flox)Smoc mice were crossed with Scgb1a1-IRES-Cre mice obtained from the Shanghai Model Organisms Center, Inc. Wild-type control mice were 8-week-old male C57BL/6 mice purchased from Cyagen Bioscience Inc. and randomly assigned to WT and WT_CS groups.

Techniques: Expressing, Control, Gene Expression, Immunohistochemistry, shRNA, Knockdown

Journal: Respiratory research

Article Title: Lsm2 is critical to club cell proliferation and its inhibition aggravates COPD progression.

doi: 10.1186/s12931-025-03126-8

Figure Lengend Snippet: Fig. 2 Lung-specific Lsm2 knockout exacerbates cigarette smoke-induced lung injury and inflammation. A The diagram of design strategy for generating Lsm2 conditional knockout mice using CRISPR/Cas9 technique. B Experimental design schematic. C Hematoxylin and eosin (HE) staining. The green arrows point to exudative red blood cells, the blue arrows highlight infiltrating inflammatory cells, and the asterisk (*) denotes thickened airways. D Lung tissue pathology scoring, including lung injury score, and MAST, E concentration of TNF-α, CXCL15 and IL-6 in bronchoalveolar lavage fluid (BALF) (pg/mL); Values represent mean ± SD, n = 3–5 for each group. *p < 0.05; **p < 0.01; ****p < 0.0001. NC group Negative control mice, NC_CS group negative control mice exposed to cigarette smoke for 3 months, Lsm2−/− group lung-specific Lsm2 knockout mice, Lsm2−/−_CS group Lung-specific Lsm2 knockout mice exposed to cigarette smoke for 3 months

Article Snippet: Construction of COPD model with club cell‐specific Lsm2 knockout mice To generate Club cell-specific Lsm2 knockout mice (Lsm2ΔScgb1a1), C57BL/6J-Lsm2em#1(flox)Smoc mice were crossed with Scgb1a1-IRES-Cre mice obtained from the Shanghai Model Organisms Center, Inc. Wild-type control mice were 8-week-old male C57BL/6 mice purchased from Cyagen Bioscience Inc. and randomly assigned to WT and WT_CS groups.

Techniques: Knock-Out, CRISPR, Staining, Concentration Assay, Negative Control

Journal: Respiratory research

Article Title: Lsm2 is critical to club cell proliferation and its inhibition aggravates COPD progression.

doi: 10.1186/s12931-025-03126-8

Figure Lengend Snippet: Fig. 4 Club cell-specific Lsm2 knockout exacerbates cigarette smoke (CS)-induced lung inflammation. A Number of differentially expressed genes in four groups (n = 3 biological replicates). B, C Differential genes with significantly increased expression following smoke exposure, which further increased upon Club cell-specific Lsm2 knockout. D Gene Ontology (GO) enrichment analysis of differentially expressed genes. E Number of white blood cells in bronchoalveolar lavage fluid (BALF). F Concentrations of IL-6, CXCL15, and TNF-α in BALF measured by ELISA (pg/ml). Values represent mean ± SD, n = 3–6 for each group. *p < 0.05; **p < 0.01; ***p < 0.001; ****p < 0.0001

Article Snippet: Construction of COPD model with club cell‐specific Lsm2 knockout mice To generate Club cell-specific Lsm2 knockout mice (Lsm2ΔScgb1a1), C57BL/6J-Lsm2em#1(flox)Smoc mice were crossed with Scgb1a1-IRES-Cre mice obtained from the Shanghai Model Organisms Center, Inc. Wild-type control mice were 8-week-old male C57BL/6 mice purchased from Cyagen Bioscience Inc. and randomly assigned to WT and WT_CS groups.

Techniques: Knock-Out, Expressing, Enzyme-linked Immunosorbent Assay

Journal: Respiratory research

Article Title: Lsm2 is critical to club cell proliferation and its inhibition aggravates COPD progression.

doi: 10.1186/s12931-025-03126-8

Figure Lengend Snippet: Fig. 5 Club cell-specific Lsm2 knockout decreases the number of ciliated epithelial cells. A Ciliary structure observed under scanning electron microscopy and transmission electron microscopy. B Length of cilia (μm). C Ciliary beat frequency (CBF, Hz) in tracheal rings. D Immunofluorescence (IF) of α-tubulin. E The percent of α-tubulin+ cells. Values represent mean ± SD, n = 3 for each group. *p < 0.05; **p < 0.01; ***p < 0.001; ****p < 0.0001

Article Snippet: Construction of COPD model with club cell‐specific Lsm2 knockout mice To generate Club cell-specific Lsm2 knockout mice (Lsm2ΔScgb1a1), C57BL/6J-Lsm2em#1(flox)Smoc mice were crossed with Scgb1a1-IRES-Cre mice obtained from the Shanghai Model Organisms Center, Inc. Wild-type control mice were 8-week-old male C57BL/6 mice purchased from Cyagen Bioscience Inc. and randomly assigned to WT and WT_CS groups.

Techniques: Knock-Out, Electron Microscopy, Transmission Assay, Immunofluorescence

Journal: Respiratory research

Article Title: Lsm2 is critical to club cell proliferation and its inhibition aggravates COPD progression.

doi: 10.1186/s12931-025-03126-8

Figure Lengend Snippet: Fig. 6 Club cell-specific Lsm2 knockout modulates cellular composition. A Schematic of lung tissue dissociation to single-cell suspension and loading into the 10× Genomics System. B tSNE visualization of all lung cells showing 29 clusters and tSNE visualization of WT, WT_CS, Lsm2ΔScgb1a1, and Lsm2ΔScgb1a1_CS groups. C tSNE visualization profiling the major cell types. D Bubble plots of the marker genes expressed in the major cell types. E The number and percentage of the major cell types. F tSNE visualization of Club cells and ciliated epithelial cells in WT, WT_CS, Lsm2ΔScgb1a1, and Lsm2ΔScgb1a1_CS groups. G Volcano plot of differential genes of ciliated epithelial cells between WT and Lsm2ΔScgb1a1 groups, and WT_CS and Lsm2ΔScgb1a1_CS groups

Article Snippet: Construction of COPD model with club cell‐specific Lsm2 knockout mice To generate Club cell-specific Lsm2 knockout mice (Lsm2ΔScgb1a1), C57BL/6J-Lsm2em#1(flox)Smoc mice were crossed with Scgb1a1-IRES-Cre mice obtained from the Shanghai Model Organisms Center, Inc. Wild-type control mice were 8-week-old male C57BL/6 mice purchased from Cyagen Bioscience Inc. and randomly assigned to WT and WT_CS groups.

Techniques: Knock-Out, Suspension, Marker

Journal: Respiratory research

Article Title: Lsm2 is critical to club cell proliferation and its inhibition aggravates COPD progression.

doi: 10.1186/s12931-025-03126-8

Figure Lengend Snippet: Fig. 8 Lsm2 regulates the progression of COPD by influencing the differentiation of Club cells into ciliated epithelial cells

Article Snippet: Construction of COPD model with club cell‐specific Lsm2 knockout mice To generate Club cell-specific Lsm2 knockout mice (Lsm2ΔScgb1a1), C57BL/6J-Lsm2em#1(flox)Smoc mice were crossed with Scgb1a1-IRES-Cre mice obtained from the Shanghai Model Organisms Center, Inc. Wild-type control mice were 8-week-old male C57BL/6 mice purchased from Cyagen Bioscience Inc. and randomly assigned to WT and WT_CS groups.

Techniques:

Journal: Frontiers in Immunology

Article Title: Persistent expression of NLRP3 in spinal microglia promotes development of lumbar disc degeneration

doi: 10.3389/fimmu.2022.1064303

Figure Lengend Snippet: Demographic information of Intervertebral disc donors.

Article Snippet: A mouse with CreERT2 knock-in under the microglia-specific Tmem119 promoter (Tmem119p-CreERT2; #031820, Jax Mice, Bar Harbor, ME, USA) ( ) was bred to a mouse with its NLRP3 exon 4 flanked by loxP sites (NLRP3 (fx/fx); #12935, Taconic Biosciences, Rensselaer, NY, USA) that allow constitutive knockout of NLRP3 in microglia after Cre-induced recombination (Tmem119p-CreERT2; NLRP3 (fx/fx)) induced by tamoxifen.

Techniques:

Journal: Frontiers in Immunology

Article Title: Persistent expression of NLRP3 in spinal microglia promotes development of lumbar disc degeneration

doi: 10.3389/fimmu.2022.1064303

Figure Lengend Snippet: Disc NLRP3 levels correlate with the pain and disc degeneration level in LDD patients. Disc specimens from 24 participants who had different levels of Thompson classification of the degeneration and scores for pain were analyzed. (A, B) The NLRP3 protein levels in disc tissue were quantified by ELISA in all 24 specimens. Reads of NLRP3 OD values at 450nm were presented. The correlation between NLRP3 protein levels and pain score ( A , r 2 = 0.85, p<0.0001) or Thompson classification of the degeneration level ( B , p=0.003) was assessed.

Article Snippet: A mouse with CreERT2 knock-in under the microglia-specific Tmem119 promoter (Tmem119p-CreERT2; #031820, Jax Mice, Bar Harbor, ME, USA) ( ) was bred to a mouse with its NLRP3 exon 4 flanked by loxP sites (NLRP3 (fx/fx); #12935, Taconic Biosciences, Rensselaer, NY, USA) that allow constitutive knockout of NLRP3 in microglia after Cre-induced recombination (Tmem119p-CreERT2; NLRP3 (fx/fx)) induced by tamoxifen.

Techniques: Enzyme-linked Immunosorbent Assay

Journal: Frontiers in Immunology

Article Title: Persistent expression of NLRP3 in spinal microglia promotes development of lumbar disc degeneration

doi: 10.3389/fimmu.2022.1064303

Figure Lengend Snippet: NLRP3 is exclusively expressed in disc microglia. Single cell expression profile for mouse spinal cord was obtained from Panglaodb. (A–F) In all analyzed 6 mouse spinal cord samples, NLRP3 (blue rectangle) was exclusively expressed in disc microglia clusters (red rectangle).

Article Snippet: A mouse with CreERT2 knock-in under the microglia-specific Tmem119 promoter (Tmem119p-CreERT2; #031820, Jax Mice, Bar Harbor, ME, USA) ( ) was bred to a mouse with its NLRP3 exon 4 flanked by loxP sites (NLRP3 (fx/fx); #12935, Taconic Biosciences, Rensselaer, NY, USA) that allow constitutive knockout of NLRP3 in microglia after Cre-induced recombination (Tmem119p-CreERT2; NLRP3 (fx/fx)) induced by tamoxifen.

Techniques: Expressing

Journal: Frontiers in Immunology

Article Title: Persistent expression of NLRP3 in spinal microglia promotes development of lumbar disc degeneration

doi: 10.3389/fimmu.2022.1064303

Figure Lengend Snippet: Generation of microglia-specific NLRP3-KO or NLRP3-overexpressing mice. (A) Illustration of mice with microglia-specific depletion of NLRP3 (Tmem119p-CreERT2; NLRP3 (fx/fx)) and their control NLRP3(fx/fx) mice, as well as mice with microglia-specific persistent expression of NLRP3 (Tmem119p-CreERT2; NLRP3mut) and their control NLRP3mut mice. (B) NLRP3 staining was done in spinal discs from tamoxifen-challenged mice. (C, D) Dissociated cells from spinal discs of the mice were FAC sorted for CD68+Tmem119+ microglia, the NLRP3 levels of which were checked by ELISA. (C) The relative levels to those from NLRP3(fx/fx) (=1) were shown. (D) The presentative flow charts of FACS sorting CD68+Tmem119+ microglia. *p<0.05. ns, non-significant. Scale bars are 100µm.

Article Snippet: A mouse with CreERT2 knock-in under the microglia-specific Tmem119 promoter (Tmem119p-CreERT2; #031820, Jax Mice, Bar Harbor, ME, USA) ( ) was bred to a mouse with its NLRP3 exon 4 flanked by loxP sites (NLRP3 (fx/fx); #12935, Taconic Biosciences, Rensselaer, NY, USA) that allow constitutive knockout of NLRP3 in microglia after Cre-induced recombination (Tmem119p-CreERT2; NLRP3 (fx/fx)) induced by tamoxifen.

Techniques: Control, Expressing, Staining, Enzyme-linked Immunosorbent Assay

Journal: Frontiers in Immunology

Article Title: Persistent expression of NLRP3 in spinal microglia promotes development of lumbar disc degeneration

doi: 10.3389/fimmu.2022.1064303

Figure Lengend Snippet: NLRP3 depletion in microglia reduces phagocytosis potential and release of pro-inflammatory cytokines. (A) Phagocytosis for zymosan was assessed in sorted disc microglia from mice with microglia-specific alteration in NLRP3 expression. (B) ELISA for IL-1β, TNFα, IFNɣ, ARG1 and CD163 in sorted disc microglia from mice with microglia-specific alteration in NLRP3 expression. The relative levels to those from NLRP3mut (=1) were shown. *p<0.05. ns, non-significant.

Article Snippet: A mouse with CreERT2 knock-in under the microglia-specific Tmem119 promoter (Tmem119p-CreERT2; #031820, Jax Mice, Bar Harbor, ME, USA) ( ) was bred to a mouse with its NLRP3 exon 4 flanked by loxP sites (NLRP3 (fx/fx); #12935, Taconic Biosciences, Rensselaer, NY, USA) that allow constitutive knockout of NLRP3 in microglia after Cre-induced recombination (Tmem119p-CreERT2; NLRP3 (fx/fx)) induced by tamoxifen.

Techniques: Expressing, Enzyme-linked Immunosorbent Assay

Journal: Frontiers in Immunology

Article Title: Persistent expression of NLRP3 in spinal microglia promotes development of lumbar disc degeneration

doi: 10.3389/fimmu.2022.1064303

Figure Lengend Snippet: NLRP3 depletion in microglia reduces disc degeneration and associated pain. The effects of altering NLRP3 levels in microglia on disc degeneration and associated pain were examined in a mouse model for LDD. A total of 8 groups of mice were included in this experiment. Group 1, NLRP3 (fx/fx) mice received sham operation (Sham); Group 2: NLRP3 (fx/fx) mice received LDD induction (LDD); Group 3: NLRP3mut mice received sham operation; Group 4: NLRP3mut mice received LDD induction; Group 5, Tmem119p-CreERT2; NLRP3 (fx/fx) mice received sham operation; Group 6: Tmem119p-CreERT2; NLRP3 (fx/fx) mice received LDD induction; Group 7: Tmem119p-CreERT2; NLRP3mut mice received sham operation; Group 8: Tmem119p-CreERT2; NLRP3mut mice received LDD induction. Mice were analyzed 8 weeks after LDD or at age of 23-week-old. (A, B) Surgical induction of LDD and the quantification of disc degeneration were performed, shown by representative images (A) and by quantification for degenerative scores (B) . (C) A Von Frey filament test for pain evaluation, shown by the relative mechanically induced withdrawal threshold and by thermally induced withdrawal latency of the paw (normalized to those from NLRP3mut (=1)). *p<0.05. ns: no significance.

Article Snippet: A mouse with CreERT2 knock-in under the microglia-specific Tmem119 promoter (Tmem119p-CreERT2; #031820, Jax Mice, Bar Harbor, ME, USA) ( ) was bred to a mouse with its NLRP3 exon 4 flanked by loxP sites (NLRP3 (fx/fx); #12935, Taconic Biosciences, Rensselaer, NY, USA) that allow constitutive knockout of NLRP3 in microglia after Cre-induced recombination (Tmem119p-CreERT2; NLRP3 (fx/fx)) induced by tamoxifen.

Techniques:

Journal: Frontiers in Immunology

Article Title: Persistent expression of NLRP3 in spinal microglia promotes development of lumbar disc degeneration

doi: 10.3389/fimmu.2022.1064303

Figure Lengend Snippet: Reduction in disc degeneration and associated pain by NLRP3 depletion in microglia may result from an alleviation of neuroinflammation. (A–D) ELISA for NLRP3 (A) , IL-1β (B) , TNFα (C) and IFNɣ (D) levels in disc tissue sham/LDD-treated mice. The relative levels to those from NLRP3mut (=1) were shown. *p<0.05. ns, no significance.

Article Snippet: A mouse with CreERT2 knock-in under the microglia-specific Tmem119 promoter (Tmem119p-CreERT2; #031820, Jax Mice, Bar Harbor, ME, USA) ( ) was bred to a mouse with its NLRP3 exon 4 flanked by loxP sites (NLRP3 (fx/fx); #12935, Taconic Biosciences, Rensselaer, NY, USA) that allow constitutive knockout of NLRP3 in microglia after Cre-induced recombination (Tmem119p-CreERT2; NLRP3 (fx/fx)) induced by tamoxifen.

Techniques: Enzyme-linked Immunosorbent Assay