Journal: Circulation research

Article Title: Cardiac Myocyte KLF5 Regulates Ppara Expression and Cardiac Function

doi: 10.1161/CIRCRESAHA.115.306383

Figure Lengend Snippet: (A) Predicted AP-1 (yellow) and KLF (framed) binding sites on mouse Ppara promoter. (B–C) Cardiac mRNA levels of Klf isoforms (B) and protein levels of KLF5 and β-actin (C) in 10–12-weeks old C57BL/6 mice treated with 5 mg/kg LPS or saline (CTRL) (n=4–5; *P<0.05; **P<0.01; ***P<0.001 vs CTRL). (D–E) Ppara, Klf5 and Klf6 mRNA levels in HL-1 cells (D) treated with 1µg/ml LPS or saline (CTRL) for 9h (n=6; *p<0.05 vs. CTRL) or in aMHC-Pparg mice (E) treated with 5mg/kg LPS or saline (CTRL) for 8–10h (n=5; *p<0.05; **p<0.01 vs. CTRL).

Article Snippet: The microarray analysis for cardiac mRNA obtained from α MHC-Klf5 −/− mice was performed by Arraystar (data deposited in {"type":"entrez-geo","attrs":{"text":"GSE63839","term_id":"63839"}} GSE63839 ).

Techniques: Binding Assay, Saline

Journal: Circulation research

Article Title: Cardiac Myocyte KLF5 Regulates Ppara Expression and Cardiac Function

doi: 10.1161/CIRCRESAHA.115.306383

Figure Lengend Snippet: (A–D) Ppara and Klf5 mRNA (A, C) and protein (B, D) levels in HL-1 cells treated with Ad-cJunAsp (A, B) or Ad-KLF5 (C, D); (n=6; *p<0.05; **p<0.01; ***p<0.001 vs CTRL). (E–I) Enrichment of −792/−772 bp region (E, F) or −719/−698 bp region (G, H) of mouse Ppara promoter with c-Jun (E, G) or KLF5 (F, H) of chromatin samples from HL-1 cells treated with Ad-GFP (CTRL) and either Ad-cJunAsp (E, G) or Ad-KLF5 (F, H); **p<0.01 vs CTRL. (I) Enrichment of −792/−772 bp region of mouse Ppara promoter with c-Jun or KLF5 of chromatin samples from HL-1 cells treated with 1 µg/ml LPS or saline (CTRL); *p<0.05 vs CTRL. Data for all bar graphs are represented as means ± SEM (statistical analysis: t-test).

Article Snippet: The microarray analysis for cardiac mRNA obtained from α MHC-Klf5 −/− mice was performed by Arraystar (data deposited in {"type":"entrez-geo","attrs":{"text":"GSE63839","term_id":"63839"}} GSE63839 ).

Techniques: Saline

Journal: Circulation research

Article Title: Cardiac Myocyte KLF5 Regulates Ppara Expression and Cardiac Function

doi: 10.1161/CIRCRESAHA.115.306383

Figure Lengend Snippet: (A, B) Klf5 mRNA in the heart, skeletal muscle, intestine, kidney, white adipose tissue, brain (A) and primary cardiac myocytes (B) of aMHC-Klf5−/− mice (n=3; *p<0.05 vs floxed). (C) Hierarchical clustering for differentially expressed mRNAs detected by whole genome microarray analysis of cardiac mRNA obtained from aMHC-Klf5−/− mice and control floxed mice. Red color indicates high relative expression and blue color indicates low relative expression. (D–G) Gene ontology analysis for classification of the downregulated (D) or upregulated (E) genes based on the metabolic process that they are associated with and pathway analysis for downregulated (F) and upregulated (G) genes detected with whole genome microarray analysis of cardiac mRNA obtained from aMHC-Klf5−/− mice and control floxed mice. Data for all bar graphs are represented as means ± SEM (statistical analysis: t-test).

Article Snippet: The microarray analysis for cardiac mRNA obtained from α MHC-Klf5 −/− mice was performed by Arraystar (data deposited in {"type":"entrez-geo","attrs":{"text":"GSE63839","term_id":"63839"}} GSE63839 ).

Techniques: Microarray, Control, Expressing

Journal: Circulation research

Article Title: Cardiac Myocyte KLF5 Regulates Ppara Expression and Cardiac Function

doi: 10.1161/CIRCRESAHA.115.306383

Figure Lengend Snippet: (A) Ingenuity pathway analysis of genes regulated over 2-fold in the aMHC-Klf5−/− mouse array that are related to FA metabolism. (B) Cardiac Klf5 and Ppara mRNA levels of 10- to 12-week-old aMHC-Klf5−/− male and female mice (n=5; **p<0.01; ***p<0.001 vs same gender floxed mice). (C) Cardiac PPARα and β-actin protein levels of 10- to 12-week-old floxed and aMHC-Klf5−/− male mice. (D–F) Cardiac mRNA levels for FA oxidation- (Ppargc-1a, Ppargc-1β, Pparg, Ppard, Acox and Cpt1b) (D), lipid uptake- (Cd36, Lpl and Angptl4) (E) and lipid storage-related genes (Dgat1, Dgat2, Plin2, Plin5) (F) (n=5; *p<0.05, **p<0.01, ***p<0.001 vs same gender floxed mice). (G) Cardiac PGC-1, CPT-1, DGAT-1, ATGL, phosphorylated AMPK, total AMPK, and GAPDH protein levels of 10- to 12-week-old floxed and aMHC-Klf5−/− male mice. (H, I) [14C]-Palmitic acid (H) and [14C]-Glucose (I) oxidation levels in cardiac muscle of 10- to 12-week-old floxed and aMHC-Klf5−/− male mice (n=4–5; *p<0.05; **p<0.01 vs floxed mice). Data for all bar graphs are represented as means ± SEM (statistical analysis: t-test).

Article Snippet: The microarray analysis for cardiac mRNA obtained from α MHC-Klf5 −/− mice was performed by Arraystar (data deposited in {"type":"entrez-geo","attrs":{"text":"GSE63839","term_id":"63839"}} GSE63839 ).

Techniques:

Journal: Circulation research

Article Title: Cardiac Myocyte KLF5 Regulates Ppara Expression and Cardiac Function

doi: 10.1161/CIRCRESAHA.115.306383

Figure Lengend Snippet: (A–F) Fractional shortening (A, D), left ventricular internal dimension during diastole (B, E), left ventricular internal dimension during systole (C, F), in 2–3 months old (A–C) and 6 months old (D–F) αMHC-Klf5−/− and floxed (WT) mice. (G–M) Photographs of echocardiograms (G), fractional shortening (H), left ventricular internal dimension during diastole (I), left ventricular internal dimension during systole (J) left ventricular posterior wall during diastole (K) left ventricular posterior wall during systole (L), and heart weight/tibia length ratio (M) in 8–12 months old αMHC-Klf5−/− and floxed (WT) mice (n=7–8; *p<0.05). (N, O) Cardiac mRNA levels for Bnp, Anf, αMHC and βMHC genes in 2–3 months old (N) and 11–12 months old (O) male floxed and αMHC-Klf5−/− mice (F) (n=5; *p<0.05, **p<0.01 vs floxed mice).

Article Snippet: The microarray analysis for cardiac mRNA obtained from α MHC-Klf5 −/− mice was performed by Arraystar (data deposited in {"type":"entrez-geo","attrs":{"text":"GSE63839","term_id":"63839"}} GSE63839 ).

Techniques:

Journal: Circulation research

Article Title: Cardiac Myocyte KLF5 Regulates Ppara Expression and Cardiac Function

doi: 10.1161/CIRCRESAHA.115.306383

Figure Lengend Snippet: (A) Ingenuity pathway analysis of cardiac genes regulated over 2-fold in the aMHC-Klf5−/− mouse array that have direct or indirect association with insulin signaling and glucose metabolism proteins. Highlighted with bold fonts within the diagram are proteins that modulate insulin signaling. (B) Fractional shortening of C57BL/6 mice 6 weeks post-STZ or saline (CTRL) administration (n=5; *p<0.05 vs CTRL). (C) Western blot analysis for cardiac KLF5 and β-actin protein levels in C57BL/6 mice 6 weeks post-STZ administration (n=3; ***p<0.001 vs CTRL). (D) Cardiac Klf5 and Ppara mRNA levels in floxed and aMHC-Klf5−/− mice 6 weeks post-STZ administration (n=5; *p<0.05, **p<0.01 vs CTRL). (E) Cardiac Klf5 and Ppara mRNA levels in 12 weeks old ob/ob mice compared with wild type C57BL/6 mice (n=4–5, *p<0.05, ***p<0.001 vs wt). (F–I) Plasma glucose levels (F, G) and cardiac Klf5 and Ppara mRNA levels (H, I) in wild type mice treated with STZ (6 weeks prior to glucose measurement), dapagliflozin (F, H), antisense oligonucleotides against SGLT2 (SGLT2-ASO) (G, I) and combination of either STZ with dapagliflozin (F, H) or STZ with SGLT2-ASO (G, I) (n=5, **p<0.01, ***p<0.001 vs CTRL).

Article Snippet: The microarray analysis for cardiac mRNA obtained from α MHC-Klf5 −/− mice was performed by Arraystar (data deposited in {"type":"entrez-geo","attrs":{"text":"GSE63839","term_id":"63839"}} GSE63839 ).

Techniques: Saline, Western Blot, Clinical Proteomics

Journal: Molecular Therapy. Nucleic Acids

Article Title: MicroRNA-26b-5p Inhibits Mouse Liver Fibrogenesis and Angiogenesis by Targeting PDGF Receptor-Beta

doi: 10.1016/j.omtn.2019.02.014

Figure Lengend Snippet: The Expression Pattern of PDGFR-β in the Fibrotic Liver of MCDHF Mice and the Correlation between PDGFR-β and Fibrosis and Angiogenesis Markers (A) Representative H&E, Sirius Red, and oil red O stainings in the fibrotic liver of MCDHF mice. The mRNA expressions of fibrosis markers (B), angiogenesis markers (C), and PDGFR-β (D) were examined by qRT-PCR in the fibrotic liver of MCDHF mice. PDGFR-β protein expression was examined (E) and quantified (F) by western blot in the fibrotic liver. Data are presented as the mean ± SEM. n = 6 per group. *p < 0.05 versus control.

Article Snippet: KEGG, Reactome, and GO analyses were performed to explore the function and pathways based on differentially expressed genes. mRNA microarray experiments and technical assistance in bioinformatic analysis were handled by Capitalbio Technology (Beijing, China).

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

Journal: Molecular Therapy. Nucleic Acids

Article Title: MicroRNA-26b-5p Inhibits Mouse Liver Fibrogenesis and Angiogenesis by Targeting PDGF Receptor-Beta

doi: 10.1016/j.omtn.2019.02.014

Figure Lengend Snippet: The Origin of PDGFR-β + Cells in MCDHF Fibrotic Mice and the Expression of PDGFR-β in TGF-β1-Treated BMSCs In Vivo (A) Representative images of immunofluorescence analysis to track PDGFR-β (green) expression in the fibrotic liver. Hollow arrows indicate PDGFR-β expression around the newly formed vessels, while solid arrows indicate PDGFR-β expression around the existing mature vessels. (B) Immunofluorescence staining for PDGFR-β (red) to track PDGFR-β + cells following 56 days of MCDHF diet. (C) The proportion of PDGFR-β + EGFP + cells accounting for total PDGFR-β + cells was measured by Image-Pro Plus software. (D) PDGFR-β mRNA expression was examined by qRT-PCR in BMSCs treated with the indicated concentrations of TGF-β1 for 24 h. (E) PDGFR-β mRNA expression in BMSCs treated with 10 ng/mL TGF-β1 at different times. (F and G) PDGFR-β protein expression was examined (F) and quantified (G) by western blot in TGF-β1-treated BMSCs. Data are presented as the mean ± SEM. n = 6 per group. *p < 0.05 versus control.

Article Snippet: KEGG, Reactome, and GO analyses were performed to explore the function and pathways based on differentially expressed genes. mRNA microarray experiments and technical assistance in bioinformatic analysis were handled by Capitalbio Technology (Beijing, China).

Techniques: Expressing, In Vivo, Immunofluorescence, Staining, Software, Quantitative RT-PCR, Western Blot, Control

Journal: Molecular Therapy. Nucleic Acids

Article Title: MicroRNA-26b-5p Inhibits Mouse Liver Fibrogenesis and Angiogenesis by Targeting PDGF Receptor-Beta

doi: 10.1016/j.omtn.2019.02.014

Figure Lengend Snippet: Downregulation of PDGFR-β Expression by miR-26b-5p in TGF-β1-Treated BMSCs (A) miR-26b-5p expression in the fibrotic liver induced by MCDHF. (B) The correlation between miR-26b-5p and PDGFR-β in liver tissue. Transfection efficiency of miR-26b-5p mimic (C) or inhibitor (F) in BMSCs is shown. PDGFR-β mRNA expression was examined by qRT-PCR with or without miR-26b-5p mimic (D) or inhibitor (G) transfection in BMSCs. Protein expression was examined by western blot with miR-26b-5p mimic (E) or inhibitor (H) transfection in BMSCs. Biotin-avidin pull-down assay (I) and luciferase reporter assay (J) demonstrated PDGFR-β was a target of miR-26b-5p. Data are presented as the mean ± SEM. n = 6 per group. *p < 0.05 versus control. #p < 0.05 versus TGF-β1 treated alone.

Article Snippet: KEGG, Reactome, and GO analyses were performed to explore the function and pathways based on differentially expressed genes. mRNA microarray experiments and technical assistance in bioinformatic analysis were handled by Capitalbio Technology (Beijing, China).

Techniques: Expressing, Transfection, Quantitative RT-PCR, Western Blot, Avidin-Biotin Assay, Pull Down Assay, Luciferase, Reporter Assay, Control

Journal: Molecular Therapy. Nucleic Acids

Article Title: MicroRNA-26b-5p Inhibits Mouse Liver Fibrogenesis and Angiogenesis by Targeting PDGF Receptor-Beta

doi: 10.1016/j.omtn.2019.02.014

Figure Lengend Snippet: Regulation of lncMEG3 on PDGFR-β in TGF-β1-Treated BMSCs (A) lncMEG3 expression was examined by qRT-PCR in the fibrotic liver induced by MCDHF. (B) The correlation between lncMEG3 and PDGFR-β in liver tissue. Transfection efficiency of lncMEG3 overexpression plasmid (C) or siRNA (F) in BMSCs is shown. PDGFR-β mRNA expression was examined by qRT-PCR with lncMEG3 overexpression plasmid (D) or siRNA (G) in BMSCs. PDGFR-β protein expression was examined by western blot with lncMEG3 overexpression plasmid (E) or siRNA (H) in BMSCs. Data are presented as the mean ± SEM. n = 6 per group. *p < 0.05 versus control. #p < 0.05 versus TGF-β1 treated alone.

Article Snippet: KEGG, Reactome, and GO analyses were performed to explore the function and pathways based on differentially expressed genes. mRNA microarray experiments and technical assistance in bioinformatic analysis were handled by Capitalbio Technology (Beijing, China).

Techniques: Expressing, Quantitative RT-PCR, Transfection, Over Expression, Plasmid Preparation, Western Blot, Control

Journal: Molecular Therapy. Nucleic Acids

Article Title: MicroRNA-26b-5p Inhibits Mouse Liver Fibrogenesis and Angiogenesis by Targeting PDGF Receptor-Beta

doi: 10.1016/j.omtn.2019.02.014

Figure Lengend Snippet: miR-26b-5p Was Sponged by lncMEG3 in TGF-β1-Treated BMSCs (A) The correlation between lncMEG3 and miR-26b-5p in liver tissue. Biotin-avidin pull-down assay (B) and luciferase reporter assay (C) demonstrated that lncMEG3 was a target of miR-26b-5p. (D) PDGFR-β mRNA expression with or without lncMEG3 overexpression plasmids in miR-26b-5p mimic-treated BMSCs. (E) PDGFR-β protein expression with or without lncMEG3 overexpression plasmids in miR-26b-5p mimic-treated BMSCs. Data are presented as the mean ± SEM. n = 6 per group. *p < 0.05 versus control. #p < 0.05 versus miR-26b-5p mimic treated alone.

Article Snippet: KEGG, Reactome, and GO analyses were performed to explore the function and pathways based on differentially expressed genes. mRNA microarray experiments and technical assistance in bioinformatic analysis were handled by Capitalbio Technology (Beijing, China).

Techniques: Avidin-Biotin Assay, Pull Down Assay, Luciferase, Reporter Assay, Expressing, Over Expression, Control

Journal: Molecular Therapy. Nucleic Acids

Article Title: MicroRNA-26b-5p Inhibits Mouse Liver Fibrogenesis and Angiogenesis by Targeting PDGF Receptor-Beta

doi: 10.1016/j.omtn.2019.02.014

Figure Lengend Snippet: Microarray Analysis Was Performed in TGF-β1-Treated BMSCs with or without miR-26b-5p Mimics BMSCs were treated with 10 ng/mL TGF-β1 for 24 h with or without miR-26b-5p mimics. Microarray analysis for mRNA was performed with RNA extracted from BMSCs. Hierarchical cluster analysis of significantly differentially expressed mRNA is shown as follows: bright green, underexpression; black, no change; bright red, overexpression. n = 3 per group. (A) Microarray heatmap comparing the signatures of PDGFR-β and angiogenesis marker and fibrosis marker genes in TGF-β1-treated BMSCs with or without miR-26b-5p mimics. KEGG and Reactome enrichment analyses (B) and GO enrichment analysis for biological process terms (C) are for the differentially expressed genes with miR-26b-5p mimics. n = 3 per group. (D) Predicted protein network visualization with STRING. The network view predicted the associations between proteins from the regulated genes involved in angiogenesis and extracellular matrix organization in TGF-β1-treated BMSCs. The network nodes were proteins. These proteins were clustered using k-means clustering algorithms.

Article Snippet: KEGG, Reactome, and GO analyses were performed to explore the function and pathways based on differentially expressed genes. mRNA microarray experiments and technical assistance in bioinformatic analysis were handled by Capitalbio Technology (Beijing, China).

Techniques: Microarray, Over Expression, Marker

Journal: Molecular Therapy. Nucleic Acids

Article Title: MicroRNA-26b-5p Inhibits Mouse Liver Fibrogenesis and Angiogenesis by Targeting PDGF Receptor-Beta

doi: 10.1016/j.omtn.2019.02.014

Figure Lengend Snippet: The Regulation of miR-26b-5p Agomir on PDGFR-β Expression, Liver Fibrosis, and Angiogenesis In Vivo (A) Transfection efficiency of 50 nM miR-26b-5p agomir (mimic in vivo ) in the fibrotic liver of MCDHF mice. (B) PDGFR-β mRNA levels in liver tissue were measured by qRT-PCR with or without miR-26b-5p agomir injection in MCDHF mice. (C) PDGFR-β protein levels in liver tissue were measured by western blot. (D) Representative images of immunofluorescence analysis to track PDGFR-β (red) expression in BMSCs (green) in the fibrotic liver. (E) The proportion of PDGFR-β + EGFP + cells of total PDGFR-β + cells was measured by Image-Pro Plus software. Hollow arrows indicate PDGFR-β − EGFP + cells, while solid arrows indicate PDGFR-β + EGFP + cells. DAPI was used to visualize nuclei (blue). The mRNA levels of angiogenesis markers (F) and fibrosis markers (G) in the fibrotic liver are shown. Data are presented as the mean ± SEM. n = 6 per group. *p < 0.05 versus control. #p < 0.05 versus MCDHF treated alone.

Article Snippet: KEGG, Reactome, and GO analyses were performed to explore the function and pathways based on differentially expressed genes. mRNA microarray experiments and technical assistance in bioinformatic analysis were handled by Capitalbio Technology (Beijing, China).

Techniques: Expressing, In Vivo, Transfection, Quantitative RT-PCR, Injection, Western Blot, Immunofluorescence, Software, Control

Journal: International Journal of Clinical and Experimental Pathology

Article Title: Long non-coding RNA P4713 contributes to the malignant phenotypes of oral squamous cell carcinoma by activating the JAK/STAT3 pathway

doi:

Figure Lengend Snippet: Analysis of long non-coding RNAs (lncRNAs) in oral squamous cell carcinoma (OSCC). A: Heat map, volcano plot, and log-log scatter plot showing differentially expressed lncRNAs between four OSCC samples and paired adjacent normal tissues (fold change > 2.0, P < 0.05). B: The expression of lncRNA P4713 was detected by quantitative real-time PCR (qRT-PCR) in 22 OSCC tissues and adjacent non-cancerous tissues. The results are expressed as log10 (2-ΔΔCt). A log2 fold change ≥ +2 or ≤ -2 was considered significant upregulation or downregulation (dotted lines). C: Relative P4713 expression in OSCC cell lines was measured by qRT-PCR. Columns represent the mean of three independent experiments; bars, the s.d; *P < 0.05; **P < 0.01. D: Confocal microscopic fluorescent in situ hybridization images and qRT-PCR results. Scale bar = 10 µm. E: Genome location analysis of human P4713 by the UCSC Genome Browser. F: Representative fluorescent images of at least three independent experiments. Scale bar = 10 µm. G: Relative levels of GFP expression by Western blot.

Article Snippet: Microarray analysis The OSCC lncRNA/mRNA microarray analysis was performed by CapitalBio Corporation (Beijing, China).

Techniques: Expressing, Real-time Polymerase Chain Reaction, Quantitative RT-PCR, In Situ Hybridization, Western Blot

Journal: International Journal of Clinical and Experimental Pathology

Article Title: Long non-coding RNA P4713 contributes to the malignant phenotypes of oral squamous cell carcinoma by activating the JAK/STAT3 pathway

doi:

Figure Lengend Snippet: The effects of P4713 on oral squamous cell carcinoma cell proliferation in vitro. A: The relative expression of P4713 was examined by qRT-PCR in HSC-3 and UM1 cells. B: Cell proliferation was measured by CCK-8 assay. C: Detection for colony-formation assays after knockdown of P4713. D: Cell cycle analysis using propidium iodide staining. E: Western blot analysis of cyclin D1, CDK4, and CDK6 after P4713 knockdown.

Article Snippet: Microarray analysis The OSCC lncRNA/mRNA microarray analysis was performed by CapitalBio Corporation (Beijing, China).

Techniques: In Vitro, Expressing, Quantitative RT-PCR, CCK-8 Assay, Knockdown, Cell Cycle Assay, Staining, Western Blot

Journal: International Journal of Clinical and Experimental Pathology

Article Title: Long non-coding RNA P4713 contributes to the malignant phenotypes of oral squamous cell carcinoma by activating the JAK/STAT3 pathway

doi:

Figure Lengend Snippet: Silencing of P4713 suppressed the migration and invasion of oral squamous cell carcinoma (OSCC) cells. A: Inhibition of migration in HSC-3 and UM1 cells after P4713 knockdown. B: A Matrigel invasion assay was performed using an invasion chamber after treatment with si-P4713. C: In vitro migration was assessed by wound healing experiments. D: E-cadherin, N-cadherin, and vimentin were analyzed by western blotting.

Article Snippet: Microarray analysis The OSCC lncRNA/mRNA microarray analysis was performed by CapitalBio Corporation (Beijing, China).

Techniques: Migration, Inhibition, Knockdown, Invasion Assay, In Vitro, Western Blot

Journal: International Journal of Clinical and Experimental Pathology

Article Title: Long non-coding RNA P4713 contributes to the malignant phenotypes of oral squamous cell carcinoma by activating the JAK/STAT3 pathway

doi:

Figure Lengend Snippet: The relationship between P4713 and the JAK/STAT3 pathway. (A) Hierarchically clustered heatmaps of mRNAs altered in oral squamous cell carcinoma (OSCC; fold change > 2, P < 0.05). (B) The lncRNA-P4713 subnetwork in the OSCC co-expression network. (C) The top twenty GO terms of upregulated and downregulated mRNAs in OSCC cases (P < 0.05). (D) Significantly enriched pathways of the indicated gene sets. (E) qRT-PCR and (F) western blotting were used to measure the JAK/STAT3 pathway affected by P4713. (G) Representative fluorescent images of the location of STAT3. Scale bar = 10 µm.

Article Snippet: Microarray analysis The OSCC lncRNA/mRNA microarray analysis was performed by CapitalBio Corporation (Beijing, China).

Techniques: Expressing, Quantitative RT-PCR, Western Blot

Journal: Oxidative Medicine and Cellular Longevity

Article Title: GLX351322, a Novel NADPH Oxidase 4 Inhibitor, Attenuates TMJ Osteoarthritis by Inhibiting the ROS/MAPK/NF- κ B Signaling Pathways

doi: 10.1155/2023/1952348

Figure Lengend Snippet: Transcriptomic analysis of the TMJ synovium samples from normal and CFA-injected rats. (a) Schematic diagram of the experimental design and procedure for sample preparation for mRNA microarray. (b) Volcano plots of differentially expressed genes (DEGs). (c) Clustered heat map of all targets. (d) Heat map of the inflammation-related genes (fold change ≥ 2.0 and P < 0.05). (e) KEGG pathway enrichment analysis on differentially expressed genes between the control and CFA-injected groups.

Article Snippet: Total RNA was extracted by using a TRIzol reagent, and gene expression was examined by mRNA microarray analysis (KangChen Bio-tech, Shanghai, China).

Techniques: Injection, Sample Prep, Microarray