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Exogenous CXCL13 promoted the fibrogenesis in mouse L929 and human CCD-18Co fibroblasts. (A) The mRNA expressions of fibrogenesis-related genes α-SMA, Tgf‐β, MMP-9, Col1a1 and Col3a1 in L929 fibroblasts. ( B ) The fluorescence intensity of COL1A1 in L929 fibroblasts with immunofluorescent staining (× 200, COL1A1 (green) and DAPI (blue)). ( C ) The protein expressions of α-SMA and COL1A1 in L929 fibroblasts. (D) The mRNA expressions of fibrogenesis-related genes α-sma, tgf‐β, and col1a1 in CCD-18Co fibroblasts. ( E ) The protein expressions of α-SMA and COL1A1 in CCD-18Co fibroblasts. ( F ) The protein expressions of p-Akt, p-p38, p-ERK, and p-JNK. ( G ) The mRNA expressions of CXCL13 specific receptor, Cxcr5 . ( H ) <t>Inhibitors</t> targeting Akt (MK-2206 dihydrochloride, 1 μM, MCE), p38 (SB233580, 10 μM, MCE), ERK (U0126, 10 μM, MCE), and JNK (SP600125, 10 μM, MCE) demonstrated a significant reversal of CXCL13-induced upregulation of fibrosis-promoting genes Col1a1 and Col3a1 . ( I ) Blocking CXCR5 with siRNA reversed the up-regulation of CXCL13-induced fibrogenesis-related genes Col1a1 and Col3a1 . Data represent the means ± SEM. * P < 0.05, ** P < 0.01, *** P < 0.001.
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Exogenous CXCL13 promoted the fibrogenesis in mouse L929 and human CCD-18Co fibroblasts. (A) The mRNA expressions of fibrogenesis-related genes α-SMA, Tgf‐β, MMP-9, Col1a1 and Col3a1 in L929 fibroblasts. ( B ) The fluorescence intensity of COL1A1 in L929 fibroblasts with immunofluorescent staining (× 200, COL1A1 (green) and DAPI (blue)). ( C ) The protein expressions of α-SMA and COL1A1 in L929 fibroblasts. (D) The mRNA expressions of fibrogenesis-related genes α-sma, tgf‐β, and col1a1 in CCD-18Co fibroblasts. ( E ) The protein expressions of α-SMA and COL1A1 in CCD-18Co fibroblasts. ( F ) The protein expressions of p-Akt, p-p38, p-ERK, and p-JNK. ( G ) The mRNA expressions of CXCL13 specific receptor, Cxcr5 . ( H ) Inhibitors targeting Akt (MK-2206 dihydrochloride, 1 μM, MCE), p38 (SB233580, 10 μM, MCE), ERK (U0126, 10 μM, MCE), and JNK (SP600125, 10 μM, MCE) demonstrated a significant reversal of CXCL13-induced upregulation of fibrosis-promoting genes Col1a1 and Col3a1 . ( I ) Blocking CXCR5 with siRNA reversed the up-regulation of CXCL13-induced fibrogenesis-related genes Col1a1 and Col3a1 . Data represent the means ± SEM. * P < 0.05, ** P < 0.01, *** P < 0.001.

Journal: Journal of Advanced Research

Article Title: Adiponectin deficiency prevents chronic colitis-associated colonic fibrosis via inhibiting CXCL13 production

doi: 10.1016/j.jare.2024.12.032

Figure Lengend Snippet: Exogenous CXCL13 promoted the fibrogenesis in mouse L929 and human CCD-18Co fibroblasts. (A) The mRNA expressions of fibrogenesis-related genes α-SMA, Tgf‐β, MMP-9, Col1a1 and Col3a1 in L929 fibroblasts. ( B ) The fluorescence intensity of COL1A1 in L929 fibroblasts with immunofluorescent staining (× 200, COL1A1 (green) and DAPI (blue)). ( C ) The protein expressions of α-SMA and COL1A1 in L929 fibroblasts. (D) The mRNA expressions of fibrogenesis-related genes α-sma, tgf‐β, and col1a1 in CCD-18Co fibroblasts. ( E ) The protein expressions of α-SMA and COL1A1 in CCD-18Co fibroblasts. ( F ) The protein expressions of p-Akt, p-p38, p-ERK, and p-JNK. ( G ) The mRNA expressions of CXCL13 specific receptor, Cxcr5 . ( H ) Inhibitors targeting Akt (MK-2206 dihydrochloride, 1 μM, MCE), p38 (SB233580, 10 μM, MCE), ERK (U0126, 10 μM, MCE), and JNK (SP600125, 10 μM, MCE) demonstrated a significant reversal of CXCL13-induced upregulation of fibrosis-promoting genes Col1a1 and Col3a1 . ( I ) Blocking CXCR5 with siRNA reversed the up-regulation of CXCL13-induced fibrogenesis-related genes Col1a1 and Col3a1 . Data represent the means ± SEM. * P < 0.05, ** P < 0.01, *** P < 0.001.

Article Snippet: Exogenous CXCL13 promoted the fibrogenesis in mouse L929 and human CCD-18Co fibroblasts. (A) The mRNA expressions of fibrogenesis-related genes α-SMA, Tgf‐β, MMP-9, Col1a1 and Col3a1 in L929 fibroblasts. ( B ) The fluorescence intensity of COL1A1 in L929 fibroblasts with immunofluorescent staining (× 200, COL1A1 (green) and DAPI (blue)). ( C ) The protein expressions of α-SMA and COL1A1 in L929 fibroblasts. (D) The mRNA expressions of fibrogenesis-related genes α-sma, tgf‐β, and col1a1 in CCD-18Co fibroblasts. ( E ) The protein expressions of α-SMA and COL1A1 in CCD-18Co fibroblasts. ( F ) The protein expressions of p-Akt, p-p38, p-ERK, and p-JNK. ( G ) The mRNA expressions of CXCL13 specific receptor, Cxcr5 . ( H ) Inhibitors targeting Akt (MK-2206 dihydrochloride, 1 μM, MCE), p38 (SB233580, 10 μM, MCE), ERK (U0126, 10 μM, MCE), and JNK (SP600125, 10 μM, MCE) demonstrated a significant reversal of CXCL13-induced upregulation of fibrosis-promoting genes Col1a1 and Col3a1 . ( I ) Blocking CXCR5 with siRNA reversed the up-regulation of CXCL13-induced fibrogenesis-related genes Col1a1 and Col3a1 .

Techniques: Fluorescence, Staining, Blocking Assay