| Objective:To assess the effect of WISP1on cells proliferation and collagenrelease of HLF-1induced by TGF-β1, and investigate the probablemolecular mechanism.Methods:HLF-1were randomly divided into5groups: the control group(saline),the TGF-β1-treated group(TGF-β1), the WISP1-treated group(WISP1), theTGF-β1+SH-5group(TGF-β1+SH-5) and the TGF-β1+anti-WISP1group(TGF-β1+anti-WISP1). Viable cells of HLF-1were assessed by MTTafter treatment for24h,48h and72h. Collagen levels were determinedusing the Sircol Collagen Assay Kit. The levels of WISP1mRNA in variousgroups were examined by Real-time PCR. Col1a1, Fn1, PI3K, p-Akt andWISP1protein levels were analyzed by Western blotting. The experimentswere performed at least3times.Results:1. The study showed that both TGF-β1and WISP1induced the cells proliferation and collagen release of HLF-1, which were concentrationdependent and time dependent(p<0.05);2. TGF-β1exposure increased the levels of WISP1expression inHLF-1in vitro.3. Anti-WISP1neutralizing antibody could partly inhibit that TGF-β1induced HLF-1cells abnormal activation, and the levels of PI3K, p-Aktwere partly down-regulated in the anti-WISP1group when compared withthat in the TGF-β1group.4. SH-5pretreatment partly inhibited that TGF-β1induced HLF-1cellsabnormal activation and resulted in partial inhibition of p-Akt expression.The levels of WISP1and PI3K didn’t show an obvious change in theTGF-β1+SH-5group when compared with that in the TGF-β1group.Conclusion:1. WISP1may play an important role in HLF-1cells proliferation andcollagen release induced by TGF-β1in vitro;2. The effect of WISP1on HLF-1cells proliferation and collagenrelease is likely due to be involved in PI3K/Akt signaling. |