| Summary: | 博士 === 中山醫學大學 === 醫學研究所 === 106 === Objective：Tubulointerstitial fibrosis can lead to end-stage renal disease. Pentraxin 3 (PTX3) is an acute phase protein produced by resident and innate immunity cells. We investigated the effect of PTX3 on cultured human proximal tubular epithelial (HK-2) cells and a rat unilateral ureteral obstruction (UUO) model of renal fibrosis.
Methods and Materials：Gain-of-function experiments were used to examine the effect of recombinant human PTX3 (Rh-PTX3) on HK-2 cells. Cell proliferation (MTT assay) and in vitro cell migration were measured. The levels of PTX3, p-JNK1/2, and EMT markers were measured using immunohistochemistry, RT-PCR, and western blotting in UUO rats and HK-2 cells.
Results：HK-2 cells treated with Rh PTX3 did not affect cell viability, but significantly increased cell migration. Moreover, Rh-PTX3 increased the expression of snail, slug, N-cadherin, and vimentin, decreased the expression of E-cadherin, and increased the phosphorylation of JNK1/2. SP600126 (a specific JNK1/2 inhibitor) enhanced the effects of Rh-PTX3. Rats with UUO exhibited time-dependent increased levels of PTX3, p-JNK1/2, and vimentin, and decreased expression of E-cadherin.
Conclusion and Suggestion：Our results suggest that PTX3 induces cell migration via upregulation of EMT in a JNK1/2-dependent mechanism, and highlight the role of PTX3 in the pathogenesis renal fibrosis.
|
|---|
