Human ucMSCs seeded in a decellularized kidney scaffold attenuate renal fibrosis by reducing epithelial-mesenchymal transition via the TGF-β/Smad signaling pathway
Human ucMSCs seeded in a decellularized kidney scaffold attenuate renal fibrosis by reducing epithelial-mesenchymal transition via the TGF-β/Smad signaling pathway
复制标题
接种在脱细胞肾支架中的人 ucMSC 通过 TGF-β/Smad 信号通路减少上皮间质转化，从而减轻肾纤维化
DOI：
10.1038/s41390-019-0736-6
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发表时间：
2020-01-02
影响因子：
3.6
通讯作者：
Wei, Guanghui
中科院分区：
文献类型：
--
作者：
Hu, Dong;Zhang, Deying;Wei, Guanghui
BACKGROUND Renal fibrosis occurs largely through epithelial-mesenchymal transition (EMT). This study explored the beneficial effects of a human umbilical cord mesenchymal stem cell-loaded decellularized kidney scaffold (ucMSC-DKS) on renal fibrosis in a rodent model of post-transplantation renal failure, and the underlying mechanism. METHODS Rat-derived DKSs were examined after preparation, and then recellularized with human ucMSCs to prepare cell-loaded patches. A rat model of renal failure was established after subtotal nephrectomy (STN). The cell patches were transplanted to remnant kidneys. Changes in renal function, histology, EMT, and proteins related to the transforming growth factor-beta (TGF-beta)/Smad signaling pathway in the remnant kidneys were examined 8 weeks after surgery, compared with non-cell patch controls. RESULTS The DKSs were acellular and porous, with rich cytokine and major extracellular matrix components. The ucMSCs were distributed uniformly in the DKSs. Renal function was improved, renal fibrosis and EMT were reduced, and the TGF-beta/Smad signaling pathway was inhibited compared with controls at 8 weeks after ucMSC-DKS patch transplantation. CONCLUSIONS The ucMSC-DKS restores renal function and reduces fibrosis by reducing EMT via the TGF-beta/Smad signaling pathway in rats that have undergone STN. It provides an alternative for renal fibrosis treatment.
