NLRC5, the largest member of the Nucleotide-binding domain and leucine-rich repeat (NLR) protein family, is recently proven to be a critical modulator in fibrogenesis. However, the role of NLRC5 in renal fibrosis remains unknown. In the present study, we investigated the effects of NLRC5 on transforming growth factor β1 (TGF-β1)-stimulated rat renal fibroblasts in vitro. Our results showed that the expression of NLRC5 was also obviously upregulated in renal fibrosis tissues and TGF-β1-treated NRK-49F cells. Knockdown of NLRC5 inhibited the proliferation of NRK-49F cells induced by TGF-β1, as well as suppressed the accumulation of extracellular matrix (ECM) in NRK-49F cells induced by TGF-β1. Furthermore, knockdown of NLRC5 inhibited the expression of phosphorylated Smad3 in TGF-β1-treated NRK-49F cells. In conclusion, our results show that knockdown of NLRC5 inhibits renal fibroblast activation via modulating TGF-β1/Smad signaling pathway. Therefore, NLRC5 may act as a key mediator in renal fibroblast activation and fibrogenesis.
Keywords: Extracellular matrix (ECM); NLRC5; Renal fibrosis; Transforming growth factor β1 (TGF-β1).
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