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Regulation of renal fibrotic factors in unilateral ureteral obstruction model and human tubular epithelial cell by Lin28a
Gwon-Soo Jung3,# (Senior researcher), Yeo Jin Hwang2,# (researcher), Jun-Hyuk Choi1 (researcher), Kyeong-Min Lee 1,* (Senior researcher)
1Division of Biotechnology and 2Division of Electronics & Information System, Daegu Gyeongbuk Institute of Science and Technology,
3New Drug Development Center, Daegu-Gyeongbuk Medical Innovation Foundation
Background: Lin28a has diverse functions including regulation of cancer, reprogramming and regeneration, but whether it promotes injury or is a protective reaction to renal injury is unknown.
Methods: We studied how Lin28a acts in UUO-induced renal fibrosis, following unilateral ureteral obstruction, in a mouse model. We further defined the role of Lin28a in transforming growth factor (TGF)-signaling pathways in renal fibrosis through in vitro study using human tubular epithelium-like HK-2 cells.
Results: In the mouse unilateral ureteral obstruction model, obstruction markedly decreased the expression of Lin28a, increased the expression of renal fibrotic markers such as type I collagen, メ-SMA, vimentin and fibronectin. In TGF-モ-stimulated HK-2 cells, the expression of Lin28a was reduced and the expression of renal fibrotic markers such as type I collagen, メ-SMA, vimentin and fibronectin was increased. Adenovirus-mediated overexpression of Lin28a inhibited the expression of TGF-モ-stimulated type I collagen, メ-SMA, vimentin and fibronectin. Lin28a inhibited TGF-モ-stimulated SMAD3 activity, via inhibition of SMAD3 phosphorylation, but not the MAPK pathway ERK, JNK or p38.
Conclusion: Lin28a attenuates renal fibrosis in obstructive nephropathy, making its mechanism a possible therapeutic target for chronic kidney disease.
Abstract, Accepted Manuscript(in press) [Submitted on July 17, 2020, Accepted on October 5, 2020]
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