Mesenchymal Stem Cells Ameliorate Fibrosis by Enhancing Autophagy via Inhibiting Galectin-3/Akt/mTOR Pathway and by Alleviating the EMT via Inhibiting Galectin-3/Akt/GSK3β/Snail Pathway in NRK-52E Fibrosis

• DOI: 10.15283/ijsc22014
• Publication Date: 2022-04-29T00:12:50Z
• Authors: Yu Zhao; Chuan Guo; Lianlin Zeng; Jialing Li; Xia Liu; Yiwei Wang; Kun Zhao; Bo Chen
• Keywords: Myofibroblast

Epithelial-Mesenchymal transition (EMT) is one of the origins myofibroblasts in renal interstitial fibrosis. Mesenchymal stem cells (MSCs) alleviating EMT has been proved, but concrete mechanism unclear. To explore mechanism, serum-free MSCs conditioned medium (SF-MSCs-CM) was used to treat rat tubular epithelial (NRK-52E) fibrosis induced by transforming growth factor-β1 (TGF-β1) which ameliorated EMT.Galectin-3 knockdown (Gal-3 KD) and overexpression OE) lentiviral vectors were established transfected into NRK-52E. NRK-52E model TGF-β1 treated with SF-MSCs-CM for 24 h after modelling. Fibrosis autophagy related indexes detected western blot immunocytochemistry. In group, expressions α-smooth muscle actin (α-SMA), fibronectin (FN), Galectin-3, Snail, Kim-1, ratios P-Akt/Akt, P-GSK3β/GSK3β, P-PI3K/PI3K, P-mTOR/mTOR, TIMP1/MMP9, LC3B-II/I obviously increased, E-Cadherin (E-cad) P62 decreased significantly compared control group. showed an opposite trend treatment Whether Gal-3 KD or OE cells, also similar trends. However, effects anti-fibrosis enhanced more obvious than those cells.SF-MSCs-CM probably alleviated via inhibiting Galectin-3/Akt/GSK3β/Snail pathway. Meanwhile, possibly Galectin-3/Akt/mTOR pathway, synergistically Targeting galectin-3 may be a potential target