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已发表论文

左右决定因子 1(LEFTY1) 减少了 NRK-49F 细胞中由 TGF-β1 诱导的成纤维细胞向肌成纤维细胞的表型转化

 

Authors Zhang LJ, Zhang J, Xu CG, Zhou XJ, Wang W, Zheng RP, Hu W, Wu P
Received 17 April 2015
Accepted for publication 23 June 2015
Published 14 August 2015 Volume 2015:9 Pages 4669—4678
DOI http://dx.doi.org/10.2147/DDDT.S86770
Checked for plagiarism Yes
Review by Single-blind
Peer reviewers approved by Dr Syed Nasir Abbas Bhukari
Peer reviewer comments 3
Editor who approved publication:  Professor Shu-Feng Zhou


Abstract: Fibroblast activation and proliferation are important for fibroblast–myofibroblast transdifferentiation, a crucial process in the pathological changes that define renal interstitial fibrosis. The left–right determination factor (Lefty) is an important cytokine of the transforming growth factor (TGF)-β family, with two variants, Lefty-1 and Lefty-2, in mice. Lefty has diverse functions, such as the regulation of embryonic development, the inhibition of TGF-β1 signaling, and the suppression of tumor activity. However, whether Lefty-1 influences fibroblast activation and proliferation, and consequently prevents fibroblast–myofibroblast transdifferentiation, remains unclear. This study aimed to investigate whether Lefty-1 can attenuate TGF-β1-induced fibroblast–myofibroblast transdifferentiation in normal rat kidney interstitial fibroblast cells (NRK-49F), as well as the mechanisms underlying any effects. Results showed that the typical fibroblast cell morphology of NRK-49F cells was altered after TGF-β1 treatment and that Lefty-1 significantly prevented this change in a dose-dependent manner. Further analyses demonstrated decreased proliferating cell nuclear antigen, cyclin D1, collagen I(A1), alpha-smooth muscle actin, and fibronectin expression. Lefty-1 further induced remarkable reductions in TGF-β1-induced Smad3 and mitogen-activated protein kinase-10/c-Jun N-terminal kinase (JNK-3) signaling, and enhanced expression of the antifibrotic factor bone morphogenetic protein (BMP)-5. However, without TGF-β1, Lefty-1 had no effect on Smad3, JNK-3, and BMP-5 activation and fibroblast–myofibroblast transdifferentiation. Taken together, these findings indicate that Lefty-1 can alleviate TGF-β1-mediated activation and the proliferation of fibroblasts. Furthermore, Lefty-1 may prevent fibroblast–myofibroblast transdifferentiation in part via modulations of Smad3, JNK-3, and BMP-5 activities in the TGF-β/BMP signaling pathway.
Keywords: Lefty-1, NRK-49F, fibroblast, myofibroblast, transdifferentiation


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