Yu Chen, Yue Ding, Li Ming Wang
Renal fibrosis has been recognized as a serious health threat in the world because of the high cost of treatment and poor prognosis. However, the molecular mechanism of renal fibrosis is still largely unknown. In this study, we aimed at illustrating the role of TRIM35 in the renal fibrosis process. A UUO mouse model and a TGF-β1-induced tubulointerstitial fibrosis model were constructed for the research of renal fibrosis at animal and cell level, respectively. Hematoxylin-eosin and Masson staining were used for visualizing the pathological change. qRT-PCR, Western blot analysis and immunohistochemical staining were used to detect the expression of fibrosis-associated proteins and TRIM35. The results showed that, after the modeling, the expressions of α-SMA, Collagen I, Collagen III, Fibronectin and Snail1 were up-regulated, while the expression of E-cadherin was down-regulated, indicating the successful construction of animal and cell models.
More importantly, TRIM35 was proved to be upregulated in both animal and cell models. Therefore, this study demonstrates the potential promotional effect of TRIM35 in the renal fibrosis process, which may prove to be a new biomarker for the diagnosis and development of new treatments of renal fibrosis.
© 2001-2024 Fundación Dialnet · Todos los derechos reservados