In vivo sodium tungstate treatment prevents E-cadherin loss induced by diabetic serum in HK-2 cell line

Journal of Cellular Physiology
Romina BertinatAlejandro J Yáñez

Abstract

Diabetic nephropathy (DN) is characterized by interstitial inflammation and fibrosis, which is the result of chronic accumulation of extracellular matrix produced by activated fibroblasts in the renal tubulointerstitium. Renal proximal tubular epithelial cells (PTECs), through the process of epithelial-to-mesenchymal transition (EMT), are the source of fibroblasts within the interstitial space, and loss of E-cadherin has shown to be one of the earliest steps in this event. Here, we studied the effect of the anti-diabetic agent sodium tungstate (NaW) in the loss of E-cadherin induced by transforming growth factor (TGF) β-1, the best-characterized in vitro EMT promoter, and serum from untreated or NaW-treated diabetic rats in HK-2 cell line, a model of human kidney PTEC. Our results showed that both TGFβ-1 and serum from diabetic rat induced a similar reduction in E-cadherin expression. However, E-cadherin loss induced by TGFβ-1 was not reversed by NaW, whereas sera from NaW-treated rats were able to protect HK-2 cells. Searching for soluble mediators of NaW effect, we compared secretion of TGFβ isoforms and vascular endothelial growth factor (VEGF)-A, which have opposite actions on EMT. One millimolar NaW alone reduced secretion...Continue Reading

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Citations

Aug 23, 2018·Journal of Cellular Physiology·Romina BertinatFrancisco Nualart
Oct 31, 2016·Journal of Cellular Physiology·Romina BertinatAlejandro J Yáñez
Dec 2, 2021·American Journal of Physiology. Cell Physiology·Michael P GrantCasimiro Gerarduzzi

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