lncRNA MALAT1 mediated high glucose-induced HK-2 cell epithelial-to-mesenchymal transition and injury.

Journal of Physiology and Biochemistry
Jun ZhangXun Tang

Abstract

Epithelial-to-mesenchymal transition (EMT) and injury of tubular cells play critical roles in the pathogenesis of diabetic nephropathy (DN). lncRNA metastasis-associated lung adenocarcinoma transcript 1 (MALAT1) has been shown to be involved in DN progression. However, whether MALAT1 induces EMT and injury in tubular cells is unclear. Here, we investigated the effects of MALAT1 on human proximal tubular cells (HK-2 cells) and the underlying mechanism. We performed qPCR to detect MALAT1, E-cadherin, α-smooth muscle actin (α-SMA), kidney injury molecule 1 (KIM-1), and neutrophil gelatinase-associated lipocalin (NGAL). Additionally, we conducted Western blot analyses to measure E-cadherin, α-SMA, cyclin D1, c-Myc, and β-catenin in HK-2 cells cultured with normal glucose and high glucose (HG) and in transfected cells or cells treated with LiCl and DKK-1. The β-catenin localization was observed using immunofluorescence, and the protein levels of NGAL and KIM-1 were evaluated by ELISA. We found that HG-upregulated MALAT1 decreased E-cadherin and increased α-SMA, KIM-1, NGAL, cyclin D1, c-Myc, and β-catenin in HK-2 cells. LiCl exposure increased the expression of α-SMA but decreased that of E-cadherin on the base of knocking down MALA...Continue Reading

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Citations

Aug 6, 2020·Life·Jinwen LinJianghua Chen
Feb 13, 2021·Frontiers in Pharmacology·Yue-Yu GuHui-Yao Lan
Mar 23, 2020·Phytomedicine : International Journal of Phytotherapy and Phytopharmacology·Xin MouWen Hong Liu
Feb 26, 2021·Diabetes, Metabolic Syndrome and Obesity : Targets and Therapy·Langen ZhuangGuoxi Jin

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Methods Mentioned

BETA
enzyme-linked immunosorbent assay
PCR
transfection

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