Inhibition of IRE1/JNK pathway in HK-2 cells subjected to hypoxia-reoxygenation attenuates mesangial cells-derived extracellular matrix production.

ABSTRACT: Endoplasmic reticulum (ER) stress and inflammatory responses play active roles in the transition of acute kidney injury (AKI) to chronic kidney disease (CKD). Inositol-requiring enzyme 1 (IRE1) activates c-Jun NH₂ -terminal kinase (JNK) in ER stress. Tubular epithelial cells (TEC) are the main injury target and source of AKI inflammatory mediators. TEC injury may lead to glomerulosclerosis, however, the underlying mechanism remains unclear. Here, hypoxia/reoxygenation (H/R) HK-2 cells were used as an AKI model. To determine the partial effects of TEC injury on the glomerulus, HK-2 cells after H/R were co-cultured with human renal mesangial cells (HRMC). H/R up-regulated ER stress, IRE1/JNK pathway, IL-6 and MCP-1 in HK-2 cells. Stimulation of HRMC with IL-6 enhanced their prolif

SUBMITTER: Liang Y 

PROVIDER: S-EPMC7701502 | biostudies-literature | 2020 Nov

REPOSITORIES: biostudies-literature