Data for: The PERK/Nrf2 pathway mediates endoplasmic reticulum stress-induced injury by upregulating endoplasmic reticulophagy in H9c2 cardiomyoblasts

Published: 17 October 2019| Version 1 | DOI: 10.17632/dxv5bfjz8s.1
Xiuhua Liu


ERS caused ER-phagy with a decrease in cell viability and an increase in cell death in H9c2 cardiomyoblasts.(A) Live/Dead staining of H9c2 cardiomyoblasts was performed using a LIVE/DEAD® Viability/Cytotoxicity Kit (bar=40 μm, n=3). TG- or TM-treated H9c2 cardiomyoblasts were incubated with calcein-AM (green) and EthD-1 (red) for 10 min, and the fluorescence was visualized using a confocal microscope. Green fluorescence indicates live cells, while red fluorescence indicates dead cells. (E) Ultrastructural lesions in the ER caused by TG or TM and the occurrence of ER-phagy were observed via transmission electron microscopy (bar=500 nm). (F) Representative confocal microscopy images corresponding to analysis of ER-phagy for TG- or TM-treated H9c2 cardiomyoblasts and showing colocalization of autophagosomes with ER-fragments (bar=15 μm; n=3). LC3B was labeled with Texas Red, while calreticulin was labeled with Alexa Fluor 488.



Autophagy, Endoplasmic Reticulum Stress