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Inhibited autophagy may contribute to heme toxicity in cardiomyoblast cells.

Abstract：

:Several groups have demonstrated that induction of heme-oxygenase-1 (HO-1) could protect the myocardium against ischemic events; however, heme accumulation could lead to toxicity. The aim of the present study was to investigate the role of autophagy in heme toxicity. H9c2 cardiomyoblast cells were treated with different dose of hemin or cobalt-protoporphyrin IX (CoPPIX) or vehicle. Cell viability was measured by MTT assay. DCF and MitoSOX staining was employed to detect reactive oxygen species. Western blot analysis was performed to analyse the levels of HO-1, certain autophagy related proteins and pro-caspase-3 as an apoptosis marker. To study the autophagic flux, CytoID staining was carried out and cells were analyzed by fluorescence microscope and flow cytometry. Decreased cell viability was detected at high dose of hemin and CoPPIX treated H9c2 cells in a dose-dependent manner. Furthermore, at concentration of the inducers used in the present study a significantly enhanced level of ROS were detected. As it was expected both treatments induced a robust elevation of HO-1 level. In addition, the Beclin-1- independent autophagy was significantly increased, but caused a defective autophagic flux with triggered activation of caspase-3. In conclusion, these results suggest that overexpression of HO-1 by high dose of hemin and CoPPIX can induce cell toxicity in H9c2 cells via enhanced ROS level and impaired autophagy.

journal_name

Biochem Biophys Res Commun

journal_title

Biochemical and biophysical research communications

authors

Gyongyosi A,Szoke K,Fenyvesi F,Fejes Z,Debreceni IB,Nagy B Jr,Tosaki A,Lekli I

doi

10.1016/j.bbrc.2019.02.140

subject

Has Abstract

pub_date

2019-04-16 00:00:00

pages

732-738

issue

4

eissn

0006-291X

issn

1090-2104

pii

S0006-291X(19)30341-9

journal_volume

511

pub_type

杂志文章

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