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Heme oxygenase1 protects H2O2insulted glomerular mesangial cells from excessive autophagy.

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Heme oxygenase1 protects H2O2insulted glomerular mesangial cells from excessive autophagy.

Content Provider	World Health Organization (WHO)-Global Index Medicus
Author	Chi, Yanchun Zhang, Kun Cui, Rui Xu, Jia Li, Jinshun Wang, Jinhua
Description	Author Affiliation: Xu J ( Department of Nephrology, The Fourth Affiliated Hospital, Harbin Medical University, Harbin, Heilongjiang 150001, P.R. China.); Li J ( Department of Cardiology, The Nangang Branch Hospital of Heilongjiang Provincial Hospital, Nangang, Heilongjiang 150000, P.R. China.); Wang J ( Department of Pharmacy Intravenous Admixture Service, The First Affiliated Hospital of Harbin Medical University, Harbin, Heilongjiang 572000, P.R. China.); Chi Y ( Department of Nephrology, The Fourth Affiliated Hospital, Harbin Medical University, Harbin, Heilongjiang 150001, P.R. China.); Zhang K ( Department of Nephrology, The Fourth Affiliated Hospital, Harbin Medical University, Harbin, Heilongjiang 150001, P.R. China.); Cui R ( Department of Nephrology, The Fourth Affiliated Hospital, Harbin Medical University, Harbin, Heilongjiang 150001, P.R. China.)
Abstract	Increasing evidence has demonstrated that the activation of heme oxygenase (HO)1 reduces autophagy stimulated by oxidative stress injury, in which the supraphysiological production of reactive oxygen species (ROS) is detected. However, the potential mechanism underlying this effect remains unclear. The present study aimed to investigate the function of HO1 activation in the regulation of autophagy in glomerular mesangial cells subjected to H2O2induced oxidative stress injury. The results demonstrated that the HO1 agonist, hemin, reduces the LC3 protein level, which was enhanced by H2O2 treatment. Furthermore, heminactivated HO1 may function as a regulator of oxidative stressinduced autophagy in a dosedependent manner. Pharmacological activation of cJun Nterminal kinase (JNK) inhibited the effect of hemin, indicating that the JNK signaling pathway is associated with the mechanism of HO1 in impeding excessive autophagy. In addition to successfully alleviating H2O2induced oxidative stress and cellular apoptosis, heminactivated HO1 may provide cytoprotection against rapamycin, a specific autophagy agonist. The present result suggested the inhibitory action of HO1 in the avoidance of a potentially enhanced linkage between autophagy and apoptosis, particularly in the setting of excessive ROS. Therefore, enhancing the intracellular activity of HO1 may assist the crosstalk between oxidative stress, autophagy and apoptosis, and represent a novel therapeutic strategy for renal ischemic disease.
ISSN	17912997
e-ISSN	17913004
Journal	Molecular Medicine Reports
Issue Number	6
Volume Number	13
Language	English
Publisher	Spandidos Publications
Publisher Date	2016-06-01
Publisher Place	Greece
Access Restriction	Open
Subject Keyword	Discipline Molecular Biology
Content Type	Text
Resource Type	Article
Subject	Genetics Biochemistry Molecular Biology Cancer Research Molecular Medicine Oncology

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