Literature DB >> 26549357

Interleukin-10 inhibits chronic angiotensin II-induced pathological autophagy.

Raj Kishore1, Prasanna Krishnamurthy2, Venkata Naga Srikanth Garikipati3, Cindy Benedict3, Emily Nickoloff3, Mohsin Khan3, Jennifer Johnson3, Anna M Gumpert3, Walter J Koch4, Suresh Kumar Verma5.   

Abstract

BACKGROUND: Although autophagy is an essential cellular salvage process to maintain cellular homeostasis, pathological autophagy can lead to cardiac abnormalities and ultimately heart failure. Therefore, a tight regulation of autophagic process would be important to treat chronic heart failure. Previously, we have shown that IL-10 strongly inhibited pressure overload-induced hypertrophy and heart failure, but role of IL-10 in regulation of pathological autophagy is unknown. Here we tested the hypothesis that IL-10 inhibits angiotensin II-induced pathological autophagy and this process, in part, leads to improve cardiac function. METHODS AND
RESULTS: Chronic Ang II strongly induced mortality, cardiac dysfunction in IL-10 Knockout mice. IL-10 deletion exaggerated pathological autophagy in response to Ang II treatment. In isolated cardiac myocytes, IL-10 attenuated Ang II-induced pathological autophagy and activated Akt/mTORC1 signaling. Pharmacological or molecular inhibition of Akt and mTORC1 signaling attenuated IL-10 effects on Ang II-induced pathological autophagy. Furthermore, lysosomal inhibition in autophagic flux experiments further confirmed that IL-10 inhibits pathological autophagy via mTORC1 signaling.
CONCLUSION: Our data demonstrate a novel role of IL-10 in regulation of pathological autophagy; thus can act as a potential therapeutic molecule for treatment of chronic heart disease.
Copyright © 2015 Elsevier Ltd. All rights reserved.

Entities:  

Keywords:  Autophagy; Cardiomyocytes; PI3K/Akt signaling; Signaling; mTORC1

Mesh:

Substances:

Year:  2015        PMID: 26549357      PMCID: PMC4689660          DOI: 10.1016/j.yjmcc.2015.11.004

Source DB:  PubMed          Journal:  J Mol Cell Cardiol        ISSN: 0022-2828            Impact factor:   5.000


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