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Globular Adiponectin Induces Endoplasmic Reticulum Stress and Autophagy in Macrophages
Author(s) -
Oh HyeJin,
Pun Nirmala Tilija,
Raut Pawan Kumar,
Kim EunHye,
Khakurel Amrita,
Shrestha Aastha,
Park PilHoon
Publication year - 2017
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.31.1_supplement.670.1
Subject(s) - endoplasmic reticulum , unfolded protein response , autophagy , microbiology and biotechnology , adiponectin , chemistry , protein kinase a , kinase , biology , endocrinology , apoptosis , biochemistry , insulin resistance , insulin
Adiponectin, a kind of adipokine predominantly secreted from adipose tissue, is known to possess various biological functions. We have previously shown that globular adiponectin induces autophagy in macrophages, which is implicated in the suppression of inflammatory cytokines production and acts as a cell survival mechanism rather than cell death. Endoplasmic reticulum (ER) is a membranous cell organelle and carries out the process of protein folding and modifying to maintain cellular homeostasis. ER stress triggered by ER malfunction and excessive demand for protein folding induces cellular oxidative stress. It has been shown that ER stress is a potent trigger of autophagy, which is implicated in cell survival pathway. In the present study, we investigated the effect of globular adiponectin on ER stress and further its role in autophagy induction in RAW 264.7 macrophages. We found that globular adiponectin treatment induces phosphorylation of protein kinase RNA‐like endoplasmic reticulum kinase (PERK) and increase in expression of CCAAT/‐enhancer‐binding protein homologous protein (CHOP), implying that adiponectin stimulates ER stress. Given that ER stress is one of the critical mechanisms leading to autophagy induction, these results suggest a possibility that adiponectin induces autophagy via ER stress. In addition, interestingly, treatment with moderate dose of globular adiponectin significantly enhanced cell viability determined by MTS assay and decreased caspase‐3 activity in RAW 264.7 macrophages, indicating that adiponectin treatment causes growth and survival of macrophages. Taken together, these findings suggest a hypothesis that adiponectin protects macrophages from various extracellular stresses such as lipopolysaccharide (LPS) via autophagy activation mediated by ER stress. Further studies would provide better insights into the mechanisms underlying adiponectin‐induced protection of macrophages, particularly in relation to the role of ER stress and autophagy.