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Group IIE secretory phospholipase A 2 regulates lipolysis in adipocytes
Author(s) -
Zhi Hui,
Qu Linbing,
Wu Fang,
Chen Ling,
Tao Jun
Publication year - 2015
Publication title -
obesity
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.438
H-Index - 199
eISSN - 1930-739X
pISSN - 1930-7381
DOI - 10.1002/oby.21015
Subject(s) - lipolysis , endocrinology , medicine , chemistry , microbiology and biotechnology , biology , adipose tissue
Objective To examine the function of group IIE secretory phospholipase A 2 (sPLA 2 ‐IIE) in adipocytes and to explore the possible signaling mechanism involved. Methods The expression of sPLA 2 ‐IIE was demonstrated using real‐time PCR and Western blot analysis. Lipid accumulation was evaluated via the measurement of cellular triglycerides (TG). Lipolysis was quantified by measuring the release of free glycerol. The expressions of M‐type sPLA 2 receptor (PLA 2 R1) and the genes encoding adipogenic proteins were measured using real‐time PCR. The activities of the Janus kinase 2 (JAK2), extracellular regulated protein kinase (ERK), and hormone‐sensitive lipase (HSL) were determined using Western blot. Results sPLA 2 ‐IIE ‐/‐ mice gained significantly more epididymal fat than wild‐type (WT) mice. When treated with adipogenic stimuli ex vivo , stromal vascular cells isolated from the adipose tissue of sPLA 2 ‐IIE ‐/‐ mice accumulated significantly more TG than those from WT mice. Conversely, a significant reduction in lipid accumulation and an increase of free glycerol were observed in OP9 cells overexpressing sPLA 2 ‐IIE and in 3T3‐L1 cells treated with sPLA 2 ‐IIE protein. Moreover, sPLA 2 ‐IIE significantly induced adipocyte glycerol release and HSL activity, which was inhibited by PD98059, an ERK inhibitor. Conclusions sPLA 2 ‐IIE regulates lipolysis in adipocytes, likely through the ERK/HSL signaling pathway.