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Medical AI Inquiry: You was designed to assist in medical decision-making based on the provided user questions. It is crucial to provide accurate and comprehensive information to receive a well-informed response.  Labels: OBJECTIVE, METHODS, RESULTS. Meshes: 3T3-L1 Cells, Adipocytes, Adipose Tissue, Animals, Extracellular Signal-Regulated MAP Kinases, Glycerol, Group II Phospholipases A2, Lipolysis, Mice, Mitogen-Activated Protein Kinases, Signal Transduction, Sterol Esterase, Triglycerides.
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Does group IIE secretory phospholipase A2 regulate lipolysis in adipocytes? Context: To examine the function of group IIE secretory phospholipase A(2) (sPLA(2) -IIE) in adipocytes and to explore the possible signaling mechanism involved. 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. 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.
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sPLA(2) -IIE regulates lipolysis in adipocytes, likely through the ERK/HSL signaling pathway. Final Decision: yes