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Group II phospholipase A 2 activates mitogen‐activated protein kinase in cultured rat mesangial cells
Author(s) -
Sugiura Toshihiro,
Wada Akira,
Itoh Takahito,
Tojo Hiromasa,
Okamoto Mitsuhiro,
Imai Enyu,
Kamada Takenobu,
Ueda Naohiko
Publication year - 1995
Publication title -
febs letters
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.593
H-Index - 257
eISSN - 1873-3468
pISSN - 0014-5793
DOI - 10.1016/0014-5793(95)00810-v
Subject(s) - mesangial cell , mitogen activated protein kinase , kinase , endocrinology , protein kinase a , medicine , mesangial proliferative glomerulonephritis , phospholipase d , secretion , protein kinase c , glomerulonephritis , chemistry , signal transduction , microbiology and biotechnology , biology , kidney
Group II phospholipase A 2 (PLA 2 ) is a mediator of inflammation in various disease including glomerulonephritis. We recently found that urinary excretion of PLA 2 was increased in patients with mesangial proliferative glomerulonephritis and that interleukin‐1 (IL‐1) enhanced platelet derived growth factor‐stimulated mesangial cell proliferation through the action of group II PLA 2 secreted in response to IL‐1 stimuli. Here we report signal transducing mechanism through group II PLA 2 in mesangial cells. Group II PLA 2 (1–15 U/ml) rapidly activated mitogen‐activated protein (MAP) kinase. IL‐1β activated MAP kinase in two phases and the slow activation in the late phase, proceeding in parallel with increased group II PLA 2 secretion elicited by IL‐1 treatment, was inhibited by the specific antibody raised against group II PLA 2 . This suggests that the late phase activation of IL‐1‐induced MAP kinase was mediated, at least in part, by secreted group II PLA 2 .