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Protective role for cytosolic phospholipase A 2 α in autoimmune diabetes of mice
Author(s) -
Oikawa Y.,
Yamato E.,
Tashiro F.,
Yamamoto M.,
Uozumi N.,
Shimada A.,
Shimizu T.,
Miyazaki J.
Publication year - 2005
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/j.febslet.2005.06.024
Subject(s) - insulitis , diabetes mellitus , endocrinology , nod , tumor necrosis factor alpha , medicine , nod mice , alpha (finance) , type 1 diabetes , prostaglandin e , immunology , phospholipase a2 , autoimmunity , cytokine , chemistry , immune system , enzyme , biochemistry , construct validity , nursing , patient satisfaction
Cytosolic phospholipase A 2 α (cPLA 2 α) plays an important role in arachidonate pathway. To investigate the contribution of cPLA 2 α to autoimmune diabetes, we established non‐obese diabetic (NOD) mouse, an excellent model for human type 1 diabetes, deficient in cPLA 2 α. These mice showed severe insulitis and a higher incidence of diabetes. In their macrophages, decreased prostaglandin E 2 (PGE 2 ) induced by cPLA 2 α deficiency, and the increase in production of tumor necrosis factor (TNF)‐α were observed. These results suggested that cPLA 2 α plays a protective role in progression of insulitis and development of autoimmune diabetes by suppression of TNF‐α production from macrophages.