Suppr超能文献

II型磷脂酶A2与培养的小鼠肥大细胞在FcepsilonRI和细胞因子依赖性激活后由环氧合酶-2介导的前列腺素D2延迟生成有关。

Type II phospholipase A2 is linked to cyclooxygenase-2-mediated delayed prostaglandin D2 generation by cultured mouse mast cells following FcepsilonRI- and cytokine-dependent activation.

作者信息

Ashraf M M, Murakami M, Shimbara S, Amakasu Y, Atsumi G, Kudo I

机构信息

Department of Health Chemistry, School of Pharmaceutical Sciences, Showa University, 1-5-8 Hatanodai, Shinagawa-ku, Tokyo, Japan.

出版信息

Biochem Biophys Res Commun. 1996 Dec 24;229(3):726-32. doi: 10.1006/bbrc.1996.1872.

Abstract

Treatment of murine bone marrow-derived mast cells (BMMC) with interleukin (IL)-10 and IL-1beta increased the expression of type II secretory phospholipase A2 (sPLA2), but not cytosolic PLA2 (cPLA2), after culture for several hours. Further stimulation with IgE and antigen (IgE/Ag) increased cyclooxygenase (COX)-2 expression dramatically, accompanied by augmented delayed prostaglandin (PG) D2 generation over several hours. BMMC were also found to express type IIC PLA2 (PLA2-IIC), a recently described novel sPLA2 possessing 16 cysteine residues, expression of which changed minimally after BMMC activation. Delayed PGD2 generation was suppressed by approximately 80% by an antibody raised against recombinant murine type II sPLA2. These results suggest that, of the three PLA2s expressed in BMMC, type II sPLA2 is the critical enzyme that is coupled with COX-2-dependent PGD2 generation elicited by IgE/Ag in the presence of IL-10 + IL-1beta.

摘要

用白细胞介素(IL)-10和IL-1β处理小鼠骨髓来源的肥大细胞(BMMC)数小时后,II型分泌型磷脂酶A2(sPLA2)的表达增加,但胞质型磷脂酶A2(cPLA2)的表达未增加。用免疫球蛋白E和抗原(IgE/Ag)进一步刺激可显著增加环氧合酶(COX)-2的表达,并在数小时内伴随延迟性前列腺素(PG)D2生成的增加。还发现BMMC表达IIC型磷脂酶A2(PLA2-IIC),这是一种最近描述的具有16个半胱氨酸残基的新型sPLA2,其表达在BMMC激活后变化极小。针对重组小鼠II型sPLA2产生的抗体可使延迟性PGD2生成抑制约80%。这些结果表明,在BMMC中表达的三种磷脂酶A2中,II型sPLA2是在存在IL-10 + IL-1β的情况下与IgE/Ag引发的COX-2依赖性PGD2生成相关的关键酶。

文献检索

告别复杂PubMed语法,用中文像聊天一样搜索,搜遍4000万医学文献。AI智能推荐,让科研检索更轻松。

立即免费搜索

文件翻译

保留排版,准确专业,支持PDF/Word/PPT等文件格式,支持 12+语言互译。

免费翻译文档

深度研究

AI帮你快速写综述,25分钟生成高质量综述,智能提取关键信息,辅助科研写作。

立即免费体验