过氧化物酶体增殖物激活受体在小鼠骨髓来源的肥大细胞中表达。

Peroxisome proliferator-activated receptors are expressed in mouse bone marrow-derived mast cells.

作者信息

Sugiyama H, Nonaka T, Kishimoto T, Komoriya K, Tsuji K, Nakahata T

机构信息

Department of Pharmacological Research, Pharmaceuticals Development Laboratories, Teijin Institute for Bio-Medical Research, 4-3-2 Asahigaoka Hino, Tokyo, Japan.

出版信息

FEBS Lett. 2000 Feb 11;467(2-3):259-62. doi: 10.1016/s0014-5793(00)01169-8.

DOI:10.1016/s0014-5793(00)01169-8

PMID:10675550

Abstract

We examined the expression of peroxisome proliferator-activated receptors (PPARs) and the role of PPARs in cytokine production in mouse bone marrow-derived mast cells (mBMMCs). mBMMCs expressed PPARbeta strongly and gamma slightly, but not alpha. Activation of mBMMCs with antigen or calcium ionophore resulted in the increased expression of PPARgamma mRNA specifically. 15-Deoxy-Delta(12, 14)-prostaglandin J(2) (15d-PGJ(2)) and troglitazone, all PPARgamma ligands, attenuated the antigen-induced cytokine production by mBMMCs. Carbaprostacyclin, a PPARbeta ligand, also inhibited cytokine production, whereas PPARalpha ligands did not. These results suggest that PPARbeta and gamma might be included in the negative regulation of mast cell activation.

摘要

我们研究了过氧化物酶体增殖物激活受体（PPARs）的表达及其在小鼠骨髓来源肥大细胞（mBMMCs）细胞因子产生中的作用。mBMMCs强烈表达PPARβ，微弱表达PPARγ，但不表达PPARα。用抗原或钙离子载体激活mBMMCs会导致PPARγ mRNA的表达特异性增加。15-脱氧-Δ（12,14）-前列腺素J2（15d-PGJ2）和曲格列酮这两种PPARγ配体，均可减弱mBMMCs抗原诱导的细胞因子产生。卡前列环素是一种PPARβ配体，也可抑制细胞因子产生，而PPARα配体则无此作用。这些结果表明，PPARβ和PPARγ可能参与肥大细胞激活的负调控。