Unlike PPARγ, PPARα or PPARβ/δ activation does not promote human monocyte differentiation toward alternative macrophages
Unlike PPARγ, PPARα or PPARβ/δ activation does not promote human monocyte differentiation toward alternative macrophages
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DOI：
10.1016/j.bbrc.2009.06.047
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发表时间：
2009-08-28
影响因子：
3.1
通讯作者：
Chinetti-Gbaguidi, Giulia
中科院分区：
文献类型：
--
作者：
Bouhlel, Mohamed Amine;Brozek, John;Chinetti-Gbaguidi, Giulia
宏观生物会根据微环境信号调整自己的反应。虽然Th 1细胞因子促进促炎M1巨噬细胞，但Th 2细胞因子促进“替代”抗炎M2巨噬细胞表型。过氧化物酶体增殖物激活受体（PPARs）是在巨噬细胞中表达的配体激活的转录因子，在巨噬细胞中它们控制炎症反应。已经表明，在人和小鼠中，PPAR γ促进单核细胞分化为抗炎M2巨噬细胞，而PHAR β/δ在该过程中的作用仅在小鼠中报道，并且没有关于PPAR α的数据。在此，我们发现与过氧化物酶体增殖物激活受体γ相反，过氧化物酶体增殖物激活受体α和过氧化物酶体增殖物激活受体β/δ的表达总体上与人类动脉粥样硬化病变中M2标记物的表达无关。与脂代谢相关基因呈正相关。此外，与PPARgamma不同，PPARalpha或PPARbeta/delta激活不影响体外人单核细胞分化为M2巨噬细胞。因此，PPARalpha和PPARbeta/delta似乎不调节人巨噬细胞的选择性分化。(C)2009 Elsevier Inc. All rights reserved.
Macrophages adapt their response to micro-environmental signals. While Th1 cytokines promote pro-inflammatory M1 macrophages, Th2 cytokines promote in "alternative" anti-inflammatory M2 macrophage phenotype. Peroxisome proliferator-activated receptors (PPARs) are ligand-activated transcription factors expressed in macrophages where they control the inflammatory response. it has been shown that PPAR gamma promotes the differentiation of monocytes into anti-inflammatory M2 macrophages in humans and mice, while a role for PHAR beta/delta in this process has been reported only in mice and no data are available for PPAR alpha. Here, we show that in contrast to PPAR gamma, expression of PPAR alpha and PPAR beta/delta overall does not correlate with the expression of M2 markers ill human atherosclerotic lesions. whereas a positive correlation with genes of lipid metabolism exists. Moreover, Unlike PPAR gamma, PPAR alpha or PPAR beta/delta activation does not influence human monocyte differentiation into M2 macrophages in vitro. Thus, PPAR alpha and PPAR beta/delta do not appear to modulate the alternative differentiation Of human macrophages. (C) 2009 Elsevier Inc. All rights reserved.