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首页> 外文期刊>International immunopharmacology >Atorvastatin promotes human monocyte differentiation toward alternative M2 macrophages through p38 mitogen-activated protein kinase-dependent peroxisome proliferator-activated receptor gamma activation
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Atorvastatin promotes human monocyte differentiation toward alternative M2 macrophages through p38 mitogen-activated protein kinase-dependent peroxisome proliferator-activated receptor gamma activation

机译：阿托伐他汀通过p38丝裂原激活的蛋白激酶依赖性过氧化物酶体增殖物激活的受体γ激活促进人类单核细胞向其他M2巨噬细胞分化

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M1 and M2 macrophages are detectable in human atherosclerotic lesions, and M2 macrophages are present at locations distant from the lipid core in more stable zones of the plaque and appear to exert anti-inflammatory properties on M1 macrophages. Peroxisome proliferator-activated receptor (PPAR) gamma promotes the differentiation of monocytes into anti-inflammatory M2 macrophages. Although both statins and PPAR gamma ligands have been reported to protect against the progression of atherosclerosis, no data are currently available regarding the implication of statins in the alternative differentiation of human monocytes. In the present study, we hypothesized that atorvastatin may exert novel effects to prime human monocytes toward an anti-inflammatory alternative M2 phenotype. To this aim, we first found that abundant M2 markers were expressed in human circulating monocytes after atorvastatin treatment. Moreover, atorvastatin was able to induce PPAR gamma expression and activation in human monocytes in vivo and in vitro, resulting in priming primary human monocytes differentiation into M2 macrophages with a more pronounced paracrine anti-inflammatory activity in M1 macrophages. Additional data with molecular approaches revealed that p38 mitogen-activated protein kinase (MAPK) but not extracellular signal-regulated kinase (ERK) 1/2 activation was involved in atorvastatin-mediated PPAR gamma activation and enhanced alternative M2 macrophage phenotype. Collectively, our data demonstrated that atorvastatin promotes human monocyte differentiation toward alternative M2 macrophages via p38 MAPK-dependent PPAR gamma activation. (C) 2015 Elsevier B.V. All rights reserved.
机译：在人的动脉粥样硬化病变中可检测到M1和M2巨噬细胞，并且M2巨噬细胞存在于离斑块更稳定区域中距脂质核心较远的位置，并且似乎对M1巨噬细胞发挥抗炎作用。过氧化物酶体增殖物激活受体（PPAR）γ促进单核细胞分化为抗炎M2巨噬细胞。尽管据报道他汀类药物和PPARγ配体均可预防动脉粥样硬化的发展，但目前尚无关于他汀类药物在人类单核细胞替代分化中的影响的数据。在本研究中，我们假设阿托伐他汀可能对引发人类单核细胞产生抗发炎性M2表型的新作用。为此，我们首先发现在阿托伐他汀治疗后人循环单核细胞中表达了丰富的M2标记。此外，阿托伐他汀能够在体内和体外诱导人单核细胞中的PPARγ表达和活化，从而引发原代人单核细胞分化为M2巨噬细胞，并在M1巨噬细胞中具有更明显的旁分泌抗炎活性。分子方法的其他数据表明，阿托伐他汀介导的PPARγ激活和增强的替代性M2巨噬细胞表型涉及p38丝裂原激活的蛋白激酶（MAPK），而不是细胞外信号调节激酶（ERK）1/2激活。总的来说，我们的数据表明阿托伐他汀通过依赖p38 MAPK的PPARγ激活促进人类单核细胞向另类M2巨噬细胞的分化。 （C）2015 Elsevier B.V.保留所有权利。

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