MicroRNA-155 抑制巨噬细胞向 M2 型极化并抑制脉络膜新生血管。
MicroRNA-155 Inhibits Polarization of Macrophages to M2-Type and Suppresses Choroidal Neovascularization.
机构信息
Department of Ophthalmology, Shanghai General Hospital (Shanghai First People's Hospital), Shanghai Jiao Tong University, School of Medicine, Shanghai, 200080, China.
Shanghai Key Laboratory of Fundus Diseases, Shanghai, 200080, China.
出版信息
Inflammation. 2018 Feb;41(1):143-153. doi: 10.1007/s10753-017-0672-8.
Arg-1Ym-1 M2-type macrophages play essential roles in the development of choroidal neovascularization (CNV). Thus, inhibition of M2-type macrophages may be effective in suppressing CNV. However, the potential mechanisms of macrophage polarization during development of CNV remain unclear. In this study, we report that microRNA-155 (miR-155) inhibited M2 polarization by targeting C/EBPβ in CNV model mice and in bone marrow-derived primary macrophages. Moreover, our data show that intravitreous injection of miR-155 mimics suppressed subretinal leakage and neovascularization. Therefore, we conclude that C/EBPβ plays a significant role in M2 macrophage polarization in CNV model, while miR-155 mimics could suppress CNV by inhibiting C/EBPβ activity and M2 macrophage polarization.
Arg-1Ym-1 M2 型巨噬细胞在脉络膜新生血管（CNV）的发展中起着至关重要的作用。因此，抑制 M2 型巨噬细胞可能对抑制 CNV 有效。然而，CNV 发展过程中巨噬细胞极化的潜在机制尚不清楚。在这项研究中，我们报告了 microRNA-155（miR-155）通过靶向 CNV 模型小鼠和骨髓来源的原代巨噬细胞中的 C/EBPβ 抑制 M2 极化。此外，我们的数据表明，玻璃体内注射 miR-155 模拟物可抑制视网膜下渗漏和新生血管形成。因此，我们得出结论，C/EBPβ 在 CNV 模型中的 M2 巨噬细胞极化中起重要作用，而 miR-155 模拟物可通过抑制 C/EBPβ 活性和 M2 巨噬细胞极化来抑制 CNV。
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