Circulation.：MicroRNA93-IRF9-IRG1-衣康酸途径调节M2样巨噬细胞极化重建缺血性肌肉血运

2017-04-05 MedSci MedSci原创

目前尚无治疗和改善严重外周动脉疾病（PAD）患者的方法。之前研究报道miR93调节血管生成并减少遗传性PAD模型的组织损失。然而，miR93介导的缺血性肌肉的新生血管形成中细胞特异性功能、下游机制或信号传导尚不清楚。巨噬细胞调节PAD中的血管生成，并且这一程度取决于M2对M1的激活/极化状态。本研究中，我们发现miR93通过调节巨噬细胞极化在PAD模型中促进血管和动脉生成改善缺血肌肉血运重建的新机

目前尚无治疗和改善严重外周动脉疾病（PAD）患者的方法。之前研究报道miR93调节血管生成并减少遗传性PAD模型的组织损失。然而，miR93介导的缺血性肌肉的新生血管形成中细胞特异性功能、下游机制或信号传导尚不清楚。巨噬细胞调节PAD中的血管生成，并且这一程度取决于M2对M1的激活/极化状态。本研究中，我们发现miR93通过调节巨噬细胞极化在PAD模型中促进血管和动脉生成改善缺血肌肉血运重建的新机制。

在PAD术后与野生型（WT）相比，miR106b-93-25簇缺陷小鼠（miR106b-93-25 - / - ）的血管和动脉生成减少，伴随M1样巨噬细胞增加。给予miR106b-93-25 - / - PAD小鼠肌肉注射miR93增加了血管生成、动脉发生、灌注程度，这都与近端远端后肢肌肉中M2样巨噬细胞增多相关。在体外，即使是M1样极化刺激下，miR93也促进并维持M2样巨噬细胞极化。将miR106b-93-25 - / - 小鼠的骨髓巨噬细胞输送给WT小鼠缺血肌肉可减少其血管生成、动脉发生和灌注程度，而野生型巨噬细胞转移到miR106b-93-25 - / - 具有相反效应。将miR106b-93-25 - / - 与WT缺血肌肉做RNA序列分析，miR93调节IRG1功能、衣康酸的产生和巨噬细胞极化。3'UTR荧光素酶测定发现IRG1不是miR93的直接靶标，但是调节IRG1表达的IRF9是miR93靶标。体外实验证实，IRF9、IRG1和衣康酸治疗显着抑制内皮血管生成。

我们发现miR93抑制IRF9降低IRG1-衣康酸产生，诱导缺血性肌肉中的M2样巨噬细胞极化，增强PAD模型中的血管生成、动脉产生和灌注恢复。

原始出处：Ganta VC， Choi MH，et al.A MicroRNA93-IRF9-IRG1-Itaconic Acid Pathway Modulates M2-like-Macrophage Polarization to Revascularize Ischemic Muscle. Circulation. 2017 Mar 29. pii： CIRCULATIONAHA.116.025490.

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2017-09-21 xjy02

#Micro#

24 0
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2017-06-03 yb6560

#衣康酸#

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2017-09-05 jiafufeng@yaho

#CRO#

33 0
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2018-01-25 yahu

#MicroRNA93#

24 0
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2018-01-05 guihongzh

#缺血性#

29 0
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2017-04-06 虈亣靌

优质资源，共同分享

49 0
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2017-04-06 zhouqu_8

#microRNA#

30 0
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2017-04-06 tastas

#细胞极化#

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