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人类外周血液单核细胞在心肌梗塞后表现出时间演变的炎症特征,并修改心肌纤维细胞表型

Elodie Miquelestorena-Standley^1,2, Ana Valéria Vinhais da Silva³, Marina Monnier³

¹EA 4245 Transplantation, Immunologie, Inflammation, Faculté de Médecine, Université de Tours, 10 boulevard tonnele, 37032, Tours Cedex 1, France. elodie.standley@univ-tours.fr.

Scientific reports

|October 5, 2023

概括

来自急性心肌梗塞 (AMI) 患者的外周血液单核细胞 (PBMC) 在AMI后48小时内显示出不断演变的炎症和修复性特征. 这些细胞影响心脏纤维细胞的行为,导致心肌纤维化.

科学领域:

心血管研究研究心血管研究
免疫学免疫学免疫学
细胞生物学细胞生物学

背景情况:

急性心肌梗塞 (AMI) 的病理生理学涉及不同的炎症,修复和纤维化阶段.
纯能受体,如P2Y11,参与调节炎症后缺血,可能有助于AMI后的解决.

研究的目的:

在AMI患者中表征外周血液单核细胞 (PBMC) 的免疫炎症和P2Y11表达特征.
分析AMI衍生的PBMC对心脏纤维细胞的体外影响.

主要方法:

从178名ST段升高AMI患者从0至12个月的再输血后收集PBMC.
通过RT-PCR和流细胞测量评估P2RY11,炎症标志物和T细胞偏振的基因和蛋白质表达.
与人类心脏纤维细胞 (HCF) 共同培养PBMC,并测量了α-SMA/vimentin比率.

主要成果:

在AMI后48小时内,PBMC显示HMOX1,STAT3,CD4表达增加,IDO1,TBX21/GATA3比率下降.
与这些变化同时,T和B细胞中的P2RY11表达升高.
来自48小时AMI患者的PBMC在体外增加了HCF中的α-SMA/vimentin比率.

结论:

人类PBMC在AMI后的最初几天表现出动态的炎症和修复性特征.
PBMC分泌的调解剂修改纤维细胞蛋白质,表明在促进心肌纤维化方面发挥了作用.

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