Prmt1 upregulated by Hdc deficiency aggravates acute myocardial infarction via NETosis.
Prmt1 upregulated by Hdc deficiency aggravates acute myocardial infarction via NETosis.
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DOI：
10.1016/j.apsb.2021.10.016
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发表时间：
2022-04
影响因子：
14.5
通讯作者：
Ge, Junbo
中科院分区：
文献类型：
--
作者：
Zhang, Zhiwei;Ding, Suling;Wang, Zhe;Zhu, Xiaowei;Zhou, Zheliang;Zhang, Weiwei;Yang, Xiangdong;Ge, Junbo
关键词：
中性粒细胞在心肌梗死后被动员并募集到受损的心脏，并且中性粒细胞计数在临床上与冠状动脉疾病的严重程度相关。组氨酸脱羧酶（HDC）参与调节活性氧化物质（ROS）和骨髓细胞的分化。然而，HDC对心肌梗死后中性粒细胞的影响尚不清楚。在这里，我们发现，中性粒细胞被无序招募到Hdc缺陷（Hdc−/−）小鼠心肌缺血损伤区。此外，Hdc缺陷导致减弱的粘附，但增强的迁移和增强的ROS/中性粒细胞胞外陷阱（NET）的生产在中性粒细胞。Hdc−/−小鼠衍生的NET促进心肌细胞死亡和心脏成纤维细胞增殖/迁移。此外，蛋白质精氨酸甲基转移酶1（PRMT 1）在Hdc−/−小鼠来源的中性粒细胞中增加，但在外源性组胺处理下减少。通过阻断组胺受体1（H1 R）、抑制ATP合成或减少SWItch/蔗糖非发酵性（SWI/SNF）染色质重塑复合物可挽救其表达。因此，组胺或MS 023处理可以离体降低ROS和NET，并改善心脏功能和纤维化，沿着体内血浆中NET的降低。总之，我们的研究结果揭示了HDC通过组胺-H1 R-ATP-SWI/SNF-PRMT 1-ROS信号传导在NETosis中的作用，并为识别和调节心血管疾病中的有害免疫状态提供了新的生物标志物和靶标。在心肌梗死期间，组氨酸脱羧酶（HDC）的缺乏减少了中性粒细胞中内源性或外源性组胺的产生，通过增强H1 R-SWI/SNF-PRMT 1途径中的中性粒细胞浸润和活性氧化物质（ROS）依赖性NETosis来加剧心肌细胞死亡和纤维化。
Neutrophils are mobilized and recruited to the injured heart after myocardial infarction, and neutrophil count has been clinically implicated to be associated with coronary disease severity. Histidine decarboxylase (HDC) has been implicated in regulating reactive oxidative species (ROS) and the differentiation of myeloid cells. However, the effect of HDC on neutrophils after myocardial infarction remains unclear. Here, we found that neutrophils were disorderly recruited into the ischemic injured area of the myocardium of Hdc deficiency (Hdc−/−) mice. Moreover, Hdc deficiency led to attenuated adhesion but enhanced migration and augmented ROS/neutrophil extracellular traps (NETs) production in neutrophils. Hdc−/− mouse-derived NETs promoted cardiomyocyte death and cardiac fibroblast proliferation/migration. Furthermore, protein arginine methyltransferase 1 (PRMT1) was increased in Hdc−/− mouse-derived neutrophils but decreased with exogenous histamine treatment. Its expression could be rescued by blocking histamine receptor 1 (H1R), inhibiting ATP synthesis or reducing SWItch/sucrose non fermentable (SWI/SNF) chromatin remodeling complex. Accordingly, histamine or MS023 treatment could decrease ROS and NETs ex vivo, and ameliorated cardiac function and fibrosis, along with the reduced NETs in plasma in vivo. Together, our findings unveil the role of HDC in NETosis by histamine–H1R–ATP–SWI/SNF–PRMT1–ROS signaling and provide new biomarkers and targets for identifying and tuning the detrimental immune state in cardiovascular disease. During myocardial infarction, the deficiency of histidine decarboxylase (HDC), diminishing endogenous or exogenous histamine generation in neutrophils, aggravates cardiomyocyte death and fibrosis, by enhancing neutrophil infiltration and reactive oxidative species (ROS) dependent NETosis in a H1R–SWI/SNF–PRMT1 pathway.
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DOI：
10.1126/science.aao4227
发表时间：
2018-09-28
期刊：
Science (New York, N.Y.)
影响因子：
--
作者：
Albrengues J;Shields MA;Ng D;Park CG;Ambrico A;Poindexter ME;Upadhyay P;Uyeminami DL;Pommier A;Küttner V;Bružas E;Maiorino L;Bautista C;Carmona EM;Gimotty PA;Fearon DT;Chang K;Lyons SK;Pinkerton KE;Trotman LC;Goldberg MS;Yeh JT;Egeblad M
通讯作者：
Egeblad M
影响因子：
20.1
作者：
Ackers-Johnson M;Li PY;Holmes AP;O'Brien SM;Pavlovic D;Foo RS
通讯作者：
Foo RS
Slc6a8介导的肌酸摄取和积累通过调节细胞因子反应重新编程巨噬细胞极化
影响因子：
32.4
作者：
Ji, Liangliang;Zhao, Xinbin;Hu, Xiaoyu
通讯作者：
Hu, Xiaoyu
影响因子：
4.4
作者：
Hori, Y;Nihei, Y;Ohtsu, H
通讯作者：
Ohtsu, H
影响因子：
15.9
作者：
Kessenbrock, Kai;Froehlich, Leopold;Jenne, Dieter E.
通讯作者：
Jenne, Dieter E.