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CC趋化因子受体9的缺失改善心肌梗死后小鼠的心室电重构。

Abrogation of CC Chemokine Receptor 9 Ameliorates Ventricular Electrical Remodeling in Mice After Myocardial Infarction.

作者信息

Huang Yan, Ding Hua-Sheng, Song Tao, Chen Yu-Ting, Wang Teng, Tang Yan-Hong, Barajas-Martinez Hector, Huang Cong-Xin, Hu Dan

机构信息

Department of Cardiology, Renmin Hospital of Wuhan University, Wuhan, China.

Cardiovascular Research Institute, Wuhan University, Wuhan, China.

出版信息

Front Cardiovasc Med. 2021 Oct 12;8:716219. doi: 10.3389/fcvm.2021.716219. eCollection 2021.

DOI:10.3389/fcvm.2021.716219
PMID:34712704
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC8545906/
Abstract

Myocardial infarction (MI) triggers structural and electrical remodeling. CC chemokine receptor 9 (CCR9) mediates chemotaxis of inflammatory cells in MI. In our previous study, CCR9 knockout has been found to improve structural remodeling after MI. Here, we further investigate the potential influence of CCR9 on electrical remodeling following MI in order to explore potential new measures to improve the prognosis of MI. Mice was used and divided into four groups: CCR9/Sham, CCR9/Sham, CCR9/MI, CCR9/MI. Animals were used at 1 week after MI surgery. Cardiomyocytes in the infracted border zone were acutely dissociated and the whole-cell patch clamp was used to record action potential duration (APD), L-type calcium current ( ) and transient outward potassium current ( ). Calcium transient and sarcoplasmic reticulum (SR) calcium content under stimulation of Caffeine were measured in isolated cardiomyocytes by confocal microscopy. Multielectrode array (MEA) was used to measure the conduction of the left ventricle. The western-blot was performed for the expression level of connexin 43. We observed prolonged APD, increased and decreased following MI, while CCR9 knockout attenuated these changes (APD: 50.57 ± 6.51 ms in CCR9/MI vs. 76.53 ± 5.98 ms in CCR9/MI, < 0.05; : -13.15 ± 0.86 pA/pF in CCR9/MI group vs. -17.05 ± 1.11 pA/pF in CCR9/MI, < 0.05; : 4.01 ± 0.17 pA/pF in CCR9/MI group vs. 2.71 ± 0.16 pA/pF in CCR9/MI, < 0.05). The confocal microscopy results revealed CCR9 knockout reversed the calcium transient and calcium content reduction in sarcoplasmic reticulum following MI. MEA measurements showed improved conduction velocity in CCR9/MI mice (290.1 ± 34.47 cm/s in CCR9/MI group vs. 113.2 ± 14.4 cm/s in CCR9/MI group, < 0.05). Western-blot results suggested connexin 43 expression was lowered after MI while CCR9 knockout improved its expression. This study shows CCR9 knockout prevents the electrical remodeling by normalizing ion currents, the calcium homeostasis, and the gap junction to maintain APD and the conduction function. It suggests CCR9 is a promising therapeutic target for MI-induced arrhythmia, which warrants further investigation.

摘要

心肌梗死（MI）会引发结构和电重构。C-C趋化因子受体9（CCR9）介导MI中炎症细胞的趋化作用。在我们之前的研究中，发现CCR9基因敲除可改善MI后的结构重构。在此，我们进一步研究CCR9对MI后电重构的潜在影响，以探索改善MI预后的潜在新措施。使用小鼠并将其分为四组：CCR9/假手术组、CCR9/假手术组、CCR9/MI组、CCR9/MI组。在MI手术后1周使用动物。急性分离梗死边缘区的心肌细胞，采用全细胞膜片钳记录动作电位时程（APD）、L型钙电流（ ）和瞬时外向钾电流（ ）。通过共聚焦显微镜测量分离的心肌细胞在咖啡因刺激下的钙瞬变和肌浆网（SR）钙含量。使用多电极阵列（MEA）测量左心室的传导。进行蛋白质免疫印迹法检测连接蛋白43的表达水平。我们观察到MI后APD延长、 增加和 减少，而CCR9基因敲除减弱了这些变化（APD：CCR9/MI组为50.57±6.51毫秒，CCR9/MI组为76.53±5.98毫秒， <0.05； ：CCR9/MI组为-13.15±0.86皮安/皮法，CCR9/MI组为-17.05±1.11皮安/皮法， <0.05； ：CCR9/MI组为4.01±0.17皮安/皮法，CCR9/MI组为2.71±0.16皮安/皮法， <0.05）。共聚焦显微镜结果显示，CCR9基因敲除可逆转MI后肌浆网钙瞬变和钙含量的降低。MEA测量显示CCR9/MI小鼠的传导速度提高（CCR9/MI组为290.1±34.47厘米/秒，CCR9/MI组为113.2±14.4厘米/秒， <0.05）。蛋白质免疫印迹结果表明，MI后连接蛋白43表达降低，而CCR9基因敲除可改善其表达。本研究表明，CCR9基因敲除通过使离子电流、钙稳态和缝隙连接正常化来防止电重构，从而维持APD和传导功能。这表明CCR9是MI诱导的心律失常的一个有前景的治疗靶点，值得进一步研究。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8c67/8545906/75b130e6702f/fcvm-08-716219-g0006.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8c67/8545906/75b130e6702f/fcvm-08-716219-g0006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8c67/8545906/3c53c79f84b5/fcvm-08-716219-g0001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8c67/8545906/e76149ad72de/fcvm-08-716219-g0002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8c67/8545906/1d3a8da700ff/fcvm-08-716219-g0003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8c67/8545906/5783946ac631/fcvm-08-716219-g0004.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8c67/8545906/75b130e6702f/fcvm-08-716219-g0006.jpg

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