{"title":"Spock2 在脓毒症诱发的心肌病中发挥着内皮细胞关键时间序列基因的功能","authors":"Jian Zhang, Yao Lu, Yihui Shen, Hui Zhang, Yuchen Xu, Xuejun Wang, Yifan Chen, Xiaozhen He, Hao Lu, Leilei Cheng","doi":"10.1097/fjc.0000000000001577","DOIUrl":null,"url":null,"abstract":"The study aimed to investigate the pathogenesis of sepsis-induced cardiomyopathy (SIC), a leading cause of mortality in septic patients. Transcriptome data from cecal ligation and puncture (CLP)-induced septic mice were analyzed at different time points (24, 48 and 72 h) using GSE171546 data. Through weighted gene co-expression network analysis (WGCNA), time series, and differential expression analyses, key time-series differentially expressed genes (DEGs) were identified. Additionally, single-cell sequencing data (GSE207363) were used for both differential and pseudotime analyses to pinpoint DEGs specific to endothelial cells. The study highlighted Spock2, S100a9, S100a8, and Xdh as differential genes specific to endothelial cells in a time-dependent manner. Immunofluorescence validation confirmed the increased expression of SPOCK2 in the endothelial cells of CLP-induced septic mice. Further, in vitro studies showed that deletion of Spock2 significantly increased LPS-induced apoptosis in human umbilical vein endothelial cells (HUVECs). In conclusion, SPOCK2 expression is increased in septic cardiac endothelial cells and LPS-induced HUVECs and may play a protective role.","PeriodicalId":15212,"journal":{"name":"Journal of Cardiovascular Pharmacology","volume":null,"pages":null},"PeriodicalIF":2.6000,"publicationDate":"2024-04-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":"{\"title\":\"Spock2 functions as a key time-series gene of endothelial cells in sepsis-induced cardiomyopathy\",\"authors\":\"Jian Zhang, Yao Lu, Yihui Shen, Hui Zhang, Yuchen Xu, Xuejun Wang, Yifan Chen, Xiaozhen He, Hao Lu, Leilei Cheng\",\"doi\":\"10.1097/fjc.0000000000001577\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"The study aimed to investigate the pathogenesis of sepsis-induced cardiomyopathy (SIC), a leading cause of mortality in septic patients. Transcriptome data from cecal ligation and puncture (CLP)-induced septic mice were analyzed at different time points (24, 48 and 72 h) using GSE171546 data. Through weighted gene co-expression network analysis (WGCNA), time series, and differential expression analyses, key time-series differentially expressed genes (DEGs) were identified. Additionally, single-cell sequencing data (GSE207363) were used for both differential and pseudotime analyses to pinpoint DEGs specific to endothelial cells. The study highlighted Spock2, S100a9, S100a8, and Xdh as differential genes specific to endothelial cells in a time-dependent manner. Immunofluorescence validation confirmed the increased expression of SPOCK2 in the endothelial cells of CLP-induced septic mice. Further, in vitro studies showed that deletion of Spock2 significantly increased LPS-induced apoptosis in human umbilical vein endothelial cells (HUVECs). In conclusion, SPOCK2 expression is increased in septic cardiac endothelial cells and LPS-induced HUVECs and may play a protective role.\",\"PeriodicalId\":15212,\"journal\":{\"name\":\"Journal of Cardiovascular Pharmacology\",\"volume\":null,\"pages\":null},\"PeriodicalIF\":2.6000,\"publicationDate\":\"2024-04-22\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"\",\"citationCount\":\"0\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Journal of Cardiovascular Pharmacology\",\"FirstCategoryId\":\"3\",\"ListUrlMain\":\"https://doi.org/10.1097/fjc.0000000000001577\",\"RegionNum\":4,\"RegionCategory\":\"医学\",\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"\",\"PubModel\":\"\",\"JCR\":\"Q2\",\"JCRName\":\"CARDIAC & CARDIOVASCULAR SYSTEMS\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"Journal of Cardiovascular Pharmacology","FirstCategoryId":"3","ListUrlMain":"https://doi.org/10.1097/fjc.0000000000001577","RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q2","JCRName":"CARDIAC & CARDIOVASCULAR SYSTEMS","Score":null,"Total":0}
Spock2 functions as a key time-series gene of endothelial cells in sepsis-induced cardiomyopathy
The study aimed to investigate the pathogenesis of sepsis-induced cardiomyopathy (SIC), a leading cause of mortality in septic patients. Transcriptome data from cecal ligation and puncture (CLP)-induced septic mice were analyzed at different time points (24, 48 and 72 h) using GSE171546 data. Through weighted gene co-expression network analysis (WGCNA), time series, and differential expression analyses, key time-series differentially expressed genes (DEGs) were identified. Additionally, single-cell sequencing data (GSE207363) were used for both differential and pseudotime analyses to pinpoint DEGs specific to endothelial cells. The study highlighted Spock2, S100a9, S100a8, and Xdh as differential genes specific to endothelial cells in a time-dependent manner. Immunofluorescence validation confirmed the increased expression of SPOCK2 in the endothelial cells of CLP-induced septic mice. Further, in vitro studies showed that deletion of Spock2 significantly increased LPS-induced apoptosis in human umbilical vein endothelial cells (HUVECs). In conclusion, SPOCK2 expression is increased in septic cardiac endothelial cells and LPS-induced HUVECs and may play a protective role.
期刊介绍:
Journal of Cardiovascular Pharmacology is a peer reviewed, multidisciplinary journal that publishes original articles and pertinent review articles on basic and clinical aspects of cardiovascular pharmacology. The Journal encourages submission in all aspects of cardiovascular pharmacology/medicine including, but not limited to: stroke, kidney disease, lipid disorders, diabetes, systemic and pulmonary hypertension, cancer angiogenesis, neural and hormonal control of the circulation, sepsis, neurodegenerative diseases with a vascular component, cardiac and vascular remodeling, heart failure, angina, anticoagulants/antiplatelet agents, drugs/agents that affect vascular smooth muscle, and arrhythmias.
Appropriate subjects include new drug development and evaluation, physiological and pharmacological bases of drug action, metabolism, drug interactions and side effects, application of drugs to gain novel insights into physiology or pathological conditions, clinical results with new and established agents, and novel methods. The focus is on pharmacology in its broadest applications, incorporating not only traditional approaches, but new approaches to the development of pharmacological agents and the prevention and treatment of cardiovascular diseases. Please note that JCVP does not publish work based on biological extracts of mixed and uncertain chemical composition or unknown concentration.