Bone Marrow-Derived Endothelial Progenitor Cells Contribute to Monocrotaline-Induced Pulmonary Arterial Hypertension in Rats via Inhibition of Store-Operated Ca2+ Channels
单位：[1]Medical Research Center, Beijing Chao-Yang Hospital, Capital Medical University, Beijing 100020, China北京朝阳医院[2]Key Laboratory of Respiratory and Pulmonary Circulation Disorders, Institute of Respiratory Medicine, Beijing 100020, China[3]Center for Respiratory Diseases, Department of Pulmonary and Critical Care Medicine, China-Japan Friendship Hospital, National Clinical Research Center for Respiratory Diseases, National Pulmonary Embolism & Pulmonary Vascular Diseases Research Group, Beijing 100029, China[4]Department of Physiology, School of Basic Medicine, Capital Medical University, Beijing 100069, China[5]Division of Translational and Regenerative Medicine,The University of Arizona College of Medicine, Tucson, Arizona, USA
Purpose. This study aimed to explore whether bone marrow- (BM-) derived endothelial progenitor cells (EPCs) contributing to monocrotaline- (MCT-) induced pulmonary arterial hypertension (PAH) in rats via modulating store-operated Ca2+ channels (SOC). Methods. Sprague Dawley (SD) rats were assigned into MCT group (n = 30) and control group (n = 20). Rats in MCT group were subcutaneously administered with 60 mg/kg MCT solution, and rats in control group were injected with equal amount of vehicle. After 3 weeks of treatment, right ventricular systolic pressure (RVSP) and right ventricular hypertrophy index (RVHI) of two groups were measured, and BM-derived EPCs were isolated. Immunochemistry identification and vasculogenesis detection of EPCs were then performed. [Ca2+](cyt) measurement was performed to detect store-operated calcium entry (SOCE) in two groups, followed by determination of Oral and canonical transient receptor potential (TRPC) channels expression. Results. After 3 weeks of treatment, there were significant increases in RVSP and RVHI in MCT group compared with control group, indicating that MCT successfully induced PAH in rats. Moreover, the SOCE ([Ca2+](cyt) rise) in BM-derived EPCs of MCT group was lower than that of control group. Furthermore, the expression levels of Orai3, TRPC1, TRPC3, and TRPC6 in BM-derived EPCs were decreased in MCT group in comparison with control group. Conclusions. The SOC activities were inhibited in BM-derived EPCs of MCT-treated rats. These results may be associated with the depressed expression of Orai3, TRPC1, TRPC3, and TRPC6, which are major mediators of SOC.
基金：
National Natural Science Foundation of ChinaNational Natural Science Foundation of China (NSFC) [81270117, 81300044]; Beijing Natural Science FoundationBeijing Natural Science Foundation [7162069]; Fund of The National Key Research and Development Program of China [2016YFC0905600]; NATIONAL HEART, LUNG, AND BLOOD INSTITUTEUnited States Department of Health & Human ServicesNational Institutes of Health (NIH) - USANIH National Heart Lung & Blood Institute (NHLBI) [R35HL135807, U01HL125208] Funding Source: NIH RePORTER; NATIONAL INSTITUTE OF ENVIRONMENTAL HEALTH SCIENCESUnited States Department of Health & Human ServicesNational Institutes of Health (NIH) - USANIH National Institute of Environmental Health Sciences (NIEHS) [P30ES006694] Funding Source: NIH RePORTER
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外文
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中科院(CAS)分区：
出版当年[2017]版：
大类|3 区生物
小类|3 区生物工程与应用微生物4 区医学：研究与实验
最新[2025]版：
大类|4 区医学
小类|4 区生物工程与应用微生物4 区医学：研究与实验
JCR分区：
出版当年[2016]版：
Q2BIOTECHNOLOGY & APPLIED MICROBIOLOGYQ3MEDICINE, RESEARCH & EXPERIMENTAL
最新[2023]版：
Q3BIOTECHNOLOGY & APPLIED MICROBIOLOGYQ3MEDICINE, RESEARCH & EXPERIMENTAL
第一作者单位：[1]Medical Research Center, Beijing Chao-Yang Hospital, Capital Medical University, Beijing 100020, China[2]Key Laboratory of Respiratory and Pulmonary Circulation Disorders, Institute of Respiratory Medicine, Beijing 100020, China
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推荐引用方式(GB/T 7714)：
Ran Miao,Jun Wan,Jie Liu,et al.Bone Marrow-Derived Endothelial Progenitor Cells Contribute to Monocrotaline-Induced Pulmonary Arterial Hypertension in Rats via Inhibition of Store-Operated Ca2+ Channels[J].BIOMED RESEARCH INTERNATIONAL.2018,2018:doi:10.1155/2018/4892349.
APA：
Ran Miao,Jun Wan,Jie Liu,Jason X.-J. Yuan,Jing Wang...&Chen Wang.(2018).Bone Marrow-Derived Endothelial Progenitor Cells Contribute to Monocrotaline-Induced Pulmonary Arterial Hypertension in Rats via Inhibition of Store-Operated Ca2+ Channels.BIOMED RESEARCH INTERNATIONAL,2018,
MLA：
Ran Miao,et al."Bone Marrow-Derived Endothelial Progenitor Cells Contribute to Monocrotaline-Induced Pulmonary Arterial Hypertension in Rats via Inhibition of Store-Operated Ca2+ Channels".BIOMED RESEARCH INTERNATIONAL 2018.(2018)
