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Sema3E/PlexinD1 inhibition is a therapeutic strategy for improving cerebral perfusion and restoring functional loss after stroke in aged rats

文献类型：期刊论文

作者Zhou, Yi-Fan3; Li, Peng-Cheng4; Wu, Jie-Hong3; Haslam, James Andrew5; Mao, Ling3; Xia, Yuan-Peng3; He, Quan-Wei3; Wang, Xu-Xia6; Lei, Hao6; Lan, Xiao-Li7
刊名NEUROBIOLOGY OF AGING
出版日期2018-10-01
卷号70页码:102-116
ISSN号0197-4580
关键词Ischemic Stroke Cerebral Perfusion Functional Neovascularization Bbb Integrity Endothelial Cells Pericytes
DOI10.1016/j.neurobiolaging.2018.06.003
文献子类Article
英文摘要Brain tissue survival and functional recovery after ischemic stroke greatly depend on cerebral vessel perfusion and functional collateral circulation in the ischemic area. Semaphorin 3E (Sema3E), one of the class 3 secreted semaphorins, has been demonstrated to be a critical regulator in embryonic and postnatal vascular formation via binding to its receptor PlexinD1. However, whether Sema3E/PlexinD1 signaling is involved in poststroke neovascularization remains unknown. To determine the contribution of Sema3E/PlexinD1 signaling to poststroke recovery, aged rats (18 months) were subjected to a transient middle cerebral artery occlusion. We found that depletion of Sema3E/PlexinD1 signaling with lentivirus-mediated PlexinD1-specific-shRNA improves tissue survival and functional outcome. Sema3E/PlexinD1 inhibition not only increases cortical perfusion but also ameliorates blood-brain barrier damage, as determined by positron emission tomography and magnetic resonance imaging. Mechanistically, we demonstrated that Sema3E suppresses endothelial cell proliferation and angiogenic capacity. More importantly, Sema3E/PlexinD1 signaling inhibits recruitment of pericytes by decreasing production of platelet derived growth factor-BB in endothelial cells. Overall, our study revealed that inhibition of Sema3E/PlexinD1 signaling in the ischemic penumbra, which increases both endothelial angiogenic capacity and recruitment of pericytes, contributed to functional neovascularization and blood-brain barrier integrity in the aged rats. Our findings imply that Sema3E/PlexinD1 signaling is a novel therapeutic target for improving brain tissue survival and functional recovery after ischemic stroke. (C) 2018 Elsevier Inc. All rights reserved.
WOS关键词CENTRAL-NERVOUS-SYSTEM ; MARROW STROMAL CELLS ; ISCHEMIC-STROKE ; ISCHEMIA/REPERFUSION INJURY ; DEVELOPMENTAL ANGIOGENESIS ; REPERFUSION INJURY ; VASCULAR NETWORK ; ARTERY OCCLUSION ; A EXPRESSION ; BRAIN
WOS研究方向Geriatrics & Gerontology ; Neurosciences & Neurology
语种英语
出版者ELSEVIER SCIENCE INC
WOS记录号WOS:000442879100012
资助机构National Natural Science Foundation of China(81601027 ; National Natural Science Foundation of China(81601027 ; National Key Research and Development Program of China(2016YFC1300600) ; National Key Research and Development Program of China(2016YFC1300600) ; National Research Foundation for the Doctoral Program of Higher Education of China(20120142110068) ; National Research Foundation for the Doctoral Program of Higher Education of China(20120142110068) ; New Century Excellent Talents in University(NCET-10-0406) ; New Century Excellent Talents in University(NCET-10-0406) ; 81571119 ; 81571119 ; 81571139 ; 81571139 ; 81771249 ; 81771249 ; 81400969 ; 81400969 ; 81400970 ; 81400970 ; 81301001) ; 81301001) ; National Natural Science Foundation of China(81601027 ; National Natural Science Foundation of China(81601027 ; National Key Research and Development Program of China(2016YFC1300600) ; National Key Research and Development Program of China(2016YFC1300600) ; National Research Foundation for the Doctoral Program of Higher Education of China(20120142110068) ; National Research Foundation for the Doctoral Program of Higher Education of China(20120142110068) ; New Century Excellent Talents in University(NCET-10-0406) ; New Century Excellent Talents in University(NCET-10-0406) ; 81571119 ; 81571119 ; 81571139 ; 81571139 ; 81771249 ; 81771249 ; 81400969 ; 81400969 ; 81400970 ; 81400970 ; 81301001) ; 81301001) ; National Natural Science Foundation of China(81601027 ; National Natural Science Foundation of China(81601027 ; National Key Research and Development Program of China(2016YFC1300600) ; National Key Research and Development Program of China(2016YFC1300600) ; National Research Foundation for the Doctoral Program of Higher Education of China(20120142110068) ; National Research Foundation for the Doctoral Program of Higher Education of China(20120142110068) ; New Century Excellent Talents in University(NCET-10-0406) ; New Century Excellent Talents in University(NCET-10-0406) ; 81571119 ; 81571119 ; 81571139 ; 81571139 ; 81771249 ; 81771249 ; 81400969 ; 81400969 ; 81400970 ; 81400970 ; 81301001) ; 81301001) ; National Natural Science Foundation of China(81601027 ; National Natural Science Foundation of China(81601027 ; National Key Research and Development Program of China(2016YFC1300600) ; National Key Research and Development Program of China(2016YFC1300600) ; National Research Foundation for the Doctoral Program of Higher Education of China(20120142110068) ; National Research Foundation for the Doctoral Program of Higher Education of China(20120142110068) ; New Century Excellent Talents in University(NCET-10-0406) ; New Century Excellent Talents in University(NCET-10-0406) ; 81571119 ; 81571119 ; 81571139 ; 81571139 ; 81771249 ; 81771249 ; 81400969 ; 81400969 ; 81400970 ; 81400970 ; 81301001) ; 81301001)
源URL[http://ir.wipm.ac.cn/handle/112942/13060]  
专题中国科学院武汉物理与数学研究所
通讯作者Li, Ya-Nan; Hu, Bo
作者单位1.Med Coll Wisconsin, Dept Pharmacol & Toxicol, Milwaukee, WI 53226 USA
2.Med Coll Wisconsin, Dept Pathol, Childrens Res Inst, Div Pediat Pathol, Milwaukee, WI 53226 USA
3.Huazhong Univ Sci & Technol, Union Hosp, Dept Neurol, Tongji Med Coll, Wuhan 430022, Hubei, Peoples R China
4.Huazhong Univ Sci & Technol, Union Hosp, Dept Ophthalmol, Tongji Med Coll, Wuhan, Hubei, Peoples R China
5.Swansea Univ, Swansea Coll Med, Singleton Pk, Swansea, W Glam, Wales
6.Chinese Acad Sci, Wuhan Inst Phys & Math, Wuhan Ctr Magnet Resonance, State Key Lab Magnet Resonance & Atom & Mol Phys, Wuhan, Hubei, Peoples R China
7.Huazhong Univ Sci & Technol, Union Hosp, Dept Nucl Med, Tongji Med Coll, Wuhan, Hubei, Peoples R China
8.Med Coll Wisconsin, Dept Surg, Div Pediat Surg, Childrens Res Inst, 8700 W Wisconsin Ave, Milwaukee, WI 53226 USA
9.Icahn Sch Med Mt Sinai, Friedman Brain Inst, Dept Neurosci, Dept Neurol, New York, NY 10029 USA
推荐引用方式
GB/T 7714		 Zhou, Yi-Fan,Li, Peng-Cheng,Wu, Jie-Hong,et al. Sema3E/PlexinD1 inhibition is a therapeutic strategy for improving cerebral perfusion and restoring functional loss after stroke in aged rats[J]. NEUROBIOLOGY OF AGING,2018,70:102-116.
APA Zhou, Yi-Fan.,Li, Peng-Cheng.,Wu, Jie-Hong.,Haslam, James Andrew.,Mao, Ling.,...&Hu, Bo.(2018).Sema3E/PlexinD1 inhibition is a therapeutic strategy for improving cerebral perfusion and restoring functional loss after stroke in aged rats.NEUROBIOLOGY OF AGING,70,102-116.
MLA Zhou, Yi-Fan,et al."Sema3E/PlexinD1 inhibition is a therapeutic strategy for improving cerebral perfusion and restoring functional loss after stroke in aged rats".NEUROBIOLOGY OF AGING 70(2018):102-116.

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来源：武汉物理与数学研究所

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