WIPM OpenIR
Sema3E/PlexinD1 inhibition is a therapeutic strategy for improving cerebral perfusion and restoring functional loss after stroke in aged rats
Zhou, Yi-Fan1; Li, Peng-Cheng2; Wu, Jie-Hong1; Haslam, James Andrew3; Mao, Ling1; Xia, Yuan-Peng1; He, Quan-Wei1; Wang, Xu-Xia4; Lei, Hao4; Lan, Xiao-Li5; Miao, Qing Robert6,7,8; Yue, Zhen-Yu9; Li, Ya-Nan1; Hu, Bo1
2018-10-01
Source PublicationNEUROBIOLOGY OF AGING
ISSN0197-4580
Volume70Pages:102-116
SubtypeArticle
AbstractBrain 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.
KeywordIschemic Stroke Cerebral Perfusion Functional Neovascularization Bbb Integrity Endothelial Cells Pericytes
WOS HeadingsScience & Technology ; Life Sciences & Biomedicine
Funding OrganizationNational 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)
DOI10.1016/j.neurobiolaging.2018.06.003
WOS KeywordCENTRAL-NERVOUS-SYSTEM ; MARROW STROMAL CELLS ; ISCHEMIC-STROKE ; ISCHEMIA/REPERFUSION INJURY ; DEVELOPMENTAL ANGIOGENESIS ; REPERFUSION INJURY ; VASCULAR NETWORK ; ARTERY OCCLUSION ; A EXPRESSION ; BRAIN
Indexed BySCI
Language英语
Funding OrganizationNational 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)
WOS Research AreaGeriatrics & Gerontology ; Neurosciences & Neurology
WOS SubjectGeriatrics & Gerontology ; Neurosciences
WOS IDWOS:000442879100012
PublisherELSEVIER SCIENCE INC
Citation statistics
Cited Times:5[WOS]   [WOS Record]     [Related Records in WOS]
Document Type期刊论文
Identifierhttp://ir.wipm.ac.cn/handle/112942/13061
Collection中国科学院武汉物理与数学研究所
Corresponding AuthorLi, Ya-Nan; Hu, Bo
Affiliation1.Huazhong Univ Sci & Technol, Union Hosp, Dept Neurol, Tongji Med Coll, Wuhan 430022, Hubei, Peoples R China
2.Huazhong Univ Sci & Technol, Union Hosp, Dept Ophthalmol, Tongji Med Coll, Wuhan, Hubei, Peoples R China
3.Swansea Univ, Swansea Coll Med, Singleton Pk, Swansea, W Glam, Wales
4.Chinese Acad Sci, Wuhan Inst Phys & Math, Wuhan Ctr Magnet Resonance, State Key Lab Magnet Resonance & Atom & Mol Phys, Wuhan, Hubei, Peoples R China
5.Huazhong Univ Sci & Technol, Union Hosp, Dept Nucl Med, Tongji Med Coll, Wuhan, Hubei, Peoples R China
6.Med Coll Wisconsin, Dept Surg, Div Pediat Surg, Childrens Res Inst, 8700 W Wisconsin Ave, Milwaukee, WI 53226 USA
7.Med Coll Wisconsin, Dept Pathol, Childrens Res Inst, Div Pediat Pathol, Milwaukee, WI 53226 USA
8.Med Coll Wisconsin, Dept Pharmacol & Toxicol, Milwaukee, WI 53226 USA
9.Icahn Sch Med Mt Sinai, Friedman Brain Inst, Dept Neurosci, Dept Neurol, New York, NY 10029 USA
Recommended Citation
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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