期刊
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA
卷 105, 期 12, 页码 4856-4861出版社
NATL ACAD SCIENCES
DOI: 10.1073/pnas.0709867105
关键词
ischemia; Notch3; vascular smooth muscle; CADASIL
资金
- NCI NIH HHS [R01 CA098402, CA098402-06] Funding Source: Medline
- NHGRI NIH HHS [HG003616-01A1, R01 HG003616] Funding Source: Medline
- NHLBI NIH HHS [HL052233, R01 HL052233] Funding Source: Medline
- NINDS NIH HHS [5 P50 NS10828-32, R37 NS026084, NS026084-18, P50 NS010828, R01 NS026084] Funding Source: Medline
Vascular smooth muscle cells (SMCs) have been implicated in the pathophysiology of stroke, the third most common cause of death and the leading cause of long-term neurological disability in the world. However, there is little insight into the underlying cellular pathways that link SMC function to brain ischemia susceptibility. Using a hitherto uncharacterized knockout mouse model of Notch 3, a Notch signaling receptor paralogue highly expressed in vascular SMCs, we uncover striking susceptibility to ischemic stroke upon challenge. Cellular and molecular analyses of vascular SMCs derived from these animals associate Notch 3 activity to the expression of specific gene targets, whereas genetic rescue experiments unambiguously link Notch 3 function in vessels to the ischemic phenotype.
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