期刊
JOURNAL OF CEREBRAL BLOOD FLOW AND METABOLISM
卷 42, 期 2, 页码 253-263出版社
SAGE PUBLICATIONS INC
DOI: 10.1177/0271678X211056392
关键词
Matricellular protein; ischemia-reperfusion; blood-brain barrier; neuroprotection; inflammation
资金
- NIH [NS099531, NS109459, NS101960]
- Department of Neurological Surgery, University of Wisconsin-Madison
The study found that TNC knockdown following a stroke can significantly reduce TNC protein expression, improve motor function deficits, decrease infarct volume, BBB damage, and inflammation.
The role of tenascin-C (TNC) in ischemic stroke pathology is not known despite its prognostic association with cerebrovascular diseases. Here, we investigated the effect of TNC knockdown on post-stroke brain damage and its putative mechanism of action in adult mice of both sexes. Male and female C57BL/6 mice were subjected to transient middle cerebral artery occlusion and injected (i.v.) with either TNC siRNA or a negative (non-targeting) siRNA at 5 min after reperfusion. Motor function (beam walk and rotarod tests) was assessed between days 1 and 14 of reperfusion. Infarct volume (T2-MRI), BBB damage (T1-MRI with contrast), and inflammatory markers were measured at 3 days of reperfusion. The TNC siRNA treated cohort showed significantly curtailed post-stroke TNC protein expression, motor dysfunction, infarction, BBB damage, and inflammation compared to the sex-matched negative siRNA treated cohort. These results demonstrate that the induction of TNC during the acute period after stroke might be a mediator of post-ischemic inflammation and secondary brain damage independent of sex.
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