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Partial loss of VE-...
Partial loss of VE-cadherin improves long-term outcome and cerebral blood flow after transient brain ischemia in mice
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- Gertz, Karen (författare)
- Charite Univ Med Berlin, Klin & Hsch Ambulanz Neurol, Charitepl 1, D-10117 Berlin, Germany.;Charite Univ Med Berlin, Ctr Stroke Res Berlin CSB, Charitepl 1, D-10117 Berlin, Germany.
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- Kronenberg, Golo (författare)
- Charite Univ Med Berlin, Ctr Stroke Res Berlin CSB, Charitepl 1, D-10117 Berlin, Germany.;Charite Univ Med Berlin, Klin & Hsch Ambulanz Psychiat & Psychotherapie, Charite Campus Mitte, Charitepl 1, D-10117 Berlin, Germany.
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- Uhlemann, Ria (författare)
- Charite Univ Med Berlin, Klin & Hsch Ambulanz Neurol, Charitepl 1, D-10117 Berlin, Germany.;Charite Univ Med Berlin, Ctr Stroke Res Berlin CSB, Charitepl 1, D-10117 Berlin, Germany.
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- Prinz, Vincent (författare)
- Charite Univ Med Berlin, Campus Virchow Klinikum, Klin Neurochirurg, Augustenburger Pl 1, D-13353 Berlin, Germany.
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- Marquina, Ruben (författare)
- Charite Univ Med Berlin, Klin & Hsch Ambulanz Neurol, Charitepl 1, D-10117 Berlin, Germany.
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- Corada, Monica (författare)
- IFOM, FIRC Inst Mol Oncol, Via Adamello 16, I-20139 Milan, Italy.;Univ Milan, Dept Biosci, Via Celoria 26, I-20133 Milan, Italy.
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- Dejana, Elisabetta (författare)
- Uppsala universitet,Vaskulärbiologi,IFOM, FIRC Inst Mol Oncol, Via Adamello 16, I-20139 Milan, Italy.;Univ Milan, Dept Biosci, Via Celoria 26, I-20133 Milan, Italy.
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- Endres, Matthias (författare)
- Charite Univ Med Berlin, Klin & Hsch Ambulanz Neurol, Charitepl 1, D-10117 Berlin, Germany.;Charite Univ Med Berlin, Ctr Stroke Res Berlin CSB, Charitepl 1, D-10117 Berlin, Germany.;Excellence Cluster NeuroCure, Charitepl 1, D-10117 Berlin, Germany.;German Ctr Neurodegenerat Dis DZNE, Charitepl 1, D-10117 Berlin, Germany.;German Ctr Cardiovasc Res DZHK, Charitepl 1, D-10117 Berlin, Germany.
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Charite Univ Med Berlin, Klin & Hsch Ambulanz Neurol, Charitepl 1, D-10117 Berlin, Germany;Charite Univ Med Berlin, Ctr Stroke Res Berlin CSB, Charitepl 1, D-10117 Berlin, Germany. Charite Univ Med Berlin, Ctr Stroke Res Berlin CSB, Charitepl 1, D-10117 Berlin, Germany.;Charite Univ Med Berlin, Klin & Hsch Ambulanz Psychiat & Psychotherapie, Charite Campus Mitte, Charitepl 1, D-10117 Berlin, Germany. (creator_code:org_t)
- 2016-08-18
- 2016
- Engelska.
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Ingår i: BMC Neurology. - : Springer Science and Business Media LLC. - 1471-2377. ; 16
- Relaterad länk:
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https://uu.diva-port... (primary) (Raw object)
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https://doi.org/10.1...
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https://urn.kb.se/re...
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https://doi.org/10.1...
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Abstract
Ämnesord
Stäng
- Background: VE-cadherin is the chief constituent of endothelial adherens junctions. However, the role of VE-cadherin in the pathogenesis of cerebrovascular diseases including brain ischemia has not yet been investigated. Methods: VE-cadherin heterozygous (VEC+/-) mice and wildtype controls were subjected to transient brain ischemia by 30 min filamentous middle cerebral artery occlusion (MCAo)/reperfusion. Results: Acute lesion sizes as assessed by MR-imaging on day 3 did not differ between genotypes. Unexpectedly, however, partial loss of VE-cadherin resulted in long-term stroke protection measured histologically on day 28. Equally surprisingly, VEC+/- mice displayed no differences in post-stroke angiogenesis compared to littermate controls, but showed increased absolute regional cerebral blood flow in ischemic striatum at four weeks. The early induction of VE-cadherin mRNA transcription after stroke was reduced in VEC+/- mice. By contrast, N-cadherin and beta-catenin mRNA expression showed a delayed, but sustained, upregulation up to 28 days after MCAo, which was increased in VEC+/ mice. Furthermore, partial loss of VE-cadherin resulted in a pattern of elevated ischemia-triggered mRNA transcription of pericyte-related molecules alpha-smooth muscle actin (alpha-SMA), aminopeptidase N (CD13), and platelet-derived growth factor receptor beta (PDGFR-beta). Conclusions: Partial loss of VE-cadherin results in long term stroke protection. On the cellular and molecular level, this effect appears to be mediated by improved endothelial/pericyte interactions and the resultant increase in cerebral blood flow. Our study reinforces accumulating evidence that long-term stroke outcome depends critically on vascular mechanisms.
Ämnesord
- MEDICIN OCH HÄLSOVETENSKAP -- Klinisk medicin -- Neurologi (hsv//swe)
- MEDICAL AND HEALTH SCIENCES -- Clinical Medicine -- Neurology (hsv//eng)
Nyckelord
- Cerebral ischemia
- Stroke
- Endothelium
- Pericyte
- Adhesion molecule
- Angiogenesis
Publikations- och innehållstyp
- ref (ämneskategori)
- art (ämneskategori)
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