RGD Reference Report - Lack of alpha 2-antiplasmin promotes re-endothelialization via over-release of VEGF after vascular injury in mice. - Rat Genome Database

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Lack of alpha 2-antiplasmin promotes re-endothelialization via over-release of VEGF after vascular injury in mice.

Authors: Matsuno, H  Ishisaki, A  Nakajima, K  Okada, K  Ueshima, S  Matsuo, O  Kozawa, O 
Citation: Matsuno H, etal., Blood 2003 Nov 15;102(10):3621-8. Epub 2003 Jul 31.
RGD ID: 1302296
Pubmed: PMID:12893771   (View Abstract at PubMed)
DOI: DOI:10.1182/blood-2003-03-0700   (Journal Full-text)

We here report that the arterial blood flow after endothelial injury in mice deficient in alpha 2-antiplasmin (alpha 2-AP-/- mice) was well maintained compared with that of wild-type mice. Moreover, the development of neointima 4 weeks after injury in alpha 2-AP-/- mice was significantly decreased. Histologic observations showed a prompt recovery of endothelial cells with a much higher proliferating index in repaired endothelium in alpha 2-AP-/- mice. The amount of secreted vascular endothelial growth factor (VEGF) by explanted vascular smooth muscle cells (SMCs) from alpha 2-AP-/- mice was significantly increased. In separate experiments using a human endothelial cell (EC) line, we could demonstrate that plasminogen binds to ECs and that this binding can be prevented by alpha 2-AP. Finally, an injection of either an anti-VEGF receptor-1 antibody or alpha 2-AP reduced the prompt endothelial healing. alpha 2-AP is the main inactivator of plasmin, which cleaves extracellular matrix-bound VEGF to release a diffusible proteolytic fragment. Lack of alpha 2-AP, therefore, could lead to a local over-release of VEGF by the continuously active plasmin in the injured area, which could result in a prompt re-endothelialization after vascular injury. Our results provide new insight into the role of alpha 2-AP and VEGF in the pathogenesis of re-endothelialization following vascular injury.

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Gene Serpinf1 serpin family F member 1 Rattus norvegicus

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