Journal
STROKE
Volume 34, Issue 10, Pages 2483-2488Publisher
LIPPINCOTT WILLIAMS & WILKINS
DOI: 10.1161/01.STR.0000088644.60368.ED
Keywords
angiogenesis; brain; endoglin; endothelium; hypoxia; mitogen-activated protein kinases; protein kinases
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Funding
- NINDS NIH HHS [NS-35965, NS-37695] Funding Source: Medline
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Background and Purpose-Endoglin (CD105) is a membrane glycoprotein that is mutated in hereditary hemorrhagic telangiectasia (Osler-Rendu-Weber disease) and shows increased expression in proliferating endothelial cells during angiogenesis. Methods-We investigated the effect of hypoxia on endoglin expression in murine cerebral microvascular endothelial (bEND.3) cells in vitro and the possible involvement of mitogen-activated protein kinase (MAPK) pathways. Results-Hypoxia increased endoglin mRNA and protein expression in bEND.3 cells, which was associated with phosphoactivation of extracellular signal-related kinase (ERK), p38 MAPK, and Jun amino-terminal kinase (JNK). Inhibitors of p38 decreased hypoxic induction of endoglin expression, as did dominant negative MAPK kinase 3 (MKK3), which activates p38. In contrast, constitutively active MKK3 or JNK1 potentiated the hypoxic induction of endoglin. Conclusions-These results indicate that hypoxia induces the expression of endoglin at both the mRNA and protein levels and that induction is regulated by the p38 and perhaps also JNK pathways.
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