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Stroke. 2003 Oct;34(10):2483-8. Epub 2003 Aug 28.

Hypoxic induction of endoglin via mitogen-activated protein kinases in mouse brain microvascular endothelial cells.

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1
Buck Institute for Age Research, 8001 Redwood Blvd, Novato, Calif 94945, USA.

Abstract

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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