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Endothelial cells are activated during hypoxia via endoglin/ALK-1/SMAD1/5 signaling in vivo and in vitro.

Forskningsöversiktsartikel
Författare Fei Tian
Xianghua Zhou
Anke M Smits
Erik Larsson
Marie-José Goumans
Carl-Henrik Heldin
Jan Borén
Levent Akyürek
Publicerad i Biochemical and Biophysical Research Communications
Volym 392
Nummer/häfte 3
Sidor 283-288
ISSN 1090-2104
Publiceringsår 2010
Publicerad vid Wallenberglaboratoriet
Institutionen för biomedicin, avdelningen för medicinsk kemi och cellbiologi
Sidor 283-288
Språk en
Länkar dx.doi.org/10.1016/j.bbrc.2009.12.1...
Ämnesord Heart; Infarction; Hypoxia; Endoglin; Signaling
Ämneskategorier Medicin och Hälsovetenskap

Sammanfattning

Endoglin (ENG) promotes angiogenesis by enhancing activation of TGF-beta type I receptors ALK-1 and ALK-5. ALK-1 phosphorylates transcription factors SMAD1/5, which bind to BMP-responsive elements (BRE), whereas ALK-5 phosphorylates SMAD3, which binds to CAGA elements. Expression of ENG is increased during myocardial infarction (MI). We investigated which ENG signaling pathway is activated in endothelial cells during hypoxia. Expression of ENG, ALK-1, ALK-5, and phosphorylated SMAD1/3/5 by immunostaining and immunoblotting in a mouse model of myocardial infarction (MI) and in hypoxic human aortic endothelial cells (HAECs) was evaluated. Activation of BRE and CAGA was measured by luciferase assays in cells transfected with plasmids expressing ENG or ALK-1 and the number of cells was quantified. mRNA expression of the target genes of TGF-beta signaling, ID1 and BCL-X, was quantified by real-time RT-PCR. Expression of ENG, ALK-1 and phosphorylated SMAD1/5, but not ALK-5 or phosphorylated SMAD3, was significantly increased in hypoxic endothelial cells in vivo and in vitro. Overexpression of both ENG and ALK-1 significantly increased BRE but not CAGA activity, expression of ID1 and BCL-X and the number of HAECs at hypoxia. ENG/ALK-1 signaling is one of the factors that regulate endothelial cell activity during adaptive cardiac angiogenesis.

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