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Activin receptor‐like kinase 1 inhibits human microvascular endothelial cell migration: Potential roles for JNK and ERK by Laurent David; Christine Mallet; Bruno Vailhé; Samy Lamouille; Jean‐Jacques Feige; Sabine Bailly is a Biochemistry, Genetics and Molecular Biology article available to read on EtoBox.

## Abstract Activin receptor‐like kinase 1 (ALK1) is an endothelial‐specific type I receptor of the TGFβ receptor family that is implicated in angiogenesis and in the pathogenesis of the vascular disease, hereditary hemorrhagic telangiectasia (HHT). In the absence of a specific ligand, ALK1 cellular functions have been mainly studied through the use of a constitutively active form of this receptor (ALK1ca) and are still debated. We previously reported that ALK1ca inhibits proliferation and migration of human endothelial cells suggesting that ALK1 plays an important role in the maturation phase of angiogenesis (Lamouille et al., 2002, Blood 100: 4495–4501). In the present work, we further analyzed the role of ALK1 in the migration of human dermal microvascular endothelial cell (HMVEC‐d) and observed that silencing endogenous ALK1 expression with siRNAs accelerates endothelial cell migration in the wound assay. Further, we demonstrate that ALK1‐induced inhibition of migration is Smad‐independent. Using a panel of kinase inhibitors, we found that HMVEC‐d wound closure was completely inhibited by a JNK inhibitor and to a lower degree by an ERK kinase inhibitor. Further, HMVEC‐d woundin

Author

Laurent David; Christine Mallet; Bruno Vailhé; Samy Lamouille; Jean‐Jacques Feige; Sabine Bailly

Publisher

John Wiley and Sons; Wiley (John Wiley & Sons); John Wiley & Sons Inc.; Wiley (ISSN 0021-9541)

Published

2007

Language

EN

Field

Biochemistry, Genetics and Molecular Biology (Life Sciences)