Thalidomide attenuates nitric oxide-driven angiogenesis by interacting with soluble guanylyl cyclase.

ABSTRACT:

Background and purpose

Nitric oxide (NO) promotes angiogenesis by activating endothelial cells. Thalidomide arrests angiogenesis by interacting with the NO pathway, but its putative targets are not known. Here, we have attempted to identify these targets.

Experimental approach

Cell-based angiogenesis assays (wound healing of monolayers and tube formation in ECV304, EAhy926 and bovine arterial endothelial cells), along with ex vivo and in vivo angiogenesis assays, were used to explore interactions between thalidomide and NO. We also carried out in silico homology modelling and docking studies to elucidate possible molecular interactions of thalidomide and soluble guanylyl cyclase (sGC).

Key results

Thalidomide inhibited pro-angiogenic functions in endothelial cell cult

SUBMITTER: Majumder S 

PROVIDER: S-EPMC2801213 | biostudies-literature | 2009 Dec

REPOSITORIES: biostudies-literature