JOURNAL ARTICLE
RESEARCH SUPPORT, NON-U.S. GOV'T
RESEARCH SUPPORT, U.S. GOV'T, NON-P.H.S.
Add like
Add dislike
Add to saved papers

Distinct regulation of gene expression in human endothelial cells by TGF-beta and its receptors.

Transforming growth factor beta (TGF-beta) and its signaling mediators play essential roles in angiogenesis-formation of new blood vessels, as evidenced by targeted gene disruption in mice and their mutations in human vascular dysplasia. However, little is known about the molecular basis of TGF-beta function in vascular formation. To study the function of TGF-beta signaling in angiogenesis and to elucidate the signaling specificity of TGF-beta receptors at the gene transcriptional level, we analyzed the expression profile of the genes regulated by TGF-beta and its type I receptors ALK1 and ALK5 in human microvessel endothelial cells (ECs). Global change of gene expression profiles was examined by microarray and RT-PCR analyses in the ECs treated with TGF-beta1 or by adenoviral expression of the active ALK1 or ALK5. We found that the profiles of the genes regulated by TGF-beta, ALK1 and ALK5 are distinct from each other, although some of genes are modulated by all of them. TGF-beta regulated far more genes than ALK1 and ALK5 did. ALK1 enhanced the formation of tube-like structures of ECs, while ALK5 stimulates EC aggregation. Our results suggest that ALK1 appears to have important functions in regulating proliferation of ECs, whereas ALK5 tends to modulate cell-cell interaction and cell adhesion and extracellular matrix remodeling.

Full text links

We have located links that may give you full text access.
Can't access the paper?
Try logging in through your university/institutional subscription. For a smoother one-click institutional access experience, please use our mobile app.

For the best experience, use the Read mobile app

Mobile app image

Get seemless 1-tap access through your institution/university

For the best experience, use the Read mobile app

All material on this website is protected by copyright, Copyright © 1994-2024 by WebMD LLC.
This website also contains material copyrighted by 3rd parties.

By using this service, you agree to our terms of use and privacy policy.

Your Privacy Choices Toggle icon

You can now claim free CME credits for this literature searchClaim now

Get seemless 1-tap access through your institution/university

For the best experience, use the Read mobile app