Skip to main page content
U.S. flag

An official website of the United States government

Dot gov

The .gov means it’s official.
Federal government websites often end in .gov or .mil. Before sharing sensitive information, make sure you’re on a federal government site.

Https

The site is secure.
The https:// ensures that you are connecting to the official website and that any information you provide is encrypted and transmitted securely.

Access keys NCBI Homepage MyNCBI Homepage Main Content Main Navigation
Review
. 2014 Nov;63(2):97-104.
doi: 10.1016/j.vph.2014.10.003.

Notch signal integration in the vasculature during remodeling

Bahman Rostama  1 , Sarah M Peterson, Calvin P H Vary, Lucy Liaw
Affiliations
Review

Notch signal integration in the vasculature during remodeling

Bahman Rostama et al. Vascul Pharmacol. 2014 Nov.

Abstract

Notch signaling plays many important roles in homeostasis and remodeling in the vessel wall, and serves a critical role in the communication between endothelial cells and smooth muscle cells. Within blood vessels, Notch signaling integrates with multiple pathways by mechanisms including direct protein–protein interaction, cooperative or synergistic regulation of signal cascades, and co-regulation of transcriptional targets. After establishment of the mature blood vessel, the spectrum and intensity of Notch signaling change during phases of active remodeling or disease progression. These changes can be mediated by regulation via microRNAs and protein stability or signaling, and corresponding changes in complementary signaling pathways. Notch also affects endothelial cells on a system level by regulating key metabolic components. This review will outline the most recent findings of Notch activity in blood vessels, with a focus on how Notch signals integrate with other molecular signaling pathways controlling vascular phenotype.

PubMed Disclaimer

Figures

Figure 1
Figure 1. Notch signaling in vascular homeostasis and remodeling
In the mature vasculature, the endothelium is a quiescent monolayer with extensive cell adhesions that extend to underlying smooth muscle cells. Quiescence signals include BMP9/BMP10 activation of ALK1, and DLL4 activation of Notch. Normal expression of endothelial cell Jagged1 activates Notch3 in smooth muscle cells to maintain their differentiated, contractile phenotype. Vascular activation under conditions of stress, injury, or disease progression is accompanied by changes in Notch ligand and receptor expression in the vessel wall. These changes regulate cellular proliferation, cell identity, cell function, and overall phenotype.
See this image and copyright information in PMC

Similar articles

See all similar articles

Cited by

See all "Cited by" articles

References

    1. Kume T. Ligand-dependent Notch signaling in vascular formation. Adv Exp Med Biol. 2012;727:210–222. - PubMed
    1. Domigan CK, Iruela-Arispe ML. Recent advances in vascular development. Curr Opin Hematol. 2012;19:176–183. - PMC - PubMed
    1. Boucher J, Gridley T, Liaw L. Molecular pathways of Notch signaling in vascular smooth muscle cells. Front Physiol. 2012;3:81. - PMC - PubMed
    1. Fouillade C, Monet-Lepretre M, Baron-Menguy C, Joutel A. Notch signalling in smooth muscle cells during development and disease. Cardiovasc Res. 2012;95:138–146. - PubMed
    1. Bellen HJ, Yamamoto S. Notch Signaling, Methods and Protcols. In: Walker JM, editor. Methods in Molecular Biology. Vol. 1187. Humana Press; 2014. p. 351. - PubMed

Substances

LinkOut - more resources