Format

Send to

Choose Destination
See comment in PubMed Commons below
Transl Res. 2014 Apr;163(4):296-306. doi: 10.1016/j.trsl.2014.01.011. Epub 2014 Jan 24.

Pericyte-endothelial crosstalk: implications and opportunities for advanced cellular therapies.

Author information

1
Program in Cellular and Molecular Physiology, Sackler School of Graduate Biomedical Sciences, Center for Innovations in Wound Healing Research, Tufts University School of Medicine, Boston, Mass.
2
Program in Cellular and Molecular Physiology, Sackler School of Graduate Biomedical Sciences, Center for Innovations in Wound Healing Research, Tufts University School of Medicine, Boston, Mass. Electronic address: iramherman@gmail.com.

Abstract

Pericytes are mural cells of the microcirculation that have been shown to play key roles in regulating microvascular morphogenesis and stability throughout each tissue bed and organ system assessed. Of note, recent work has revealed that pericytes share several characteristics with mesenchymal- and adipose-derived stem cells, suggesting there may be lineage-related connections among bona fide pericytes and these vascular "progenitors," which can assume a perivascular position in association with endothelial cells. Hence, pericyte identity as a mediator of vascular remodeling may be confounded by its close relationships with its progenitors or pluripotent cell counterparts and yet demonstrates their potential utility as cell-based therapies for unmet clinical needs. Crucial to the development of such therapies is a comprehensive understanding of the origin and fate regulating these related cell types as well as the unveiling of the molecular mechanisms by which pericytes and endothelial cells communicate. Such mechanistic inputs, which disrupt normal cellular crosstalk during disease inception and progression, offer opportunities for intervention and are discussed in the context of the vasculopathies accompanying tumor growth, diabetes, and fibrosis.

PMID:
24530608
PMCID:
PMC3976718
DOI:
10.1016/j.trsl.2014.01.011
[Indexed for MEDLINE]
Free PMC Article
PubMed Commons home

PubMed Commons

0 comments
How to join PubMed Commons

    Supplemental Content

    Full text links

    Icon for Elsevier Science Icon for PubMed Central
    Loading ...
    Support Center