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
. 2006 Oct;135(2):305-11.
doi: 10.1016/j.jss.2006.06.010. Epub 2006 Aug 23.

Pericytes and their role in microvasculature homeostasis

Affiliations
Review

Pericytes and their role in microvasculature homeostasis

David A Edelman et al. J Surg Res. 2006 Oct.

Abstract

Background: The microvascular pericyte was first described in 1873, though it is a cell that has largely been ignored in the clinical literature. Pericytes are multifunctional, polymorphic, perivascular cells that lie within, and contribute to the production of the microvessel basil lamina.

Materials: The pericyte is the second cell that comprises the capillary wall, and is in a prime location to be involved with microvascular permeability. The exact sequence of events in Acute Respiratory Distress Syndrome (ARDS) is unknown, though increased permeability (pulmonary edema) is the primary physiological abnormality seen in the early stages. Pericytes are crucial in the development of capillary leak and pulmonary edema seen in ARDS. Pericytes regulate permeability through contractility and apoptosis.

Results: Changes in pericyte contractility alter the physical capillary barrier by opening the endothelial junctional space, and are reversible. Pericyte apoptosis leads to a compromise of the barrier effect of the capillary wall, and is a more permanent change.

Conclusions: The purpose of this paper is to review publications of pericyte physiological and pathophysiologic interactions in regards to contractility, apoptosis, and permeability.

PubMed Disclaimer

LinkOut - more resources