Format

Send to

Choose Destination
Microcirculation. 2013 Nov;20(8):679-92. doi: 10.1111/micc.12068.

Emerging understanding of roles for arterioles in inflammation.

Author information

1
Department of Pharmacology and Physiology, University of Rochester, Rochester, New York, USA.

Abstract

Arterioles, capillaries, and venules all actively change their cellular functions and phenotypes during inflammation in ways that are essential for maintenance of homeostasis and self-defense, and are also associated with many inflammatory disorders. ECs, together with pericytes and ECM proteins, can regulate blood flow, the coagulation cascade, fluid and solute exchange, and leukocyte trafficking. While capillary and venular functions in inflammation are well characterized, the arteriolar contribution to inflammation has only recently come into focus. Arterioles differ from venules in structure, EC morphology, shear environment, expression, and distribution of surface ligands; hence, regulation and function of arteriolar wall cells during inflammation may also be distinct from venules. Recent work indicates that in response to proinflammatory stimuli, arterioles alter barrier function, and support leukocyte and platelet interactions through upregulation of adhesion molecules. This suggests that in addition to their role in blood flow regulation, arterioles may also participate in inflammatory responses. In this review, we will discuss mechanisms that characterize arteriolar responses to proinflammatory stimuli. We will detail how distinct arteriolar features contribute to regulation of barrier function and leukocyte-EC interactions in inflammation, and further highlight the potential priming effects of arteriolar responses on venular function and progression of inflammatory responses.

KEYWORDS:

adhesion molecules; endothelial cells; inflammatory responses; leukocytes; morphology; neutrophils; permeability; shear stress

PMID:
23701383
PMCID:
PMC3797166
DOI:
10.1111/micc.12068
[Indexed for MEDLINE]
Free PMC Article

Supplemental Content

Full text links

Icon for Wiley Icon for PubMed Central
Loading ...
Support Center