Adiponectin is a protein hormone excreted into the bloodstream by fatty tissue and it plays a role in the suppression of inflammation-associated metabolic disorders that may result in type 2 diabetes, obesity, and atherosclerosis. In the Journal of Clinical Investigation, Rosario Scalia and colleagues from Thomas Jefferson University studied the vascular protective actions of adiponectin in mice. The authors found that adiponectin-deficient (Ad-/-) mice possessed high levels of nitric oxide and a 5-fold increase in the adhesion of leukocytes to the blood vessel wall. This effect could be blocked and reversed by the addition of the recombinant globular adiponectin domain (gAd). Importantly, prior administration of gAd was also shown to protect healthy mice against the induction of leukocyte-endothelium interactions. The study demonstrates a clear role for normal levels of adiponectin in the regulation of leukocyte-endothelium interactions in mice. The data also suggest that gAd may serve as a potential pharmacological treatment of abnormal endothelial dysfunction occurring in pathological conditions associated with adiponectin deficiency.
TITLE: Adiponectin deficiency increases leukocyte-endothelium interactions via upregulation of endothelial cell adhesion molecules in vivo
AUTHOR CONTACT:
Rosario Scalia
Thomas Jefferson University, Philadelphia, Pennsylvania, USA.
Barry J. Goldstein
Jefferson Medical College, Philadelphia, Pennsylvania, USA.
JCI table of contents -- June 1, 2007
Contact: Brooke Grindlinger
Journal of Clinical Investigation
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