Inhibition of smooth muscle cell proliferation by adiponectin requires proteolytic conversion to its globular form.

Accelerated atherosclerosis is the primary cardiovascular manifestation of diabetes and correlates inversely with levels of circulating adiponectin, an anti-atherosclerotic adipokine that declines in diabetes. We therefore initiated a study to examine the mechanisms by which adiponectin, a hormone released from adipose tissue, influences the proliferation of vascular smooth muscle cells (SMCs). Addition of adiponectin to quiescent porcine coronary artery SMCs increased both protein and DNA synthesis and concurrently activated ERK1/2 and Akt.

Peroxisome proliferator-activated receptor alpha and gamma ligands differentially affect smooth muscle cell proliferation and migration.

Peroxisome proliferator-activated receptors (PPARs) alpha and gamma are expressed in smooth muscle cells (SMCs). This study was designed to compare the effects of PPARalpha and PPARgamma on SMC proliferation and migration and to determine how they operate. Treatment of SMCs from porcine coronary artery revealed that mitogen-stimulated DNA synthesis was blocked by the PPARalpha ligand 4-chloro-6-(2,3-xylidino)-2-pyrimidinylthioacetic acid (WY14,643) and 15-deoxy-Delta(12,14) prostaglandin J(2) (15d-PGJ(2)) (a putative PPARgamma agonist) but not by the PPARgamma agonist rosiglitazone or the PPARbeta/delta ligand 2-methyl-4-((4-methyl-2-(4-trifluoromethylphenyl)-1,3-thiazol-5-yl)-methylsulfanyl)phenoxy acetic acid (GW501516).