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Tumor Suppressor Protein Linked to Atherosclerosis

p19ARF deficiency in mice reduces plaque apoptosis and promotes atherosclerosis

FRIDAY, April 9 (HealthDay News) -- In mice, deficiency of the tumor suppressor protein p19ARF encoded by the CDKN2A gene reduces macrophage and vascular smooth muscle cell apoptosis, and aggravates atherosclerosis, according to a study published online April 7 in the Journal of the American College of Cardiology.

Herminia González-Navarro, Ph.D., of the Instituto de Biomedicina de Valencia in Spain, and colleagues fed an atherogenic diet to atherosclerosis-prone apolipoprotein E (apoE)-null and doubly deficient apoE-p19ARF mice and quantified the atherosclerosis burden in whole-mounted aortas and in aortic cross-sections.

The researchers found that genetic disruption of p19ARF augmented aortic atherosclerosis without affecting body weight, plasma lipoproteins, or plaque's proliferative activity. They also note that p19ARF deficiency significantly attenuated apoptosis in atherosclerotic lesions and in cultured macrophages and vascular smooth muscle cells, which are major cellular constituents of atheromatous plaques.

"These findings suggest that interventions aimed at increasing the expression of ARF may lessen plaque progression," the authors write. "Our results also support the notion that decreased plaque apoptosis might contribute to increased risk of atherosclerosis in individuals homozygous for the G allele of rs10757278, who exhibit reduced levels of not only ARF, but also p15INK4b, p16INK4a, and ANRIL transcripts in blood-borne T cells."

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