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Effect of intermittent hypoxia on atherosclerosis in apolipoprotein E-deficient mice.

ABSTRACT: Obstructive sleep apnea causes intermittent hypoxia (IH) and is associated with increased cardiovascular mortality. This increased risk may be attributable to more extensive or unstable atherosclerotic plaques in subjects with OSA. We studied the effect of chronic IH in atherosclerosis-prone mice.Apolipoprotein E-deficient (ApoE(-/-)) mice fed a high cholesterol diet were exposed to 4 or 12 weeks of IH and compared to intermittent air-exposed controls. At 4 weeks, IH increased plaque size in the aortic sinus and the descending aorta. At 12 weeks, atherosclerosis progressed in all groups, but more rapidly in the descending aorta of IH-exposed animals. Plaque composition was similar between IH and controls. Between 4 and 12 weeks, there were progressive increases in blood pressure, with relatively stable increases in serum lipids and arterial stiffness.IH accelerates atherosclerotic plaque growth in ApoE(-/-) mice without affecting plaque composition. The mechanisms may include non-additive increases in serum lipids, and cumulative increases in blood pressure.

SUBMITTER: Jun J

PROVIDER: S-EPMC2846209 | biostudies-literature | 2010 Apr

REPOSITORIES: biostudies-literature

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Effect of intermittent hypoxia on atherosclerosis in apolipoprotein E-deficient mice.

Jun Jonathan J Reinke Christian C Bedja Djahida D Berkowitz Dan D Bevans-Fonti Shannon S Li Jianguo J Barouch Lili A LA Gabrielson Kathleen K Polotsky Vsevolod Y VY

Atherosclerosis 20091017 2

<h4>Objective</h4>Obstructive sleep apnea causes intermittent hypoxia (IH) and is associated with increased cardiovascular mortality. This increased risk may be attributable to more extensive or unstable atherosclerotic plaques in subjects with OSA. We studied the effect of chronic IH in atherosclerosis-prone mice.<h4>Methods and results</h4>Apolipoprotein E-deficient (ApoE(-/-)) mice fed a high cholesterol diet were exposed to 4 or 12 weeks of IH and compared to intermittent air-exposed control ...[more]

PMID: 19897196

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Project description:Fat inflammation may play an important role in comorbidities associated with obesity such as atherosclerosis.To first establish feasibility of fat transplantation, epididymal fat pads were harvested from wild-type C57BL/6J mice and transplanted into leptin-deficient (Lep(ob/ob)) mice. Fat transplantation produced physiological leptin levels and prevented obesity and infertility in Lep(ob/ob) mice. However, the transplanted fat depots were associated with chronically increased macrophage infiltration with characteristics identical to those observed in fat harvested from obese animals. The inflammation in transplanted adipose depots was regulated by the same factors that have been implicated in endogenous fat inflammation such as monocyte chemoattractant protein-1. To determine whether this inflamed adipose depot could affect vascular disease in mice, epididymal fat depots were transplanted into atherosclerosis-prone apolipoprotein E-deficient ApoE(-/-) mice. Plasma from ApoE(-/-) mice receiving fat transplants contained increased leptin, resistin, and monocyte chemoattractant protein-1 compared with plasma from sham-operated ApoE(-/-) mice. Furthermore, mice transplanted with visceral fat developed significantly more atherosclerosis compared with sham-operated animals, whereas transplants with subcutaneous fat did not affect atherosclerosis despite a similar degree of fat inflammation. Treatment of transplanted ApoE(-/-) mice with pioglitazone decreased macrophage content of the transplanted visceral fat pad and reduced plasma monocyte chemoattractant protein-1. Importantly, pioglitazone also reduced atherosclerosis triggered by inflammatory visceral fat but had no protective effect on atherosclerosis in the absence of the visceral fat transplantation.Our results indicate that visceral adipose-related inflammation accelerates atherosclerosis in mice. Drugs such as thiazolidinediones might be a useful strategy to specifically attenuate the vascular disease induced by visceral inflammatory fat.

Dataset Information

Effect of intermittent hypoxia on atherosclerosis in apolipoprotein E-deficient mice.

Publications

Effect of intermittent hypoxia on atherosclerosis in apolipoprotein E-deficient mice.

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