C-reactive protein accelerates the progression of atherosclerosis in apolipoprotein E-deficient mice

Area of Science:

• Cardiovascular Research
• Immunology
• Genetics

Background:

• Plasma C-reactive protein (CRP) is a known predictor of atherosclerosis.
• Previous research lacked in vivo evidence to confirm CRP's proatherogenic role.

Purpose of the Study:

• To investigate the in vivo effect of human CRP transgene expression on atherosclerosis development in apolipoprotein E-deficient mice.

Main Methods:

• Utilized apolipoprotein E-deficient (apoE-/-) mice with human CRP transgene (tg).
• Assessed atherosclerosis in basal and turpentine-stimulated conditions.
• Analyzed aortic atherosclerotic lesion size, C3 deposition, vascular cell adhesion molecule-1, collagen, and angiotensin type 1 receptor (AT1-R) expression.

Main Results:

• Human CRP transgene expression significantly increased aortic atherosclerotic lesion size in apoE-/- mice.
• CRP and complement C3 deposition were elevated within lesions.
• Increased expression of AT1-R, vascular cell adhesion molecule-1, and collagen was observed in lesions of CRP-expressing mice.
• No significant difference in blood pressure was noted, indicating a local effect.

Conclusions:

• Human CRP transgene expression accelerates aortic atherosclerosis in apoE-/- mice.
• CRP is proatherogenic in vivo, associated with complement activation and increased expression of inflammatory markers and AT1-R within atherosclerotic lesions.