Key result
Heart failure in hypertensive rats is linked to increased myocardial decorin and type I collagen.
Why the study?
The temporal and spatial expression of decorin during progression to heart failure and its role in extracellular matrix remodeling are not well understood.
Answers are grounded in this paper and cite their sources.
Decorin dynamics in SHHF rats may reflect ECM remodeling in hypertensive HF; leaves open translation to human disease.
The proteoglycan, decorin, is a regulator of collagen fibril organization and its resulting functional properties. The temporal and spatial expression of decorin during the progression to heart failure is not well understood and may play a significant role in extracellular matrix remodeling. Decorin and types I and III collagen levels were measured in male Spontaneously Hypertensive Heart Failure (SHHF) and control Wistar-Furth rats at 2 and 8 mo, and at congestive heart failure (CHF). Decorin levels increased in the SHHF rats relative to the control rats in CHF. Type I collagen levels increased while type III levels decreased in the SHHF rats in CHF relative to the age matched controls. The SHHF rats have 48 and 45 KDa isoforms of the decorin core protein expressed at all ages while control Wistar-Furths produced only a 45 KDa form. Decorin was localized in the outer ventricle wall but during CHF, decorin was expressed throughout the ventricular myocardium. Immunogold localization of decorin demonstrated an increased distribution of decorin along the myocardium collagen fibrils at CHF. The enhanced expression and greater distribution of decorin may be linked to extracellular matrix remodeling which occurs with the development of heart failure.
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Medeiros et al. (2002) studied Heart failure. Spontaneously Hypertensive Heart Failure (SHHF) vs. Control Wistar-Furth rats was evaluated on Decorin and types I and III collagen levels. Decorin levels and distribution, along with type I collagen, increased in the myocardium of Spontaneously Hypertensive Heart Failure rats during congestive heart failure compared to controls.
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