Pressure overload-induced alterations in fibrillar collagen content and myocardial diastolic function: role of secreted protein acidic and rich in cysteine (SPARC) in post-synthetic procollagen processing.

ABSTRACT:

Background

Chronic pressure overload causes myocardial hypertrophy, increased fibrillar collagen content, and abnormal diastolic function. We hypothesized that one determinant of these pressure overload-induced changes is the extracellular processing of newly synthesized procollagen into mature collagen fibrils. We further hypothesized that secreted protein acidic and rich in cysteine (SPARC) plays a key role in post-synthetic procollagen processing in normal and pressure-overloaded myocardium.

Methods and results

To determine whether pressure overload-induced changes in collagen content and diastolic function are affected by the absence of SPARC, age-matched wild-type (WT) and SPARC-null mice underwent either transverse aortic constriction (TAC) for 4 weeks or served as non

SUBMITTER: Bradshaw AD 

PROVIDER: S-EPMC2734276 | biostudies-literature | 2009 Jan

REPOSITORIES: biostudies-literature