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Collagen formation was disorganized in SPARC-less mice, leaving them vulnerable to cardiac rupture.
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A little SPARC may help a broken heart rebound, according to Schellings et al. on page 113.
Like other extracellular matrix proteins, SPARC helps to heal wounds by modulating cell–matrix interactions and promoting cell proliferation, migration, and angiogenesis. Here, Schellings et al. find that SPARC uses its wound-healing skills to form strong scars that help prevent cardiac rupture after a heart attack.
Mice lacking SPARC developed normal, healthy hearts. But after a heart attack, SPARC-less mice—particularly males—had a hard time recovering. Without the protein, which is known to bind directly to type I collagen, the normally strong and structured collagen bundles that form at the site of injury were loose, creating a disorganized scar. Similar collagen defects are seen in healing skin when SPARC is absent.
When people (or mice) suffer heart attacks, SPARC levels are known to rise. The protein also appears to be elevated in people with chronic heart dysfunction. Predicting that SPARC provides a protective service to hearts trying to heal, the authors overexpressed SPARC after heart injury in normal mice. As expected, mice with more SPARC survived longer. In nonheart cells, SPARC amplifies signals induced by TGFβ, a cytokine with known heart-healing properties. Indeed, treating SPARC-deficient mice with TGFβ rescued collagen deposition and hastened healing.
Whether SPARC expression varies in humans has not yet been examined, but low levels could be an underlying factor in heart recovery. And as matrix proteins tend to decrease over time, diminishing SPARC expression may help explain why the elderly suffer higher rates of mortality after heart attacks. The authors suggest that in the future, treating people with recombinant SPARC might help heart attack victims recover.
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