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Published on: November 11, 2022
Osteoglycin prevents cardiac dilatation and dysfunction after myocardial infarction through infarct collagen
Lucas N L Van Aelst1, Sandra Voss1, Paolo Carai1
1From the Department of Cardiovascular Sciences, Center for Molecular and Vascular Biology, Catholic University of Leuven, Leuven, Belgium (L.N.L.V.A., P.C., A.-P.P., S.H.); Department of Cardiology (L.N.L.V.A., M.S.) and Department of Pathology (E.V.), University Hospitals Leuven, Leuven, Belgium; Department of Cardiology, Kerckhoff Heart Center, Bad Nauheim, Germany (S.V., H.N., C.T., H.M.); Department of Cardiology, Cardiovascular Research Institute Maastricht (CARIM), University Hospital Maastricht, Maastricht, The Netherlands (P.C., R.V.L., S.S.-v.W., L.E., H.-P.B.-L.R., A.-P.P., S.H.); Department of Pediatrics, Molecular Cardiovascular Biology, Cincinnati Children's Hospital Medical Center, University of Cincinnati, OH (D.V.); Department of Molecular Cell Biology, Cardiovascular Research Institute Maastricht, Maastricht University, Maastricht, The Netherlands (F.K.V.); National Heart and Lung Institute, Cardiovascular Genetics and Genomics, London, United Kingdom (S.A.C.); National Heart Centre Singapore, Department of Cardiology, Singapore (S.A.C.); Duke-NUS Graduate Medical School, Singapore (S.A.C.); Department of Cardiology, University Hospital Basel, Basel, Switzerland (H.-P.B.-L.R.); and ICIN-Netherlands Heart Institute, Utrecht, The Netherlands (S.H.).
Rationale:
To maintain cardiac mechanical and structural integrity after an ischemic insult, profound alterations occur within the extracellular matrix. Osteoglycin is a small leucine-rich proteoglycan previously described as a marker of cardiac hypertrophy.
Objective:
To establish whether osteoglycin may play a role in cardiac integrity and function after myocardial infarction (MI).
Methods And Results:
Osteoglycin expression is associated with collagen deposition and scar formation in mouse and human MI. Absence of osteoglycin in mice resulted in significantly increased rupture-related mortality with tissue disruption, intramyocardial bleeding, and increased cardiac dysfunction, despite equal infarct sizes. Surviving osteoglycin null mice had greater infarct expansion in comparison with wild-type mice because of impaired collagen fibrillogenesis and maturation in the infarcts as revealed by electron microscopy and collagen polarization. Absence of osteoglycin did not affect cardiomyocyte hypertrophy in the remodeling remote myocardium. In cultured fibroblasts, osteoglycin knockdown or supplementation did not alter transforming growth factor-β signaling. Adenoviral overexpression of osteoglycin in wild-type mice significantly improved collagen quality, thereby blunting cardiac dilatation and dysfunction after MI. In osteoglycin null mice, adenoviral overexpression of osteoglycin was unable to prevent rupture-related mortality because of insufficiently restoring osteoglycin protein levels in the heart. Finally, circulating osteoglycin levels in patients with heart failure were significantly increased in the patients with a previous history of MI compared with those with nonischemic heart failure and correlated with survival, left ventricular volumes, and other markers of fibrosis.
Conclusions:
Increased osteoglycin expression in the infarct scar promotes proper collagen maturation and protects against cardiac disruption and adverse remodeling after MI. In human heart failure, osteoglycin is a promising biomarker for ischemic heart failure.
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