Please use this identifier to cite or link to this item:
Title: Osteoglycin prevents cardiac dilatation and dysfunction after myocardial infarction through infarct collagen strengthening
Authors: Van Aelst L.N.L.
Voss S.
Carai P.
Van Leeuwen R.
Vanhoutte D.
Sanders-Van Wijk S.
Eurlings L.
Swinnen M.
Verheyen F.K.
Verbeken E.
Nef H.
Troidl C.
Cook S.A. 
Brunner-La Rocca H.-P.
M”llmann H.
Papageorgiou A.-P.
Heymans S.
Keywords: Cardiac remodeling
Heart failure
Heart rupture
Myocardial infarction
Issue Date: 2015
Publisher: Lippincott Williams and Wilkins
Citation: Van Aelst L.N.L., Voss S., Carai P., Van Leeuwen R., Vanhoutte D., Sanders-Van Wijk S., Eurlings L., Swinnen M., Verheyen F.K., Verbeken E., Nef H., Troidl C., Cook S.A., Brunner-La Rocca H.-P., M”llmann H., Papageorgiou A.-P., Heymans S. (2015). Osteoglycin prevents cardiac dilatation and dysfunction after myocardial infarction through infarct collagen strengthening. Circulation Research 116 (3) : 425-436. ScholarBank@NUS Repository.
Abstract: 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-? 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 ? 2014 American Heart Association, Inc.
Source Title: Circulation Research
ISSN: 97330
DOI: 10.1161/CIRCRESAHA.116.304599
Appears in Collections:Elements
Staff Publications

Show full item record
Files in This Item:
File Description SizeFormatAccess SettingsVersion 
CIRCRESAHA.116.304599.pdf5.25 MBAdobe PDF




checked on Sep 18, 2020

Page view(s)

checked on Sep 18, 2020

Google ScholarTM



Items in DSpace are protected by copyright, with all rights reserved, unless otherwise indicated.