Osteopontin: A potential biomarker for heart failure and reverse remodeling after left ventricular assist device support

Schipper, Marguérite E.I.; Scheenstra, Maaike R.; Kuik, J. van; Wichen, D.F. van; Weide, Petra van der; Dullens, H. F. J.; Lahpor, Jaap R.; Jonge, Nicolaas de; Weger, Roel A. de

doi:10.1016/j.healun.2011.03.015

Cited by 30 publications

(27 citation statements)

References 18 publications

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“…These findings indicate that distinct expression profiles of Corin in ventricular and atrial tissues and reduced levels of soluble corin protein in the plasma may be important in the pathogenesis of HF. In addition, we noted in the failing heart a high increase of the expression levels of trombospondin 4 ( Thbs4 ), osteopontin ( Ssp1 ) and periostin ( Postn ), in support of previously published results indicating that these proteins could have high therapeutic and diagnostic potential in HF [6,29]. …”

Section: Discussionsupporting

confidence: 87%

Transcriptional profiling of left ventricle and peripheral blood mononuclear cells in a rat model of postinfarction heart failure

et al. 2013

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BackgroundMyocardial infarction (MI) often results in left ventricular (LV) remodeling followed by heart failure (HF). It is of great clinical importance to understand the molecular mechanisms that trigger transition from compensated LV injury to HF and to identify relevant diagnostic biomarkers. The aim of this study was to investigate gene expression in the LV and to evaluate their reflection in peripheral blood mononuclear cells (PBMCs).MethodsMI was induced in rats by ligation of the proximal left coronary artery. Rats with small, moderate, and large MI size were included into the experiment two months after the operation. The development of heart failure was estimated by echocardiography and catheterization. Microarrays were used to compare the LV and PBMCs transcriptomes of control and experimental animals.ResultsOnly rats with a large MI developed extensive LV remodeling and heart failure. 840 transcripts were altered in LV of failing hearts, and especially numerous were those associated with the extracellular matrix. In contrast, no significant gene expression changes were seen in LVs of rats with moderate or small MI that had compensated LV injury. We showed that ceruloplasmin was similarly overexpressed in the heart and blood in response to HF, whereas downregulation of tetraspanin 12 was significant only in the PBMCs.ConclusionA large size of infarcted area is critical for progression of LV remodeling and HF development, associated with altered gene expression in the heart. Ceruloplasmin and tetraspanin 12 are potential convenient markers in readily obtainable PBMCs.

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Section: Discussionsupporting

confidence: 87%

Transcriptional profiling of left ventricle and peripheral blood mononuclear cells in a rat model of postinfarction heart failure

et al. 2013

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“…In contrast, in patients with heart failure and preserved ejection fraction OPN levels predicted death or heart failure events only in single variable analysis, but not when introduced into a multivariable model (235). Moreover, unloading the failing ventricle through left ventricular assist device support did not consistently reduce OPN levels in heart failure patients (400). A recent study suggested that in patients with stable ischemic heart disease, OPN levels are an independent predictor of adverse outcome (159).…”

Section: The Matricellular Proteins Key Modulators Of Cell:cellmentioning

confidence: 99%

Matricellular Proteins in Cardiac Adaptation and Disease

Frangogiannis

2012

Physiological Reviews

375

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The term matricellular proteins describes a family of structurally unrelated extracellular macromolecules that, unlike structural matrix proteins, do not play a primary role in tissue architecture, but are induced following injury and modulate cell-cell and cell-matrix interactions. When released to the matrix, matricellular proteins associate with growth factors, cytokines, and other bioactive effectors and bind to cell surface receptors transducing signaling cascades. Matricellular proteins are upregulated in the injured and remodeling heart and play an important role in regulation of inflammatory, reparative, fibrotic and angiogenic pathways. Thrombospondin (TSP)-1, -2, and -4 as well as tenascin-C and -X secreted protein acidic and rich in cysteine (SPARC), osteopontin, periostin, and members of the CCN family (including CCN1 and CCN2/connective tissue growth factor) are involved in a variety of cardiac pathophysiological conditions, including myocardial infarction, cardiac hypertrophy and fibrosis, aging-associated myocardial remodeling, myocarditis, diabetic cardiomyopathy, and valvular disease. This review discusses the properties and characteristics of the matricellular proteins and presents our current knowledge on their role in cardiac adaptation and disease. Understanding the role of matricellular proteins in myocardial pathophysiology and identification of the functional domains responsible for their actions may lead to design of peptides with therapeutic potential for patients with heart disease.

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“…234 Specifically in the heart, OPN upregulation in response to MI, primarily localized in macrophages, 236 is crucial for proper collagen deposition and reduction of chamber dilatation, thereby protecting from adverse cardiac remodeling. 231 Most importantly, in patients with heart failure, 237 MI, 238 or stenotic valvular [239][240][241] disease, OPN plasma levels seem to be a very promising biomarker for prediction 242 or progression 243 of heart diseases related to adverse cardiac remodeling.…”

Section: Osteopontinmentioning

confidence: 99%

Myocardial Extracellular Matrix

Rienks

Papageorgiou

Frangogiannis

et al. 2014

Circulation Research

307

170

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Abstract:The cardiac extracellular matrix (ECM) is a complex architectural network consisting of structural and nonstructural proteins, creating strength and plasticity. The nonstructural compartment of the ECM houses a variety of proteins, which are vital for ECM plasticity, and can be divided into 3 major groups: glycoproteins, proteoglycans, and glycosaminoglycans. The common denominator for these groups is glycosylation, which refers to the decoration of proteins or lipids with sugars. This review will discuss the fundamental role of the matrix in cardiac development, homeostasis, and remodeling, from a glycobiology point of view. Glycoproteins (eg, thrombospondins, secreted protein acidic and rich in cysteine, tenascins), proteoglycans (eg, versican, syndecans, biglycan), and glycosaminoglycans (eg, hyaluronan, heparan sulfate) are upregulated on cardiac injury and regulate key processes in the remodeling myocardium such as inflammation, fibrosis, and angiogenesis. Albeit some parallels can be made regarding the processes these proteins are involved in, their specific functions are extremely diverse. In fact, under varying conditions, individual proteins can even have opposing functions, making spatiotemporal contribution of these proteins in the rearrangement of multifaceted ECM very hard to grasp. Alterations of protein characteristics by the addition of sugars may explain the immense, yet tightly regulated, variability of the remodeling cardiac matrix. Understanding the role of glycosylation in altering the ultimate function of glycoproteins, proteoglycans, and glycosaminoglycans in the myocardium may lead to the development of new biochemical structures or compounds with great therapeutic potential for patients with heart disease. (Circ Res. 2014;114:872-888.)

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Osteopontin: A potential biomarker for heart failure and reverse remodeling after left ventricular assist device support

Cited by 30 publications

References 18 publications

Transcriptional profiling of left ventricle and peripheral blood mononuclear cells in a rat model of postinfarction heart failure

Transcriptional profiling of left ventricle and peripheral blood mononuclear cells in a rat model of postinfarction heart failure

Matricellular Proteins in Cardiac Adaptation and Disease

Myocardial Extracellular Matrix

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