Article

Effect of coronary thrombolysis on the plasma concentration of osteonectin (SPARC, BM40) in patients with acute myocardial infarction.

Sinai Center for Thrombosis Research, Baltimore, Maryland 21215, USA.
Journal of Thrombosis and Thrombolysis (Impact Factor: 2.04). 11/2000; 10(2):197-202. DOI: 10.1023/A:1018774812613
Source: PubMed

ABSTRACT Osteonectin is a phosphoglycoprotein exclusively located in bone and platelet alpha-granules. Human platelet-derived osteonectin is released into plasma after thrombin-induced activation. Recognizing the unique distribution of the osteonectin pool, we first sought to investigate whether osteonectin could serve as a sensitive marker of platelet activity, and identify patients with acute myocardial infarction (AMI). The second objective was to define the effects of thrombolytic therapy in these patients on the plasma concentrations of osteonectin at prespecified time points following attempted reperfusion. Osteonectin levels by ELISA were determined in AMI patients before thrombolysis and at 3, 6, 12, and 24 hours thereafter and compared with 12 healthy controls. At baseline, soluble osteonectin plasma levels were similar between controls (447. 7+/-20.6 ng/ml) and AMI patients (425.7+/-43.3 ng/mL; p=NS). A significant increase of the soluble osteonectin was observed at 3 hours after thrombolysis (519.4+/-26.9 ng/mL; p=0.03), and was followed by a decrease to baseline levels at 6 hours after attempted reperfusion. Contrary to expectations, the plasma osteonectin level in our pilot study was not a sensitive marker distinguishing patients with AMI. The early peak of soluble osteonectin at 3 hours after thrombolytic therapy is most likely not related to coronary thrombolysis per se but rather to the phasic changes of platelet activity during myocardial ischemia-reperfusion. The unquestionable platelet origin of this protein and the lack of elevated plasma levels of this alpha-granule constituent, challenge the postulate of uniform platelet activation in AMI patients.

0 Followers
 · 
63 Views
  • [Show abstract] [Hide abstract]
    ABSTRACT: Migraine has strong genetic and environmental components and may also be a significant contributor to chronic migraine (CM). It is hypothesized that gene expression changes in peripheral blood cells can be used to detect the interaction of these influences. Distinct genomic expression patterns for migraine and CM will be present. These genomic profiles will help clarify the interactions of inheritance and environment. This initial study begins to examine the feasibility of peripheral blood cell genomic analysis to assist in the understanding of the pathophysiology of migraine and CM. Blood samples from patients were obtained either during an acute migraine or CM. Genomic expression patterns were analyzed using Affymetrix U95A microarrays. Expression patterns of 7 migraine and 15 CM patients were compared to four distinct control groups (total patients, n=56) including healthy subjects. A group of platelet genes were upregulated in both migraine and CM samples. Different gene expression patterns were also seen between migraine and CM. A group of immediate early genes including c-fos and cox-2 were expressed at higher levels in migraine, whereas specific mitochondrial genes were expressed at higher levels in CM. Increased expression of platelet genes in patients with migraine and CM suggests similar underlying pathophysiology. The differences seen between migraine and CM in other genes suggest an overlapping but not identical pathophysiology. Further genomic profiling studies will help define these relationships and provide further insights into headache pathogenesis.
    Headache The Journal of Head and Face Pain 11/2004; 44(10):994-1004. DOI:10.1111/j.1526-4610.2004.04193.x · 3.19 Impact Factor
  • [Show abstract] [Hide abstract]
    ABSTRACT: 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.
    Physiological Reviews 04/2012; 92(2):635-88. DOI:10.1152/physrev.00008.2011 · 29.04 Impact Factor
  • [Show abstract] [Hide abstract]
    ABSTRACT: In the present study, we evaluated functional activity of the alternative pathway of complement in schizophrenia by measuring the alternative pathway hemolytic activity (AH50) of complement as well as hemolytic activity of the complement C3 component (C3H50) in the blood of patients with schizophrenia and healthy subjects. To assess the influence of neuroleptic treatment on measured parameters, both drug-free and medicated patients were examined. In addition, correlation analysis between AH50 and C3H50 has been performed. The results of the present study clearly demonstrate upregulation of the alternative complement cascade in schizophrenia and activator effect of neuroleptics on complement alternative pathway. Based upon the results obtained we hypothesize that hyperactivation of the alternative complement pathway in schizophrenia is stimulated by apoptotic cells.
    Neurochemical Research 06/2010; 35(6):894-8. DOI:10.1007/s11064-010-0126-2 · 2.55 Impact Factor