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Arteriosclerosis, Thrombosis, and Vascular Biology
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Arteriosclerosis, Thrombosis, and Vascular Biology. 2008;28:611-614
doi: 10.1161/ATVBAHA.107.159608
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(Arteriosclerosis, Thrombosis, and Vascular Biology. 2008;28:611.)
© 2008 American Heart Association, Inc.


Editorials

Serum or Plasma Samples?

The "Cinderella" Role of Blood Collection Procedures Preanalytical Methodological Issues Influence the Release and Activity of Circulating Matrix Metalloproteinases and Their Tissue Inhibitors, Hampering Diagnostic Trueness and Leading to Misinterpretation

Ferdinando Mannello

From the Institute of Histology and Laboratory Analysis, Faculty of Sciences and Technologies, University "Carlo Bo", Urbino, Italy.

Correspondence to Ferdinando Mannello, Institute of Histology and Laboratory Analysis, Faculty of Sciences and Technologies, University "Carlo Bo", Via O. Ubaldini, 7-61029 Urbino (PU), Italy. E-mail ferdinando.mannello@uniurb.it


An extract of the first 250 words of the full text is provided, because this article has no abstract.
 

Dysregulations of the synthesis and breakdown of the extracellular matrix (ECM) is a key processes in the physiopathology of vascular remodeling and the development of atherothrombotic syndromes.1–4 Matrix metalloproteinases (MMPs) are endopeptidases, belonging to the matrixin family that can degrade almost all the ECM components.5 Although there is little doubt that MMPs are an important components in cancer invasion and metastasis,6 they are also regarded as key regulatory molecules in degenerative processes and inflammation,5,7 as playing roles also in physiopathological remodeling of the vascular wall2,8 and as the pathogenesis of cardio- and cerebrovascular diseases.9,10 Thus, MMPs have emerged as potential biomarkers of atherothrombotic risk and predictors of coronary and cerebrovascular disease recurrence.8

ATVB 2008;28:e15–e16.

Normal and diseased blood vessel wall cells may upregulate and activate MMPs in a multistep fashion, driven in part by soluble cytokines and cell–cell interactions with platelets and white blood cells. Enhanced MMP activation (alone or in concert with the fibrinolytic system) contributes to increased matrix turnover, which may have beneficial effects (eg, in vascular repair and atherosclerotic plaque stabilization)11 but also detrimental effects (eg, in vascular intimal thickening, atherosclerosis, and in thrombotic syndromes).12

Because the changes on the cellular level are reflected in body fluids, determination of MMPs in blood have been recommended as noninvasive tools in the diagnosis and monitoring of several diseases.13 It has been demonstrated repeatedly that both the MMP/tissue inhibitor of matrix metalloproteinase (TIMP) assay and zymography essentially depend on the blood sampling procedures, with some MMPs and TIMPs having higher . . . [Full Text of this Article]




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Consideration of preanalytical impact of blood sampling on measurement of matrix metalloproteinases and their inhibitors as precondition to evaluate their relationship to clinical data
Multiple Sclerosis, November 1, 2009; 15(11): 1372 - 1373.
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