alexa Metabolic and Inflammatory Proteins Differentially Expressed in Platelets from Unprovoked Deep Vein Thrombosis Patients | OMICS International | Abstract
ISSN: 0974-276X

Journal of Proteomics & Bioinformatics
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Research Article

Metabolic and Inflammatory Proteins Differentially Expressed in Platelets from Unprovoked Deep Vein Thrombosis Patients

Mariane C Flores-Nascimento1*, Karina Kleinfelder-Fontanesi2, Thiago Matos de Araújo3, Gabriel Forato Anhê3, Rodrigo Secolin4, Fernanda Andrade Orsi1, Erich Vinicius de Paula1 and Joyce M Annichino-Bizzacchi1

1Hematology-Hemotherapy Center, University of Campinas (UNICAMP), Campinas, SP, Brazil

2Biology Institute, University of Campinas (UNICAMP), Campinas, SP, Brazil

3Department of Pharmacology, University of Campinas (UNICAMP), Campinas, SP, Brazil

4Medical Genetic Department, University of Campinas (UNICAMP), Campinas, SP, Brazil

*Corresponding Author:
Mariane C Flores-Nascimento
Hematology-Hemotherapy Center/University of
Campinas (UNICAMP) P.O. Box 6198
13083-970, Campinas - SP, Brazil
Tel: +55 19 3521 8601
Fax: +55 19 3289 1089
E-mail: [email protected]

Received Date: November 12, 2013; Accepted Date: January 20, 2014; Published Date: January 24, 2014

Citation: Flores-Nascimento MC, Kleinfelder-Fontanesi K, de Araújo TM, Anhê GF, Secolin R, et al. (2014) Metabolic and Inflammatory Proteins Differentially Expressed in Platelets from Unprovoked Deep Vein Thrombosis Patients. J Proteomics Bioinform 7:017-022. doi:10.4172/jpb.1000298

Copyright: © 2014 Flores-Nascimento MC, et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.

Abstract

Deep vein thrombosis (DVT) is multi-causal disease associated to high morbidity and mortality due to complications, especially from pulmonary embolism. New factors of relevance on the DVT pathophysiology enhance our understanding of disease mechanisms and can be translated into improved management of patients, prevention of recurrence and development of new therapies. In this context, the precise role of platelets in the pathogenesis of DVT is not completely understood. Our objectives were to acquire and to analyze the whole platelet protein profile of samples from 3 DVT patients and to compare them to results obtained from 1 sibling and 1 neighbor from each patient (in order to minimize genetic and environmental interferences). These patients presented unprovoked and recurrent episodes of proximal DVT as well as a family history of DVT. Platelets were washed, lysed, and the proteins were hydrolyzed by trypsin. Peptides were first separated by HPLC and peptide fractions were further detected by LC-MS/MS. Five proteins was present on patients and absent in all the controls: Apolipoprotein A1 Binding-Protein, Coatomer (zeta1 sub-unit), 17β-hydroxysteroid dehydrogenase type XI, Leukotriene A-4 Hydrolase and Sorbitol Dehydrogenase. The analysis identified proteins that currently are not related to the pathophysiology of DVT, and the persistence of these inflammatory and lipid transportation-related proteins emphasize the relevance of these phenomena on DVT.

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