ORCID Profile
0000-0001-7683-3189
Current Organisations
Vanderbilt University Medical Center
,
Indian Institute of Technology Mandi
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Publisher: Elsevier BV
Date: 12-2019
DOI: 10.1016/J.SLEEP.2019.07.002
Abstract: Due to low predictive values of obstructive sleep apnea (OSA) screening tools, there is a need for biomarker for screening of OSA patients at an early stage. The aim of the study was to evaluate differentially expressed proteins in blood and urine s les of OSA patients. In this study, we used isobaric tagging for relative and absolute quantification (iTRAQ) based proteomics approach to identify differentially expressed proteins, which were subsequently verified and validated using enzyme-linked immunosorbent assay (ELISA) technique in adult OSA patients. Seventeen differentially expressed proteins were selected from iTRAQ data for verification, based on their clinical significance and reproducibility among different iTRAQ experiment sets. Five of these proteins (plasma = 2 urine = 3) were further validated in plasma (non-OSA- = 42 OSA = 198) and urine s les (non-OSA = 46 OSA = 197). ROC curve analysis for all OSA vs. non-OSA subjects ensured optimal diagnostic utility of two urinary proteins: Endothelial protein c receptor (EPCR) (AUC = 73%, cut-off: 35 pg/ml) and dermcidin (AUC = 74%, cut-off: 4.6 pg/ml). For severe OSA, diagnostic accuracy significantly improved with AUC as 88% and 82% for EPCR (cut-off: 46 pg/ml) and dermcidin (cut-off: 5.2 pg/ml) respectively. Sensitivity and specificity of combined performance of both urinary proteins for severe OSA were 94% and 91% respectively. In this study, urinary EPCR and dermcidin emerged as novel biomarkers for screening severe OSA patients.
Publisher: Elsevier BV
Date: 2017
DOI: 10.1016/J.JPROT.2016.11.017
Abstract: Myocardial infarction is one of the leading causes of cardiac dysfunction, failure and sudden death. Post infarction cardiac remodeling presents a poor prognosis, with 30%-45% of patients developing heart failure, in a period of 5-25years. Oxidative stress has been labelled as the primary causative factor for cardiac damage during infarction, however, the impact it may have during the process of post infarction remodeling has not been well probed. In this study, we have implemented iTRAQ proteomics to catalogue proteins and functional processes, participating both temporally (early and late phases) and spatially (infarct and remote zones), during post myocardial infarction remodeling of the heart as functions of the differential oxidative stress manifest during the remodeling process. Cardiac metabolism was the dominant network to be affected during infarction and the remodeling time points considered in this study. A distinctive expression pattern of cytoskeletal proteins was also observed with increased remodeling time points. Further, it was found that the cytoskeletal protein Desmin, aggregated in the infarct zone during the remodeling process, mediated by the protease Calpain1. Taken together, all of these data in conjunction may lay the foundation to understand the effects of oxidative stress on the remodeling process and elaborate the mechanism behind the compromised cardiac function observed during post myocardial infarction remodeling. Oxidative stress is the major driving force for cardiac damage during myocardial infarction. However, the impact of oxidative stress on the process of post MI remodeling in conducting the heart towards functional failure has not been well explored. In this study, a spatial and temporal approach was taken to elaborate the major proteins and cellular processes involved in post MI remodeling. Based on level/ intensity of ROS, spatially, infarct and noninfarct zones were chosen for analysis while on the temporal scale, early (30days) and late time points (120days) post MI were included in the study. This design enabled us to delineate the differential protein expression on a spectrum of maximum oxidative stress at infarct zone during MI to minimum oxidative stress at noninfarct zone during late time point post MI. The proteome profiles for each of the study groups when comparatively analysed gave a holistic idea about the dominant cellular processes involved in post MI remodeling such as cardiac metabolism, both for short term and long term remodeling as well as unique processes such as Desmin mediated cytoskeletal remodeling of the infarcted myocardium that are involved in the compromise of cardiac function.
Publisher: Elsevier BV
Date: 09-2015
DOI: 10.1016/J.JPROT.2015.04.027
Abstract: Cardiovascular disease has remained as the largest cause of morbidity and mortality worldwide. From dissecting the disease aetiology to identifying prognostic markers for better management of the disease is still a challenge for researchers. In the post human genome sequencing era much of the thrust has been focussed towards application of advanced genomic tools along with evaluation of traditional risk factors. With the advancement of next generation proteomics and metabolomics approaches it has now become possible to understand the protein interaction network & metabolic rewiring which lead to the perturbations of the disease phenotype. Further, elucidating different post translational modifications using advanced mass spectrometry based methods have provided an impetus towards in depth understanding of the proteome. The past decade has observed a plethora of studies where proteomics has been applied successfully to identify potential prognostic and diagnostic markers as well as to understand the disease mechanisms for various types of cardiovascular diseases. In this review, we attempted to document relevant proteomics based studies that have been undertaken either to identify potential biomarkers or have elucidated newer mechanistic insights into understanding the patho-physiology of cardiovascular disease, primarily coronary artery disease, cardiomyopathy, and myocardial ischemia. We have also provided a perspective on the potential of proteomics in combating this deadly disease. This review has catalogued recent studies on proteomics and metabolomics involved in understanding several cardiovascular diseases (CVDs). A holistic systems biology based approach, of which proteomics and metabolomics are two very important components, would help in delineating various pathways associated with complex disorders like CVD. This would ultimately provide better mechanistic understanding of the disease biology leading to development of prognostic biomarkers. This article is part of a Special Issue entitled: Proteomics in India.
Publisher: Wiley
Date: 15-04-2019
DOI: 10.1002/PROT.25681
Abstract: An increased level of homocysteine, a reactive thiol amino acid, is associated with several complex disorders and is an independent risk factor for cardiovascular disease. A majority (>80%) of circulating homocysteine is protein bound. Homocysteine exclusively binds to protein cysteine residues via thiol disulfide exchange reaction, the mechanism of which has been reported. In contrast, homocysteine thiolactone, the cyclic thioester of homocysteine, is believed to exclusively bind to the primary amine group of lysine residue leading to N-homocysteinylation of proteins and hence studies on binding of homocysteine thiolactone to proteins thus far have only focused on N-homocysteinylation. Although it is known that homocysteine thiolactone can hydrolyze to homocysteine at physiological pH, surprisingly the extent of S-homocysteinylation during the exposure of homocysteine thiolactone with proteins has never been looked into. In this study, we clearly show that the hydrolysis of homocysteine thiolactone is pH dependent, and at physiological pH, 1 mM homocysteine thiolactone is hydrolysed to ~0.71 mM homocysteine within 24 h. Using albumin, we also show that incubation of HTL with albumin leads to a greater proportion of S-homocysteinylation (0.41 mol/mol of albumin) than N-homocysteinylation (0.14 mol/mol of albumin). S-homocysteinylation at Cys
Publisher: Elsevier BV
Date: 09-2015
DOI: 10.1016/J.JPROT.2015.03.011
Abstract: Coronary artery disease (CAD), a complex metabolic disorder, is one of the largest causes of death worldwide. Both environmental and genetic factors contribute to the etiology of this metabolic disease. The gene-environment interaction could lead to modulation of various metabolic pathways resulting in altered levels of various metabolites. Thus, identifying metabolites could aid in deciphering pathways that could be involved in the pathophysiology of the disease. With the advent of high resolution mass spectrometry based methodologies, it is now possible to screen thousands of metabolites in a single snapshot thus, allowing the identification of potential disease metabolite markers. In this work, using an untargeted metabolomic approach, we attempted to identify metabolites that have altered levels in CAD patients. Using reverse phase and HILIC based chromatography followed by mass spectrometry we identified a total of 32 metabolites (2 fold p<0.05) in plasma whose levels were significantly altered in CAD s les. Further, we have validated the discriminative ability of these metabolites in an independent set of CAD and control s les using multivariate PLS-DA analysis. Interestingly, Lyso PC (18:0), Cortisol, Lyso PC (P-17:0), and glycerophosphocholine were among the top discriminators for CAD which implies involvement of phosphatidylcholine pathway in the pathogenesis of atherosclerosis. Herein, we report that an unbiased metabolomic study has the potential to identify newer markers which are involved in several important biological pathways like lipid metabolism, phosphatidylcholine pathway etc. which in turn are implicated in CAD. These markers could be of potential clinical importance for screening subjects at risk of CAD. This article is part of a Special Issue entitled: Proteomics in India.
Location: United States of America
No related grants have been discovered for Trayambak Basak.