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      • Record: found
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      Oxidized low density lipoprotein, stem cells, and atherosclerosis

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          Abstract

          Oxidized low density lipoprotein (ox-LDL), a risk factor of atherosclerosis, facilitates the formation and vulnerability of atherosclerotic plaque, thus contributing to several clinical complications. Stem cells participate in vascular repair after damage and atherosclerosis is a process of inflammation accompanied with vascular injury. Researchers have proposed that stem cells participate in the formation of atherosclerotic plaque. Also, because ox-LDL is capable of inducing toxic effects on stem cells, it is reasonable to postulate that ox-LDL promotes the progress of atherosclerosis via acting on stem cells. In the present article, we review the relationship between ox-LDL, stem cells, and atherosclerosis and a portion of the associated mechanisms.

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          The protein kinase complement of the human genome.

          G. Manning (2002)
          We have catalogued the protein kinase complement of the human genome (the "kinome") using public and proprietary genomic, complementary DNA, and expressed sequence tag (EST) sequences. This provides a starting point for comprehensive analysis of protein phosphorylation in normal and disease states, as well as a detailed view of the current state of human genome analysis through a focus on one large gene family. We identify 518 putative protein kinase genes, of which 71 have not previously been reported or described as kinases, and we extend or correct the protein sequences of 56 more kinases. New genes include members of well-studied families as well as previously unidentified families, some of which are conserved in model organisms. Classification and comparison with model organism kinomes identified orthologous groups and highlighted expansions specific to human and other lineages. We also identified 106 protein kinase pseudogenes. Chromosomal mapping revealed several small clusters of kinase genes and revealed that 244 kinases map to disease loci or cancer amplicons.
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            Transcriptional regulation and transformation by Myc proteins.

            Sovana Adhikary, Martin Eilers (2005)
            Myc genes are key regulators of cell proliferation, and their deregulation contributes to the genesis of most human tumours. Recently, a wealth of data has shed new light on the biochemical functions of Myc proteins and on the mechanisms through which they function in cellular transformation.
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              Mesenchymal stem cells: biology, pathophysiology, translational findings, and therapeutic implications for cardiac disease.

              Adam Williams, Joshua Hare (2011)
              Mesenchymal stem cells (MSCs) are a prototypical adult stem cell with capacity for self-renewal and differentiation with a broad tissue distribution. Initially described in bone marrow, MSCs have the capacity to differentiate into mesoderm- and nonmesoderm-derived tissues. The endogenous role for MSCs is maintenance of stem cell niches (classically the hematopoietic), and as such, MSCs participate in organ homeostasis, wound healing, and successful aging. From a therapeutic perspective, and facilitated by the ease of preparation and immunologic privilege, MSCs are emerging as an extremely promising therapeutic agent for tissue regeneration. Studies in animal models of myocardial infarction have demonstrated the ability of transplanted MSCs to engraft and differentiate into cardiomyocytes and vasculature cells, recruit endogenous cardiac stem cells, and secrete a wide array of paracrine factors. Together, these properties can be harnessed to both prevent and reverse remodeling in the ischemically injured ventricle. In proof-of-concept and phase I clinical trials, MSC therapy improved left ventricular function, induced reverse remodeling, and decreased scar size. This article reviews the current understanding of MSC biology, mechanism of action in cardiac repair, translational findings, and early clinical trial data of MSC therapy for cardiac disease.
              Article 0 comments Cited 271 times – based on 0 reviews     Review now
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                Author and article information

                Journal
                Journal ID (nlm-ta): Lipids Health Dis
                Journal ID (iso-abbrev): Lipids Health Dis
                Title: Lipids in Health and Disease
                Publisher: BioMed Central
                ISSN (Electronic): 1476-511X
                Publication date Collection: 2012
                Publication date (Electronic): 2 July 2012
                Volume: 11
                Page: 85
                Affiliations
                [1 ]Department of Cardiology, Second Xiangya Hospital, Central South University, Changsha, Hunan, 410011, China
                Article
                Publisher ID: 1476-511X-11-85
                DOI: 10.1186/1476-511X-11-85
                PMC ID: 3475066
                PubMed ID: 22747902
                SO-VID: 6c9a39ac-9179-4885-a590-eb64c80200d7
                Copyright © Copyright ©2012 Yang et al.;licensee BioMed Central Ltd.
                License:

                This is an Open Access article distributed under the terms of the Creative Commons Attribution License ( http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

                History
                Date received : 10 May 2012
                Date accepted : 16 June 2012
                Categories
                Subject: Review

                ScienceOpen disciplines: Biochemistry
                Keywords: oxidative stress,atherosclerosis,lox-1,stem cells,oxidized ldl
                Data availability:
                ScienceOpen disciplines: Biochemistry
                Keywords: oxidative stress, atherosclerosis, lox-1, stem cells, oxidized ldl

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