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      Drug Design, Development and Therapy (submit here)

      This international, peer-reviewed Open Access journal by Dove Medical Press focuses on the design and development of drugs, as well as the clinical outcomes, patient safety, and programs targeted at the effective and safe use of medicines. Sign up for email alerts here.

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      Protein kinase C-mediated sodium glucose transporter 1 activation in precondition-induced cardioprotection

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          Abstract

          The concept of cardioprotection through preconditioning against ischemia–reperfusion (I/R) injury is well known and established. However, among different proposed mechanisms regarding the concept of ischemic preconditioning, protein kinase C (PKC)-mediated cardioprotection through ischemic preconditioning plays a key role in myocardial I/R injury. Thus, this study was designed to find the relationship between PKC and sodium glucose transporter 1 (SGLT1) in preconditioning-induced cardioprotection, which is ill reported till now. By applying a multifaceted approach, we demonstrated that PKC activates SGLT1, which curbed oxidative stress and apoptosis against I/R injury. PKC activation enhances cardiac glucose uptake through SGLT1 and seems essential in preventing I/R-induced cardiac injury, indicating a possible cross-talk between PKC and SGLT1.

          Most cited references20

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          SwarmDock: a server for flexible protein-protein docking.

          Iain Moal, Paul A Bates, Raphael Chaleil … (2013)
          Protein-protein interactions are central to almost all biological functions, and the atomic details of such interactions can yield insights into the mechanisms that underlie these functions. We present a web server that wraps and extends the SwarmDock flexible protein-protein docking algorithm. After uploading PDB files of the binding partners, the server generates low energy conformations and returns a ranked list of clustered docking poses and their corresponding structures. The user can perform full global docking, or focus on particular residues that are implicated in binding. The server is validated in the CAPRI blind docking experiment, against the most current docking benchmark, and against the ClusPro docking server, the highest performing server currently available.
          Article 0 comments Cited 49 times – based on 0 reviews     Review now
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            Protein phosphorylation and signal transduction.

            J D Graves, E G Krebs (2015)
            It is now generally accepted that protein phosphorylation-dephosphorylation has a role in the regulation of essentially all cellular functions. Thus, it is of interest that this process is involved in signal transduction. Nonetheless, the extent to which protein phosphorylation participates in signaling is truly remarkable. Almost every known signaling pathway eventually impinges on a protein kinase, or in some instances, a protein phosphatase. The diversity of these enzymes is noteworthy, and it is of interest that many biotechnology companies are eyeing them as potentially important targets for drugs. Such drugs may have important therapeutic applications, and in any event, they certainly will be useful to investigators who study signal transduction. Indeed, this already has been proven to be true.
            Article 0 comments Cited 48 times – based on 0 reviews     Review now
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              Ischemic preconditioning slows energy metabolism and delays ultrastructural damage during a sustained ischemic episode.

              C Murry, V Richard, K. Reimer … (1990)
              We have shown previously that preconditioning myocardium with four 5-minute episodes of ischemia and reperfusion dramatically limited the size of infarcts caused by a subsequent 40-minute episode of sustained ischemia. The current study was undertaken to assess whether the same preconditioning protocol slowed the loss of high energy phosphates, limited catabolite accumulation, and/or delayed ultrastructural damage during a sustained ischemic episode. Myocardial metabolites and ultrastructure in the severely ischemic subendocardial regions were compared between control and preconditioned canine hearts. Hearts (four to 10 per group) were excised after 0, 5, 10, 20, or 40 minutes of sustained ischemia. All groups had comparable collateral blood flow. Preconditioned hearts developed ultrastructural injury more slowly than controls; evidence of irreversible injury was observed after 20 minutes in controls but not until 40 minutes in preconditioned hearts. Furthermore, after 40 minutes of ischemia, irreversible injury was homogeneous in controls but only focal in preconditioned myocardium. Preconditioning reduced starting levels of ATP by 29%. Nevertheless, it also slowed the rate of ATP depletion during the episode of sustained ischemia, so that after 10 minutes of ischemia, preconditioned hearts had more ATP than controls. However, after 40 minutes, ATP contents were not significantly different between groups. Preservation of ATP resulted from reduced ATP utilization and was not due to increased ATP production. Accumulation of purine nucleosides and bases (products of adenine nucleotide degradation) was limited in preconditioned myocardium. Accumulation of glucose-1-phosphate, glucose-6-phosphate, and lactate also was reduced markedly by preconditioning, due to reduced rates of glycogen breakdown and and anaerobic glycolysis. We propose that preconditioning reduces myocardial energy demand during ischemia, which results in a reduced rate of high energy phosphate utilization and a reduced rate of anaerobic glycolysis. Either preservation of ATP or reduction of the cellular load of catabolites may be responsible for delaying ischemic cell death.
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                Author and article information

                Journal
                Journal ID (nlm-ta): Drug Des Devel Ther
                Journal ID (iso-abbrev): Drug Des Devel Ther
                Journal ID (publisher-id): Drug Design, Development and Therapy
                Title: Drug Design, Development and Therapy
                Publisher: Dove Medical Press
                ISSN (Electronic): 1177-8881
                Publication date Collection: 2016
                Publication date (Electronic): 14 September 2016
                Volume: 10
                Pages: 2929-2938
                Affiliations
                [1 ]Division of Medicinal Chemistry and Pharmacology, Indian Institute of Chemical Technology, Hyderabad, India
                [2 ]Drug Discovery Research Center (DDRC), Translational Health Science and Technology Institute (THSTI), Faridabad, Haryana, India
                [3 ]Department of Pharmacology, National Institute of Pharmaceutical Education and Research, Hyderabad, India
                [4 ]Department of Pathology, National Institute of Nutrition, Hyderabad, India
                Author notes
                Correspondence: Shailendra Asthana; Sanjay K Banerjee, Drug Discovery Research Center (DDRC), Translational Health Science and Technology Institute (THSTI), NCR Biotech Science Cluster, 3rd Milestone Faridabad – Gurgaon Expressway, Haryana 121001, India, Email sasthana@ 123456thsti.res.in ; skbanerjee@ 123456thsti.res.in
                Article
                Publisher ID: dddt-10-2929
                DOI: 10.2147/DDDT.S105482
                PMC ID: 5028101
                PubMed ID: 27695290
                SO-VID: 5dd5ef53-8303-44cf-9246-27f49bb31c37
                Copyright © © 2016 Kanwal et al. This work is published and licensed by Dove Medical Press Limited
                License:

                The full terms of this license are available at https://www.dovepress.com/terms.php and incorporate the Creative Commons Attribution – Non Commercial (unported, v3.0) License ( http://creativecommons.org/licenses/by-nc/3.0/). By accessing the work you hereby accept the Terms. Non-commercial uses of the work are permitted without any further permission from Dove Medical Press Limited, provided the work is properly attributed.

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                Categories
                Subject: Original Research

                ScienceOpen disciplines: Pharmacology & Pharmaceutical medicine
                Keywords: ischemic preconditioning,ischemia-reperfusion injury,phorbol-12-myristate,oxidative stress,sglt1,phlorizin
                Data availability:
                ScienceOpen disciplines: Pharmacology & Pharmaceutical medicine
                Keywords: ischemic preconditioning, ischemia-reperfusion injury, phorbol-12-myristate, oxidative stress, sglt1, phlorizin

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