Molecular basis of impaired glycogen metabolism during ischemic stroke and hypoxia
Ischemic stroke is the combinatorial effect of many pathological processes including the loss of energy supplies, excessive intracellular calcium accumulation, oxidative stress, and inflammatory responses. The brain's ability to maintain energy demand through this process involves metabolism of...
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| description | Ischemic stroke is the combinatorial effect of many pathological processes including the loss of energy supplies, excessive intracellular calcium accumulation, oxidative stress, and inflammatory responses. The brain's ability to maintain energy demand through this process involves metabolism of glycogen, which is critical for release of stored glucose. However, regulation of glycogen metabolism in ischemic stroke remains unknown. In the present study, we investigate the role and regulation of glycogen metabolizing enzymes and their effects on the fate of glycogen during ischemic stroke.
Ischemic stroke was induced in rats by peri-vascular application of the vasoconstrictor endothelin-1 and forebrains were collected at 1, 3, 6 and 24 hours post-stroke. Glycogen levels and the expression and activity of enzymes involved in glycogen metabolism were analyzed. We found elevated glycogen levels in the ipsilateral hemispheres compared with contralateral hemispheres at 6 and 24 hours (25% and 39% increase respectively; P |
| doi_str_mv | 10.1371/journal.pone.0097570 |
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Ischemic stroke was induced in rats by peri-vascular application of the vasoconstrictor endothelin-1 and forebrains were collected at 1, 3, 6 and 24 hours post-stroke. Glycogen levels and the expression and activity of enzymes involved in glycogen metabolism were analyzed. We found elevated glycogen levels in the ipsilateral hemispheres compared with contralateral hemispheres at 6 and 24 hours (25% and 39% increase respectively; P<0.05). Glycogen synthase activity and glycogen branching enzyme expression were found to be similar between the ipsilateral, contralateral, and sham control hemispheres. In contrast, the rate-limiting enzyme for glycogen breakdown, glycogen phosphorylase, had 58% lower activity (P<0.01) in the ipsilateral hemisphere (24 hours post-stroke), which corresponded with a 48% reduction in cAMP-dependent protein kinase A (PKA) activity (P<0.01). In addition, glycogen debranching enzyme expression 24 hours post-stroke was 77% (P<0.01) and 72% lower (P<0.01) at the protein and mRNA level, respectively. In cultured rat primary cerebellar astrocytes, hypoxia and inhibition of PKA activity significantly reduced glycogen phosphorylase activity and increased glycogen accumulation but did not alter glycogen synthase activity. Furthermore, elevated glycogen levels provided metabolic support to astrocytes during hypoxia.
Our study has identified that glycogen breakdown is impaired during ischemic stroke, the molecular basis of which includes reduced glycogen debranching enzyme expression level together with reduced glycogen phosphorylase and PKA activity.</description><identifier>ISSN: 1932-6203</identifier><identifier>EISSN: 1932-6203</identifier><identifier>DOI: 10.1371/journal.pone.0097570</identifier><identifier>PMID: 24858129</identifier><language>eng</language><publisher>United States: Public Library of Science</publisher><subject>Accumulation ; Alzheimer's disease ; Alzheimers disease ; Analysis ; Animals ; Astrocytes ; Astrocytes - drug effects ; Astrocytes - metabolism ; Astrocytes - pathology ; Biology and life sciences ; Brain ; Brain Ischemia - complications ; Brain research ; Breakdown ; Calcium ; Calcium (intracellular) ; Cell Hypoxia - drug effects ; Cell Survival - drug effects ; Cerebellum ; Combinatorial analysis ; Cyclic AMP-Dependent Protein Kinases - antagonists & inhibitors ; Cyclic AMP-Dependent Protein Kinases - metabolism ; Diabetes ; Endothelin 1 ; Endothelins ; Energy ; Energy demand ; Energy Metabolism - drug effects ; Enzymes ; Gene Expression Regulation, Enzymologic - drug effects ; Glucose ; Glucose metabolism ; Glycogen ; Glycogen - metabolism ; Glycogen branching enzyme ; Glycogen Debranching Enzyme System - genetics ; Glycogen phosphorylase ; Glycogen Phosphorylase - genetics ; Glycogen synthase ; Glycogen synthesis ; Hemispheres ; Hypoglycemia ; Hypotheses ; Hypoxia ; Inflammation ; Ischemia ; Kinases ; Laboratory animals ; Male ; Metabolism ; mRNA ; Musculoskeletal system ; Neurons ; Oxidative stress ; Pathology ; Phosphorylase ; Physiological aspects ; Physiology ; Protein kinase A ; Protein Kinase Inhibitors - pharmacology ; Proteins ; Rats ; Rats, Wistar ; Reperfusion ; Rodents ; Stroke ; Stroke - complications ; Stroke - metabolism ; Stroke - pathology ; Stroke - physiopathology ; Supply and demand ; Surgery</subject><ispartof>PloS one, 2014-05, Vol.9 (5), p.e97570</ispartof><rights>COPYRIGHT 2014 Public Library of Science</rights><rights>2014 Hossain et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License: http://creativecommons.org/licenses/by/4.0/ (the “License”), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited. Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License.</rights><rights>2014 Hossain et al 2014 Hossain et al</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c692t-a811659cb17d4821b4e95d600b096091d4f1a5f9c7c31aa41afc54cb7b7ac7a03</citedby><cites>FETCH-LOGICAL-c692t-a811659cb17d4821b4e95d600b096091d4f1a5f9c7c31aa41afc54cb7b7ac7a03</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC4032261/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC4032261/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,727,780,784,864,885,2100,2926,23864,27922,27923,53789,53791,79370,79371</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/24858129$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><contributor>Coles, Jonathan A.</contributor><creatorcontrib>Hossain, Mohammed Iqbal</creatorcontrib><creatorcontrib>Roulston, Carli Lorraine</creatorcontrib><creatorcontrib>Stapleton, David Ian</creatorcontrib><title>Molecular basis of impaired glycogen metabolism during ischemic stroke and hypoxia</title><title>PloS one</title><addtitle>PLoS One</addtitle><description>Ischemic stroke is the combinatorial effect of many pathological processes including the loss of energy supplies, excessive intracellular calcium accumulation, oxidative stress, and inflammatory responses. The brain's ability to maintain energy demand through this process involves metabolism of glycogen, which is critical for release of stored glucose. However, regulation of glycogen metabolism in ischemic stroke remains unknown. In the present study, we investigate the role and regulation of glycogen metabolizing enzymes and their effects on the fate of glycogen during ischemic stroke.
Ischemic stroke was induced in rats by peri-vascular application of the vasoconstrictor endothelin-1 and forebrains were collected at 1, 3, 6 and 24 hours post-stroke. Glycogen levels and the expression and activity of enzymes involved in glycogen metabolism were analyzed. We found elevated glycogen levels in the ipsilateral hemispheres compared with contralateral hemispheres at 6 and 24 hours (25% and 39% increase respectively; P<0.05). Glycogen synthase activity and glycogen branching enzyme expression were found to be similar between the ipsilateral, contralateral, and sham control hemispheres. In contrast, the rate-limiting enzyme for glycogen breakdown, glycogen phosphorylase, had 58% lower activity (P<0.01) in the ipsilateral hemisphere (24 hours post-stroke), which corresponded with a 48% reduction in cAMP-dependent protein kinase A (PKA) activity (P<0.01). In addition, glycogen debranching enzyme expression 24 hours post-stroke was 77% (P<0.01) and 72% lower (P<0.01) at the protein and mRNA level, respectively. In cultured rat primary cerebellar astrocytes, hypoxia and inhibition of PKA activity significantly reduced glycogen phosphorylase activity and increased glycogen accumulation but did not alter glycogen synthase activity. Furthermore, elevated glycogen levels provided metabolic support to astrocytes during hypoxia.
Our study has identified that glycogen breakdown is impaired during ischemic stroke, the molecular basis of which includes reduced glycogen debranching enzyme expression level together with reduced glycogen phosphorylase and PKA activity.</description><subject>Accumulation</subject><subject>Alzheimer's disease</subject><subject>Alzheimers disease</subject><subject>Analysis</subject><subject>Animals</subject><subject>Astrocytes</subject><subject>Astrocytes - drug effects</subject><subject>Astrocytes - metabolism</subject><subject>Astrocytes - pathology</subject><subject>Biology and life sciences</subject><subject>Brain</subject><subject>Brain Ischemia - complications</subject><subject>Brain research</subject><subject>Breakdown</subject><subject>Calcium</subject><subject>Calcium (intracellular)</subject><subject>Cell Hypoxia - drug effects</subject><subject>Cell Survival - drug effects</subject><subject>Cerebellum</subject><subject>Combinatorial analysis</subject><subject>Cyclic AMP-Dependent Protein Kinases - antagonists & inhibitors</subject><subject>Cyclic AMP-Dependent Protein Kinases - metabolism</subject><subject>Diabetes</subject><subject>Endothelin 1</subject><subject>Endothelins</subject><subject>Energy</subject><subject>Energy demand</subject><subject>Energy Metabolism - drug effects</subject><subject>Enzymes</subject><subject>Gene Expression Regulation, Enzymologic - drug effects</subject><subject>Glucose</subject><subject>Glucose metabolism</subject><subject>Glycogen</subject><subject>Glycogen - metabolism</subject><subject>Glycogen branching enzyme</subject><subject>Glycogen Debranching Enzyme System - genetics</subject><subject>Glycogen phosphorylase</subject><subject>Glycogen Phosphorylase - genetics</subject><subject>Glycogen synthase</subject><subject>Glycogen synthesis</subject><subject>Hemispheres</subject><subject>Hypoglycemia</subject><subject>Hypotheses</subject><subject>Hypoxia</subject><subject>Inflammation</subject><subject>Ischemia</subject><subject>Kinases</subject><subject>Laboratory animals</subject><subject>Male</subject><subject>Metabolism</subject><subject>mRNA</subject><subject>Musculoskeletal system</subject><subject>Neurons</subject><subject>Oxidative stress</subject><subject>Pathology</subject><subject>Phosphorylase</subject><subject>Physiological aspects</subject><subject>Physiology</subject><subject>Protein kinase A</subject><subject>Protein Kinase Inhibitors - pharmacology</subject><subject>Proteins</subject><subject>Rats</subject><subject>Rats, Wistar</subject><subject>Reperfusion</subject><subject>Rodents</subject><subject>Stroke</subject><subject>Stroke - complications</subject><subject>Stroke - metabolism</subject><subject>Stroke - pathology</subject><subject>Stroke - physiopathology</subject><subject>Supply and demand</subject><subject>Surgery</subject><issn>1932-6203</issn><issn>1932-6203</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2014</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>AZQEC</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><sourceid>DWQXO</sourceid><sourceid>GNUQQ</sourceid><sourceid>DOA</sourceid><recordid>eNqNkluL1DAYhoso7jr6D0QLguDFjEmTHnIjLIuHgZWF9XAbvhzaZkybmrSy8-_NON1lCgqSi4Tk-d4k7_cmyXOMNpiU-O3OTb4HuxlcrzcIsTIv0YPkHDOSrYsMkYcn67PkSQg7hHJSFcXj5CyjVV7hjJ0nN5-d1XKy4FMBwYTU1anpBjBeq7Sxe-ka3aedHkE4a0KXqsmbvklNkK3ujEzD6N0PnUKv0nY_uFsDT5NHNdign83zKvn24f3Xy0_rq-uP28uLq7UsWDauocK4yJkUuFS0yrCgmuWqQEggViCGFa0x5DWTpSQYgGKoZU6lKEUJsgREVsnLo-5gXeCzHYHjPKtQSar42VWyPRLKwY4P3nTg99yB4X82nG84-NFIqznFGEtEFKuRphpYhYpSEEGRQoKJTEStd_Ntk-i0krofPdiF6PKkNy1v3C9OEcmyAkeBV7OAdz8nHcZ_PHmmGoivMn3topjsot38guLYs0ObI7X5CxWHOvQkBqI2cX9R8GZREJlR344NTCHw7Zeb_2evvy_Z1ydsq8GObXB2Go3rwxKkR1B6F4LX9b1zGPFDnu_c4Ic88znPsezFqev3RXcBJr8B7aDwWQ</recordid><startdate>20140523</startdate><enddate>20140523</enddate><creator>Hossain, Mohammed Iqbal</creator><creator>Roulston, Carli Lorraine</creator><creator>Stapleton, David Ian</creator><general>Public Library of Science</general><general>Public Library of Science (PLoS)</general><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>IOV</scope><scope>ISR</scope><scope>3V.</scope><scope>7QG</scope><scope>7QL</scope><scope>7QO</scope><scope>7RV</scope><scope>7SN</scope><scope>7SS</scope><scope>7T5</scope><scope>7TG</scope><scope>7TM</scope><scope>7U9</scope><scope>7X2</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8AO</scope><scope>8C1</scope><scope>8FD</scope><scope>8FE</scope><scope>8FG</scope><scope>8FH</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABJCF</scope><scope>ABUWG</scope><scope>AEUYN</scope><scope>AFKRA</scope><scope>ARAPS</scope><scope>ATCPS</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BENPR</scope><scope>BGLVJ</scope><scope>BHPHI</scope><scope>C1K</scope><scope>CCPQU</scope><scope>D1I</scope><scope>DWQXO</scope><scope>FR3</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>H94</scope><scope>HCIFZ</scope><scope>K9.</scope><scope>KB.</scope><scope>KB0</scope><scope>KL.</scope><scope>L6V</scope><scope>LK8</scope><scope>M0K</scope><scope>M0S</scope><scope>M1P</scope><scope>M7N</scope><scope>M7P</scope><scope>M7S</scope><scope>NAPCQ</scope><scope>P5Z</scope><scope>P62</scope><scope>P64</scope><scope>PATMY</scope><scope>PDBOC</scope><scope>PIMPY</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>PTHSS</scope><scope>PYCSY</scope><scope>RC3</scope><scope>5PM</scope><scope>DOA</scope></search><sort><creationdate>20140523</creationdate><title>Molecular basis of impaired glycogen metabolism during ischemic stroke and hypoxia</title><author>Hossain, Mohammed Iqbal ; Roulston, Carli Lorraine ; Stapleton, David Ian</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c692t-a811659cb17d4821b4e95d600b096091d4f1a5f9c7c31aa41afc54cb7b7ac7a03</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2014</creationdate><topic>Accumulation</topic><topic>Alzheimer's disease</topic><topic>Alzheimers disease</topic><topic>Analysis</topic><topic>Animals</topic><topic>Astrocytes</topic><topic>Astrocytes - drug effects</topic><topic>Astrocytes - metabolism</topic><topic>Astrocytes - pathology</topic><topic>Biology and life sciences</topic><topic>Brain</topic><topic>Brain Ischemia - complications</topic><topic>Brain research</topic><topic>Breakdown</topic><topic>Calcium</topic><topic>Calcium (intracellular)</topic><topic>Cell Hypoxia - drug effects</topic><topic>Cell Survival - drug effects</topic><topic>Cerebellum</topic><topic>Combinatorial analysis</topic><topic>Cyclic AMP-Dependent Protein Kinases - antagonists & inhibitors</topic><topic>Cyclic AMP-Dependent Protein Kinases - metabolism</topic><topic>Diabetes</topic><topic>Endothelin 1</topic><topic>Endothelins</topic><topic>Energy</topic><topic>Energy demand</topic><topic>Energy Metabolism - drug effects</topic><topic>Enzymes</topic><topic>Gene Expression Regulation, Enzymologic - drug effects</topic><topic>Glucose</topic><topic>Glucose metabolism</topic><topic>Glycogen</topic><topic>Glycogen - metabolism</topic><topic>Glycogen branching enzyme</topic><topic>Glycogen Debranching Enzyme System - genetics</topic><topic>Glycogen phosphorylase</topic><topic>Glycogen Phosphorylase - genetics</topic><topic>Glycogen synthase</topic><topic>Glycogen synthesis</topic><topic>Hemispheres</topic><topic>Hypoglycemia</topic><topic>Hypotheses</topic><topic>Hypoxia</topic><topic>Inflammation</topic><topic>Ischemia</topic><topic>Kinases</topic><topic>Laboratory animals</topic><topic>Male</topic><topic>Metabolism</topic><topic>mRNA</topic><topic>Musculoskeletal system</topic><topic>Neurons</topic><topic>Oxidative stress</topic><topic>Pathology</topic><topic>Phosphorylase</topic><topic>Physiological aspects</topic><topic>Physiology</topic><topic>Protein kinase A</topic><topic>Protein Kinase Inhibitors - pharmacology</topic><topic>Proteins</topic><topic>Rats</topic><topic>Rats, Wistar</topic><topic>Reperfusion</topic><topic>Rodents</topic><topic>Stroke</topic><topic>Stroke - complications</topic><topic>Stroke - metabolism</topic><topic>Stroke - pathology</topic><topic>Stroke - physiopathology</topic><topic>Supply and demand</topic><topic>Surgery</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Hossain, Mohammed Iqbal</creatorcontrib><creatorcontrib>Roulston, Carli Lorraine</creatorcontrib><creatorcontrib>Stapleton, David Ian</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Gale In Context: Opposing Viewpoints</collection><collection>Gale In Context: Science</collection><collection>ProQuest Central (Corporate)</collection><collection>Animal Behavior Abstracts</collection><collection>Bacteriology Abstracts (Microbiology B)</collection><collection>Biotechnology Research Abstracts</collection><collection>Nursing & Allied Health Database</collection><collection>Ecology Abstracts</collection><collection>Entomology Abstracts (Full archive)</collection><collection>Immunology Abstracts</collection><collection>Meteorological & Geoastrophysical Abstracts</collection><collection>Nucleic Acids Abstracts</collection><collection>Virology and AIDS Abstracts</collection><collection>Agricultural Science Collection</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Medical Database (Alumni Edition)</collection><collection>ProQuest Pharma Collection</collection><collection>Public Health Database</collection><collection>Technology Research Database</collection><collection>ProQuest SciTech Collection</collection><collection>ProQuest Technology Collection</collection><collection>ProQuest Natural Science Collection</collection><collection>Hospital Premium Collection</collection><collection>Hospital Premium Collection (Alumni Edition)</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>Materials Science & Engineering Collection</collection><collection>ProQuest Central (Alumni Edition)</collection><collection>ProQuest One Sustainability</collection><collection>ProQuest Central UK/Ireland</collection><collection>Advanced Technologies & Aerospace Collection</collection><collection>Agricultural & Environmental Science Collection</collection><collection>ProQuest Central Essentials</collection><collection>Biological Science Collection</collection><collection>ProQuest Central</collection><collection>Technology Collection (ProQuest)</collection><collection>Natural Science Collection (ProQuest)</collection><collection>Environmental Sciences and Pollution Management</collection><collection>ProQuest One Community College</collection><collection>ProQuest Materials Science Collection</collection><collection>ProQuest Central Korea</collection><collection>Engineering Research Database</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Central Student</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>SciTech Premium Collection</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Materials Science Database</collection><collection>Nursing & Allied Health Database (Alumni Edition)</collection><collection>Meteorological & Geoastrophysical Abstracts - 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The brain's ability to maintain energy demand through this process involves metabolism of glycogen, which is critical for release of stored glucose. However, regulation of glycogen metabolism in ischemic stroke remains unknown. In the present study, we investigate the role and regulation of glycogen metabolizing enzymes and their effects on the fate of glycogen during ischemic stroke.
Ischemic stroke was induced in rats by peri-vascular application of the vasoconstrictor endothelin-1 and forebrains were collected at 1, 3, 6 and 24 hours post-stroke. Glycogen levels and the expression and activity of enzymes involved in glycogen metabolism were analyzed. We found elevated glycogen levels in the ipsilateral hemispheres compared with contralateral hemispheres at 6 and 24 hours (25% and 39% increase respectively; P<0.05). Glycogen synthase activity and glycogen branching enzyme expression were found to be similar between the ipsilateral, contralateral, and sham control hemispheres. In contrast, the rate-limiting enzyme for glycogen breakdown, glycogen phosphorylase, had 58% lower activity (P<0.01) in the ipsilateral hemisphere (24 hours post-stroke), which corresponded with a 48% reduction in cAMP-dependent protein kinase A (PKA) activity (P<0.01). In addition, glycogen debranching enzyme expression 24 hours post-stroke was 77% (P<0.01) and 72% lower (P<0.01) at the protein and mRNA level, respectively. In cultured rat primary cerebellar astrocytes, hypoxia and inhibition of PKA activity significantly reduced glycogen phosphorylase activity and increased glycogen accumulation but did not alter glycogen synthase activity. Furthermore, elevated glycogen levels provided metabolic support to astrocytes during hypoxia.
Our study has identified that glycogen breakdown is impaired during ischemic stroke, the molecular basis of which includes reduced glycogen debranching enzyme expression level together with reduced glycogen phosphorylase and PKA activity.</abstract><cop>United States</cop><pub>Public Library of Science</pub><pmid>24858129</pmid><doi>10.1371/journal.pone.0097570</doi><oa>free_for_read</oa></addata></record> |
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| recordid | cdi_plos_journals_1528073805 |
| source | MEDLINE; DOAJ Directory of Open Access Journals; Public Library of Science (PLoS) Journals Open Access; EZB-FREE-00999 freely available EZB journals; PubMed Central; Free Full-Text Journals in Chemistry |
| subjects | Accumulation Alzheimer's disease Alzheimers disease Analysis Animals Astrocytes Astrocytes - drug effects Astrocytes - metabolism Astrocytes - pathology Biology and life sciences Brain Brain Ischemia - complications Brain research Breakdown Calcium Calcium (intracellular) Cell Hypoxia - drug effects Cell Survival - drug effects Cerebellum Combinatorial analysis Cyclic AMP-Dependent Protein Kinases - antagonists & inhibitors Cyclic AMP-Dependent Protein Kinases - metabolism Diabetes Endothelin 1 Endothelins Energy Energy demand Energy Metabolism - drug effects Enzymes Gene Expression Regulation, Enzymologic - drug effects Glucose Glucose metabolism Glycogen Glycogen - metabolism Glycogen branching enzyme Glycogen Debranching Enzyme System - genetics Glycogen phosphorylase Glycogen Phosphorylase - genetics Glycogen synthase Glycogen synthesis Hemispheres Hypoglycemia Hypotheses Hypoxia Inflammation Ischemia Kinases Laboratory animals Male Metabolism mRNA Musculoskeletal system Neurons Oxidative stress Pathology Phosphorylase Physiological aspects Physiology Protein kinase A Protein Kinase Inhibitors - pharmacology Proteins Rats Rats, Wistar Reperfusion Rodents Stroke Stroke - complications Stroke - metabolism Stroke - pathology Stroke - physiopathology Supply and demand Surgery |
| title | Molecular basis of impaired glycogen metabolism during ischemic stroke and hypoxia |
| url | https://sfx.bib-bvb.de/sfx_tum?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&ctx_tim=2025-01-13T13%3A49%3A34IST&url_ver=Z39.88-2004&url_ctx_fmt=infofi/fmt:kev:mtx:ctx&rfr_id=info:sid/primo.exlibrisgroup.com:primo3-Article-gale_plos_&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.atitle=Molecular%20basis%20of%20impaired%20glycogen%20metabolism%20during%20ischemic%20stroke%20and%20hypoxia&rft.jtitle=PloS%20one&rft.au=Hossain,%20Mohammed%20Iqbal&rft.date=2014-05-23&rft.volume=9&rft.issue=5&rft.spage=e97570&rft.pages=e97570-&rft.issn=1932-6203&rft.eissn=1932-6203&rft_id=info:doi/10.1371/journal.pone.0097570&rft_dat=%3Cgale_plos_%3EA418127570%3C/gale_plos_%3E%3Curl%3E%3C/url%3E&disable_directlink=true&sfx.directlink=off&sfx.report_link=0&rft_id=info:oai/&rft_pqid=1528073805&rft_id=info:pmid/24858129&rft_galeid=A418127570&rft_doaj_id=oai_doaj_org_article_4111c03d9f0e4ea98067b3b40d0b9b2b&rfr_iscdi=true |