Hyperglycemia Induces Cellular Hypoxia through Production of Mitochondrial ROS Followed by Suppression of Aquaporin-1
We previously proposed that hyperglycemia-induced mitochondrial reactive oxygen species (mtROS) generation is a key event in the development of diabetic complications. Interestingly, some common aspects exist between hyperglycemia and hypoxia-induced phenomena. Thus, hyperglycemia may induce cellula...
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| creator | Sada, Kiminori Nishikawa, Takeshi Kukidome, Daisuke Yoshinaga, Tomoaki Kajihara, Nobuhiro Sonoda, Kazuhiro Senokuchi, Takafumi Motoshima, Hiroyuki Matsumura, Takeshi Araki, Eiichi |
| description | We previously proposed that hyperglycemia-induced mitochondrial reactive oxygen species (mtROS) generation is a key event in the development of diabetic complications. Interestingly, some common aspects exist between hyperglycemia and hypoxia-induced phenomena. Thus, hyperglycemia may induce cellular hypoxia, and this phenomenon may also be involved in the pathogenesis of diabetic complications. In endothelial cells (ECs), cellular hypoxia increased after incubation with high glucose (HG). A similar phenomenon was observed in glomeruli of diabetic mice. HG-induced cellular hypoxia was suppressed by mitochondria blockades or manganese superoxide dismutase (MnSOD) overexpression, which is a specific SOD for mtROS. Overexpression of MnSOD also increased the expression of aquaporin-1 (AQP1), a water and oxygen channel. AQP1 overexpression in ECs suppressed hyperglycemia-induced cellular hypoxia, endothelin-1 and fibronectin overproduction, and apoptosis. Therefore, hyperglycemia-induced cellular hypoxia and mtROS generation may promote hyperglycemic damage in a coordinated manner. |
| doi_str_mv | 10.1371/journal.pone.0158619 |
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Interestingly, some common aspects exist between hyperglycemia and hypoxia-induced phenomena. Thus, hyperglycemia may induce cellular hypoxia, and this phenomenon may also be involved in the pathogenesis of diabetic complications. In endothelial cells (ECs), cellular hypoxia increased after incubation with high glucose (HG). A similar phenomenon was observed in glomeruli of diabetic mice. HG-induced cellular hypoxia was suppressed by mitochondria blockades or manganese superoxide dismutase (MnSOD) overexpression, which is a specific SOD for mtROS. Overexpression of MnSOD also increased the expression of aquaporin-1 (AQP1), a water and oxygen channel. AQP1 overexpression in ECs suppressed hyperglycemia-induced cellular hypoxia, endothelin-1 and fibronectin overproduction, and apoptosis. Therefore, hyperglycemia-induced cellular hypoxia and mtROS generation may promote hyperglycemic damage in a coordinated manner.</description><identifier>ISSN: 1932-6203</identifier><identifier>EISSN: 1932-6203</identifier><identifier>DOI: 10.1371/journal.pone.0158619</identifier><identifier>PMID: 27383386</identifier><language>eng</language><publisher>United States: Public Library of Science</publisher><subject>Animals ; Apoptosis ; Apoptosis - drug effects ; Aquaporin 1 ; Aquaporins ; Biology and life sciences ; Blotting, Western ; Care and treatment ; Cattle ; Cell Hypoxia ; Cell Line ; Cellular manufacture ; Complications ; Complications and side effects ; Deoxyguanosine - analogs & derivatives ; Deoxyguanosine - biosynthesis ; Diabetes ; Diabetes mellitus ; Diabetes Mellitus, Experimental - complications ; Diabetes Mellitus, Experimental - metabolism ; Endothelial cells ; Endothelial Cells - drug effects ; Endothelial Cells - metabolism ; Endothelin 1 ; Endothelin-1 - genetics ; Endothelin-1 - metabolism ; Endothelins ; Experiments ; Fibronectin ; Fibronectins - genetics ; Fibronectins - metabolism ; Glucose ; Glucose - pharmacology ; Hyperglycemia ; Hyperglycemia - complications ; Hyperglycemia - metabolism ; Hypoxia ; Hypoxia - metabolism ; Influence ; Kinases ; Life sciences ; Manganese ; Medical research ; Medicine ; Medicine and Health Sciences ; Metabolism ; Mice, Inbred C57BL ; Mice, Transgenic ; Mitochondria ; Mitochondria - metabolism ; Oxidative stress ; Oxygen ; Pathogenesis ; Phosphorylation ; Physical Sciences ; Reactive oxygen species ; Reactive Oxygen Species - metabolism ; Research and Analysis Methods ; Reverse Transcriptase Polymerase Chain Reaction ; Rodents ; Superoxide dismutase ; Superoxide Dismutase - genetics ; Superoxide Dismutase - metabolism</subject><ispartof>PloS one, 2016-07, Vol.11 (7), p.e0158619-e0158619</ispartof><rights>COPYRIGHT 2016 Public Library of Science</rights><rights>2016 Sada 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>2016 Sada et al 2016 Sada et al</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c791t-ce06f50d2d491aaa2b488a630e175ce497d602229634c91ae771440bebf9a0833</citedby><cites>FETCH-LOGICAL-c791t-ce06f50d2d491aaa2b488a630e175ce497d602229634c91ae771440bebf9a0833</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/PMC4934928/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC4934928/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,723,776,780,860,881,2096,2915,23845,27901,27902,53766,53768,79569,79570</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/27383386$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Sada, Kiminori</creatorcontrib><creatorcontrib>Nishikawa, Takeshi</creatorcontrib><creatorcontrib>Kukidome, Daisuke</creatorcontrib><creatorcontrib>Yoshinaga, Tomoaki</creatorcontrib><creatorcontrib>Kajihara, Nobuhiro</creatorcontrib><creatorcontrib>Sonoda, Kazuhiro</creatorcontrib><creatorcontrib>Senokuchi, Takafumi</creatorcontrib><creatorcontrib>Motoshima, Hiroyuki</creatorcontrib><creatorcontrib>Matsumura, Takeshi</creatorcontrib><creatorcontrib>Araki, Eiichi</creatorcontrib><title>Hyperglycemia Induces Cellular Hypoxia through Production of Mitochondrial ROS Followed by Suppression of Aquaporin-1</title><title>PloS one</title><addtitle>PLoS One</addtitle><description>We previously proposed that hyperglycemia-induced mitochondrial reactive oxygen species (mtROS) generation is a key event in the development of diabetic complications. 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drug effects</topic><topic>Aquaporin 1</topic><topic>Aquaporins</topic><topic>Biology and life sciences</topic><topic>Blotting, Western</topic><topic>Care and treatment</topic><topic>Cattle</topic><topic>Cell Hypoxia</topic><topic>Cell Line</topic><topic>Cellular manufacture</topic><topic>Complications</topic><topic>Complications and side effects</topic><topic>Deoxyguanosine - analogs & derivatives</topic><topic>Deoxyguanosine - biosynthesis</topic><topic>Diabetes</topic><topic>Diabetes mellitus</topic><topic>Diabetes Mellitus, Experimental - complications</topic><topic>Diabetes Mellitus, Experimental - metabolism</topic><topic>Endothelial cells</topic><topic>Endothelial Cells - drug effects</topic><topic>Endothelial Cells - metabolism</topic><topic>Endothelin 1</topic><topic>Endothelin-1 - genetics</topic><topic>Endothelin-1 - metabolism</topic><topic>Endothelins</topic><topic>Experiments</topic><topic>Fibronectin</topic><topic>Fibronectins - genetics</topic><topic>Fibronectins - metabolism</topic><topic>Glucose</topic><topic>Glucose - 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Interestingly, some common aspects exist between hyperglycemia and hypoxia-induced phenomena. Thus, hyperglycemia may induce cellular hypoxia, and this phenomenon may also be involved in the pathogenesis of diabetic complications. In endothelial cells (ECs), cellular hypoxia increased after incubation with high glucose (HG). A similar phenomenon was observed in glomeruli of diabetic mice. HG-induced cellular hypoxia was suppressed by mitochondria blockades or manganese superoxide dismutase (MnSOD) overexpression, which is a specific SOD for mtROS. Overexpression of MnSOD also increased the expression of aquaporin-1 (AQP1), a water and oxygen channel. AQP1 overexpression in ECs suppressed hyperglycemia-induced cellular hypoxia, endothelin-1 and fibronectin overproduction, and apoptosis. Therefore, hyperglycemia-induced cellular hypoxia and mtROS generation may promote hyperglycemic damage in a coordinated manner.</abstract><cop>United States</cop><pub>Public Library of Science</pub><pmid>27383386</pmid><doi>10.1371/journal.pone.0158619</doi><oa>free_for_read</oa></addata></record> |
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| recordid | cdi_plos_journals_1802192735 |
| source | MEDLINE; DOAJ Directory of Open Access Journals; Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals; PubMed Central; Free Full-Text Journals in Chemistry; Public Library of Science (PLoS) |
| subjects | Animals Apoptosis Apoptosis - drug effects Aquaporin 1 Aquaporins Biology and life sciences Blotting, Western Care and treatment Cattle Cell Hypoxia Cell Line Cellular manufacture Complications Complications and side effects Deoxyguanosine - analogs & derivatives Deoxyguanosine - biosynthesis Diabetes Diabetes mellitus Diabetes Mellitus, Experimental - complications Diabetes Mellitus, Experimental - metabolism Endothelial cells Endothelial Cells - drug effects Endothelial Cells - metabolism Endothelin 1 Endothelin-1 - genetics Endothelin-1 - metabolism Endothelins Experiments Fibronectin Fibronectins - genetics Fibronectins - metabolism Glucose Glucose - pharmacology Hyperglycemia Hyperglycemia - complications Hyperglycemia - metabolism Hypoxia Hypoxia - metabolism Influence Kinases Life sciences Manganese Medical research Medicine Medicine and Health Sciences Metabolism Mice, Inbred C57BL Mice, Transgenic Mitochondria Mitochondria - metabolism Oxidative stress Oxygen Pathogenesis Phosphorylation Physical Sciences Reactive oxygen species Reactive Oxygen Species - metabolism Research and Analysis Methods Reverse Transcriptase Polymerase Chain Reaction Rodents Superoxide dismutase Superoxide Dismutase - genetics Superoxide Dismutase - metabolism |
| title | Hyperglycemia Induces Cellular Hypoxia through Production of Mitochondrial ROS Followed by Suppression of Aquaporin-1 |
| url | https://sfx.bib-bvb.de/sfx_tum?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&ctx_tim=2025-02-13T19%3A12%3A29IST&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=Hyperglycemia%20Induces%20Cellular%20Hypoxia%20through%20Production%20of%20Mitochondrial%20ROS%20Followed%20by%20Suppression%20of%20Aquaporin-1&rft.jtitle=PloS%20one&rft.au=Sada,%20Kiminori&rft.date=2016-07-06&rft.volume=11&rft.issue=7&rft.spage=e0158619&rft.epage=e0158619&rft.pages=e0158619-e0158619&rft.issn=1932-6203&rft.eissn=1932-6203&rft_id=info:doi/10.1371/journal.pone.0158619&rft_dat=%3Cgale_plos_%3EA457195732%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=1802192735&rft_id=info:pmid/27383386&rft_galeid=A457195732&rft_doaj_id=oai_doaj_org_article_1e8e9edd94f64678a9679772181b4248&rfr_iscdi=true |