p21 protects cardiomyocytes against ischemia-reperfusion injury by inhibiting oxidative stress
Ischemic heart disease is a major health threat, resulting in a large number of mortalities annually worldwide. Oxidative stress is one of the main causes of cell death during ischemia‑reperfusion (IR) injury. Cyclin dependent kinase inhibitor 1A (known as p21) is important in protecting tissues aga...
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| Veröffentlicht in: | Molecular medicine reports 2018-03, Vol.17 (3), p.4665-4671 |
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| creator | Li, Hong Zou, Tong Meng, Shuai Peng, Yun-Zhu Yang, Jie-Fu |
| description | Ischemic heart disease is a major health threat, resulting in a large number of mortalities annually worldwide. Oxidative stress is one of the main causes of cell death during ischemia‑reperfusion (IR) injury. Cyclin dependent kinase inhibitor 1A (known as p21) is important in protecting tissues against IR injury, however the mechanism remains unknown. In the present study, oxygen‑glucose deprivation and subsequent reoxygenation (OGD/R) in H9c2 heart‑derived myocytes was used as a model to study myocardial IR injury in vitro. mRNA and protein expression levels were determined by reverse transcription‑quantitative polymerase chain reaction and western blotting, respectively. The levels of reactive oxygen species were measured using the fluorescence dye 2',7'‑dichlorodihydrofluorescein diacetate. The present data demonstrated that p21 expression was upregulated by tumor protein p53 (p53) in H9c2 cells exposed to OGD/R. p21 protected H9c2 cells against OGD/R‑induced oxidative stress. In addition, p21 mediated upregulation of NF‑E2‑related factor‑2 (Nrf2), a regulator of antioxidant responses, which in turn suppressed cell death in H9c2 cells subjected to OGD/R. Thus, activation of the p53/p21/Nrf2 signaling pathway may be an important adaptive response that limits oxidative injury during IR. |
| doi_str_mv | 10.3892/mmr.2018.8382 |
| format | Article |
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Oxidative stress is one of the main causes of cell death during ischemia‑reperfusion (IR) injury. Cyclin dependent kinase inhibitor 1A (known as p21) is important in protecting tissues against IR injury, however the mechanism remains unknown. In the present study, oxygen‑glucose deprivation and subsequent reoxygenation (OGD/R) in H9c2 heart‑derived myocytes was used as a model to study myocardial IR injury in vitro. mRNA and protein expression levels were determined by reverse transcription‑quantitative polymerase chain reaction and western blotting, respectively. The levels of reactive oxygen species were measured using the fluorescence dye 2',7'‑dichlorodihydrofluorescein diacetate. The present data demonstrated that p21 expression was upregulated by tumor protein p53 (p53) in H9c2 cells exposed to OGD/R. p21 protected H9c2 cells against OGD/R‑induced oxidative stress. In addition, p21 mediated upregulation of NF‑E2‑related factor‑2 (Nrf2), a regulator of antioxidant responses, which in turn suppressed cell death in H9c2 cells subjected to OGD/R. Thus, activation of the p53/p21/Nrf2 signaling pathway may be an important adaptive response that limits oxidative injury during IR.</description><identifier>ISSN: 1791-2997</identifier><identifier>EISSN: 1791-3004</identifier><identifier>DOI: 10.3892/mmr.2018.8382</identifier><identifier>PMID: 29328456</identifier><language>eng</language><publisher>Greece: Spandidos Publications</publisher><subject>Antioxidants ; Biotechnology ; Cardiomyocytes ; Care and treatment ; Cell cycle ; Cell death ; Cellular signal transduction ; Coronary artery disease ; Cyclin-dependent kinase inhibitor p21 ; Enzyme inhibitors ; Enzymes ; Gene expression ; Glucose ; GTP-binding protein ; Health aspects ; Heart diseases ; Immunoglobulins ; Ischemia ; Kinases ; Myocytes ; Oxidative stress ; Oxygen consumption (Metabolism) ; p53 Protein ; Polymerase chain reaction ; Proteins ; Reactive oxygen species ; Reperfusion ; Reperfusion injury ; Reverse transcription ; Rodents ; Signal transduction ; Testing ; Transcription factors ; Western blotting</subject><ispartof>Molecular medicine reports, 2018-03, Vol.17 (3), p.4665-4671</ispartof><rights>COPYRIGHT 2018 Spandidos Publications</rights><rights>Copyright Spandidos Publications UK Ltd. 2018</rights><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c427t-381e2a8c43c978b281aa6f3587c8198b8edba0f76a8d3f4c09318c469cef3fa63</citedby><cites>FETCH-LOGICAL-c427t-381e2a8c43c978b281aa6f3587c8198b8edba0f76a8d3f4c09318c469cef3fa63</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,776,780,27903,27904</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/29328456$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Li, Hong</creatorcontrib><creatorcontrib>Zou, Tong</creatorcontrib><creatorcontrib>Meng, Shuai</creatorcontrib><creatorcontrib>Peng, Yun-Zhu</creatorcontrib><creatorcontrib>Yang, Jie-Fu</creatorcontrib><title>p21 protects cardiomyocytes against ischemia-reperfusion injury by inhibiting oxidative stress</title><title>Molecular medicine reports</title><addtitle>Mol Med Rep</addtitle><description>Ischemic heart disease is a major health threat, resulting in a large number of mortalities annually worldwide. Oxidative stress is one of the main causes of cell death during ischemia‑reperfusion (IR) injury. Cyclin dependent kinase inhibitor 1A (known as p21) is important in protecting tissues against IR injury, however the mechanism remains unknown. In the present study, oxygen‑glucose deprivation and subsequent reoxygenation (OGD/R) in H9c2 heart‑derived myocytes was used as a model to study myocardial IR injury in vitro. mRNA and protein expression levels were determined by reverse transcription‑quantitative polymerase chain reaction and western blotting, respectively. The levels of reactive oxygen species were measured using the fluorescence dye 2',7'‑dichlorodihydrofluorescein diacetate. The present data demonstrated that p21 expression was upregulated by tumor protein p53 (p53) in H9c2 cells exposed to OGD/R. p21 protected H9c2 cells against OGD/R‑induced oxidative stress. In addition, p21 mediated upregulation of NF‑E2‑related factor‑2 (Nrf2), a regulator of antioxidant responses, which in turn suppressed cell death in H9c2 cells subjected to OGD/R. Thus, activation of the p53/p21/Nrf2 signaling pathway may be an important adaptive response that limits oxidative injury during IR.</description><subject>Antioxidants</subject><subject>Biotechnology</subject><subject>Cardiomyocytes</subject><subject>Care and treatment</subject><subject>Cell cycle</subject><subject>Cell death</subject><subject>Cellular signal transduction</subject><subject>Coronary artery disease</subject><subject>Cyclin-dependent kinase inhibitor p21</subject><subject>Enzyme inhibitors</subject><subject>Enzymes</subject><subject>Gene expression</subject><subject>Glucose</subject><subject>GTP-binding protein</subject><subject>Health aspects</subject><subject>Heart diseases</subject><subject>Immunoglobulins</subject><subject>Ischemia</subject><subject>Kinases</subject><subject>Myocytes</subject><subject>Oxidative stress</subject><subject>Oxygen consumption (Metabolism)</subject><subject>p53 Protein</subject><subject>Polymerase chain reaction</subject><subject>Proteins</subject><subject>Reactive oxygen species</subject><subject>Reperfusion</subject><subject>Reperfusion injury</subject><subject>Reverse transcription</subject><subject>Rodents</subject><subject>Signal transduction</subject><subject>Testing</subject><subject>Transcription factors</subject><subject>Western blotting</subject><issn>1791-2997</issn><issn>1791-3004</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2018</creationdate><recordtype>article</recordtype><sourceid>BENPR</sourceid><recordid>eNptkc1LwzAUwIMobk6PXqXguTUfbZMcx_ALBC96NaRpsmWszUxSsf-9GZuKIDm8x-P3krz3A-ASwYIwjm-6zhcYIlYwwvARmCLKUU4gLI8POeacTsBZCGsI6wpX_BRMMCeYlVU9BW9bjLKtd1GrGDIlfWtdNzo1Rh0yuZS2DzGzQa10Z2Xu9VZ7MwTr-sz268GPWTOmbGUbG22_zNynbWW0HzoL0esQzsGJkZugLw5xBl7vbl8WD_nT8_3jYv6UqxLTmBOGNJZMlURxyhrMkJS1IRWjiiHOGqbbRkJDa8laYkoFOUGJrrnShhhZkxm43t-bRnkfdIhi7QbfpycF4rykpKaU_VJLudHC9sZFL1WXxhPzKi0kQRglqviHSqdNO1Cu18am-p-GfN-gvAvBayO23nbSjwJBsZMkkiSxkyR2khJ_dfjs0HS6_aG_rZAvOLKNpw</recordid><startdate>20180301</startdate><enddate>20180301</enddate><creator>Li, Hong</creator><creator>Zou, Tong</creator><creator>Meng, Shuai</creator><creator>Peng, Yun-Zhu</creator><creator>Yang, Jie-Fu</creator><general>Spandidos Publications</general><general>Spandidos Publications UK Ltd</general><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>3V.</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8AO</scope><scope>8FE</scope><scope>8FH</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AN0</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BENPR</scope><scope>BHPHI</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>HCIFZ</scope><scope>K9.</scope><scope>LK8</scope><scope>M0S</scope><scope>M1P</scope><scope>M7P</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope></search><sort><creationdate>20180301</creationdate><title>p21 protects cardiomyocytes against ischemia-reperfusion injury by inhibiting oxidative stress</title><author>Li, Hong ; Zou, Tong ; Meng, Shuai ; Peng, Yun-Zhu ; Yang, Jie-Fu</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c427t-381e2a8c43c978b281aa6f3587c8198b8edba0f76a8d3f4c09318c469cef3fa63</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2018</creationdate><topic>Antioxidants</topic><topic>Biotechnology</topic><topic>Cardiomyocytes</topic><topic>Care and treatment</topic><topic>Cell cycle</topic><topic>Cell death</topic><topic>Cellular signal transduction</topic><topic>Coronary artery disease</topic><topic>Cyclin-dependent kinase inhibitor p21</topic><topic>Enzyme inhibitors</topic><topic>Enzymes</topic><topic>Gene expression</topic><topic>Glucose</topic><topic>GTP-binding protein</topic><topic>Health aspects</topic><topic>Heart diseases</topic><topic>Immunoglobulins</topic><topic>Ischemia</topic><topic>Kinases</topic><topic>Myocytes</topic><topic>Oxidative stress</topic><topic>Oxygen consumption (Metabolism)</topic><topic>p53 Protein</topic><topic>Polymerase chain reaction</topic><topic>Proteins</topic><topic>Reactive oxygen species</topic><topic>Reperfusion</topic><topic>Reperfusion injury</topic><topic>Reverse transcription</topic><topic>Rodents</topic><topic>Signal transduction</topic><topic>Testing</topic><topic>Transcription factors</topic><topic>Western blotting</topic><toplevel>online_resources</toplevel><creatorcontrib>Li, Hong</creatorcontrib><creatorcontrib>Zou, Tong</creatorcontrib><creatorcontrib>Meng, Shuai</creatorcontrib><creatorcontrib>Peng, Yun-Zhu</creatorcontrib><creatorcontrib>Yang, Jie-Fu</creatorcontrib><collection>PubMed</collection><collection>CrossRef</collection><collection>ProQuest Central (Corporate)</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>ProQuest SciTech 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>ProQuest Central (Alumni Edition)</collection><collection>ProQuest Central UK/Ireland</collection><collection>British Nursing Database</collection><collection>ProQuest Central Essentials</collection><collection>Biological Science Collection</collection><collection>ProQuest Central</collection><collection>Natural Science Collection</collection><collection>ProQuest One Community College</collection><collection>ProQuest Central Korea</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Central Student</collection><collection>SciTech Premium Collection</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>ProQuest Biological Science Collection</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>Biological Science Database</collection><collection>ProQuest One Academic Eastern Edition (DO NOT USE)</collection><collection>ProQuest One Academic</collection><collection>ProQuest One Academic UKI Edition</collection><collection>ProQuest Central China</collection><jtitle>Molecular medicine reports</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Li, Hong</au><au>Zou, Tong</au><au>Meng, Shuai</au><au>Peng, Yun-Zhu</au><au>Yang, Jie-Fu</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>p21 protects cardiomyocytes against ischemia-reperfusion injury by inhibiting oxidative stress</atitle><jtitle>Molecular medicine reports</jtitle><addtitle>Mol Med Rep</addtitle><date>2018-03-01</date><risdate>2018</risdate><volume>17</volume><issue>3</issue><spage>4665</spage><epage>4671</epage><pages>4665-4671</pages><issn>1791-2997</issn><eissn>1791-3004</eissn><abstract>Ischemic heart disease is a major health threat, resulting in a large number of mortalities annually worldwide. Oxidative stress is one of the main causes of cell death during ischemia‑reperfusion (IR) injury. Cyclin dependent kinase inhibitor 1A (known as p21) is important in protecting tissues against IR injury, however the mechanism remains unknown. In the present study, oxygen‑glucose deprivation and subsequent reoxygenation (OGD/R) in H9c2 heart‑derived myocytes was used as a model to study myocardial IR injury in vitro. mRNA and protein expression levels were determined by reverse transcription‑quantitative polymerase chain reaction and western blotting, respectively. The levels of reactive oxygen species were measured using the fluorescence dye 2',7'‑dichlorodihydrofluorescein diacetate. The present data demonstrated that p21 expression was upregulated by tumor protein p53 (p53) in H9c2 cells exposed to OGD/R. p21 protected H9c2 cells against OGD/R‑induced oxidative stress. In addition, p21 mediated upregulation of NF‑E2‑related factor‑2 (Nrf2), a regulator of antioxidant responses, which in turn suppressed cell death in H9c2 cells subjected to OGD/R. Thus, activation of the p53/p21/Nrf2 signaling pathway may be an important adaptive response that limits oxidative injury during IR.</abstract><cop>Greece</cop><pub>Spandidos Publications</pub><pmid>29328456</pmid><doi>10.3892/mmr.2018.8382</doi><tpages>7</tpages><oa>free_for_read</oa></addata></record> |
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| ispartof | Molecular medicine reports, 2018-03, Vol.17 (3), p.4665-4671 |
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| source | Spandidos Publications Journals; EZB-FREE-00999 freely available EZB journals; Alma/SFX Local Collection |
| subjects | Antioxidants Biotechnology Cardiomyocytes Care and treatment Cell cycle Cell death Cellular signal transduction Coronary artery disease Cyclin-dependent kinase inhibitor p21 Enzyme inhibitors Enzymes Gene expression Glucose GTP-binding protein Health aspects Heart diseases Immunoglobulins Ischemia Kinases Myocytes Oxidative stress Oxygen consumption (Metabolism) p53 Protein Polymerase chain reaction Proteins Reactive oxygen species Reperfusion Reperfusion injury Reverse transcription Rodents Signal transduction Testing Transcription factors Western blotting |
| title | p21 protects cardiomyocytes against ischemia-reperfusion injury by inhibiting oxidative stress |
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