HSP70 inhibits smac release from the mitochondria and protects against H2O2-induced apoptosis in C2C12 myogenic cells
To observe whether HSP70 could protect against H2O2-induced apoptosis in C2C12 myogenic cells by inhibiting Smac release from the mitochondria. HSP70 gene and full length Smac gene was transiently transfected in C2C12 myogenic cells by lipofectamine and the protein levels of HSP70 and Smac were anal...
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| Veröffentlicht in: | Zhong nan da xue xue bao. Journal of Central South University. Yi xue ban 2005-02, Vol.30 (1), p.32-37 |
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| container_title | Zhong nan da xue xue bao. Journal of Central South University. Yi xue ban |
| container_volume | 30 |
| creator | Jiang, Bi-mei Xiao, Wei-min Shi, Yong-zhong Liu, Mei-dong Xiao, Xian-zhong |
| description | To observe whether HSP70 could protect against H2O2-induced apoptosis in C2C12 myogenic cells by inhibiting Smac release from the mitochondria.
HSP70 gene and full length Smac gene was transiently transfected in C2C12 myogenic cells by lipofectamine and the protein levels of HSP70 and Smac were analysed by Western blotting. Hoechst 33 258 staining was used to examine cell morphological changes and to calculate percentage of apoptotic nuclei. DNA ladder pattern on agarose gel electrophoresis was used to observe the DNA fragmentation. Activities of caspase-3 and caspase-9 were assayed with Western blotting. The release of Smac from the mitochondria to the cytoplasm was observed by immunofluorescence.
H2O2 ( 0.5 mmol/L ) activated caspase-3, caspase-9 8 h after the treatment and specific morphological changes of apoptosis 12 h after the treatment, and overexpression of Smac significantly promoted H2O2-induced activation of caspase-3, caspase-9 and apoptosis in C2C12 myogenic cells. HSP70 overexpression significa |
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HSP70 gene and full length Smac gene was transiently transfected in C2C12 myogenic cells by lipofectamine and the protein levels of HSP70 and Smac were analysed by Western blotting. Hoechst 33 258 staining was used to examine cell morphological changes and to calculate percentage of apoptotic nuclei. DNA ladder pattern on agarose gel electrophoresis was used to observe the DNA fragmentation. Activities of caspase-3 and caspase-9 were assayed with Western blotting. The release of Smac from the mitochondria to the cytoplasm was observed by immunofluorescence.
H2O2 ( 0.5 mmol/L ) activated caspase-3, caspase-9 8 h after the treatment and specific morphological changes of apoptosis 12 h after the treatment, and overexpression of Smac significantly promoted H2O2-induced activation of caspase-3, caspase-9 and apoptosis in C2C12 myogenic cells. HSP70 overexpression significa</description><identifier>ISSN: 1672-7347</identifier><identifier>PMID: 15871184</identifier><language>chi</language><publisher>China</publisher><subject>Apoptosis - drug effects ; Cells, Cultured ; HSP70 Heat-Shock Proteins - pharmacology ; Humans ; Hydrogen Peroxide ; Intracellular Signaling Peptides and Proteins - metabolism ; Mitochondria, Heart - drug effects ; Mitochondria, Heart - metabolism ; Mitochondrial Proteins - antagonists & inhibitors ; Mitochondrial Proteins - metabolism ; Myoblasts - metabolism ; Myocytes, Cardiac - drug effects ; Myocytes, Cardiac - metabolism</subject><ispartof>Zhong nan da xue xue bao. Journal of Central South University. Yi xue ban, 2005-02, Vol.30 (1), p.32-37</ispartof><woscitedreferencessubscribed>false</woscitedreferencessubscribed></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,776,780</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/15871184$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Jiang, Bi-mei</creatorcontrib><creatorcontrib>Xiao, Wei-min</creatorcontrib><creatorcontrib>Shi, Yong-zhong</creatorcontrib><creatorcontrib>Liu, Mei-dong</creatorcontrib><creatorcontrib>Xiao, Xian-zhong</creatorcontrib><title>HSP70 inhibits smac release from the mitochondria and protects against H2O2-induced apoptosis in C2C12 myogenic cells</title><title>Zhong nan da xue xue bao. Journal of Central South University. Yi xue ban</title><addtitle>Zhong Nan Da Xue Xue Bao Yi Xue Ban</addtitle><description>To observe whether HSP70 could protect against H2O2-induced apoptosis in C2C12 myogenic cells by inhibiting Smac release from the mitochondria.
HSP70 gene and full length Smac gene was transiently transfected in C2C12 myogenic cells by lipofectamine and the protein levels of HSP70 and Smac were analysed by Western blotting. Hoechst 33 258 staining was used to examine cell morphological changes and to calculate percentage of apoptotic nuclei. DNA ladder pattern on agarose gel electrophoresis was used to observe the DNA fragmentation. Activities of caspase-3 and caspase-9 were assayed with Western blotting. The release of Smac from the mitochondria to the cytoplasm was observed by immunofluorescence.
H2O2 ( 0.5 mmol/L ) activated caspase-3, caspase-9 8 h after the treatment and specific morphological changes of apoptosis 12 h after the treatment, and overexpression of Smac significantly promoted H2O2-induced activation of caspase-3, caspase-9 and apoptosis in C2C12 myogenic cells. HSP70 overexpression significa</description><subject>Apoptosis - drug effects</subject><subject>Cells, Cultured</subject><subject>HSP70 Heat-Shock Proteins - pharmacology</subject><subject>Humans</subject><subject>Hydrogen Peroxide</subject><subject>Intracellular Signaling Peptides and Proteins - metabolism</subject><subject>Mitochondria, Heart - drug effects</subject><subject>Mitochondria, Heart - metabolism</subject><subject>Mitochondrial Proteins - antagonists & inhibitors</subject><subject>Mitochondrial Proteins - metabolism</subject><subject>Myoblasts - metabolism</subject><subject>Myocytes, Cardiac - drug effects</subject><subject>Myocytes, Cardiac - metabolism</subject><issn>1672-7347</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2005</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNo1kM9LwzAAhXNQ3Jj7FyQnb4Xmd3OUolYYTFDPJU3SNdAktUkP---tul3eu3x8PN4N2CIucCEIFRuwT8l1ZSmlJLwSd2CDWCUQqugWLM3HuyihC4PrXE4weaXhbEerkoX9HD3Mg4Xe5aiHGMzsFFTBwGmO2eqVVyflQsqwwUdcuGAWbQ1UU5xyTC6tXljjGmHoz_Fkg9NQ23FM9-C2V2Oy-0vvwNfL82fdFIfj61v9dCgmhGkuCFVlpw3TvdVEYEOl5BVBrO-YIYQzKjHjtFcSc2OIlLrEiHfUmDWZpojswOO_d937vdiUW-_S7wIVbFxSy4WQtPwDHy7g0nlr2ml2Xs3n9noU-QE8TWQb</recordid><startdate>200502</startdate><enddate>200502</enddate><creator>Jiang, Bi-mei</creator><creator>Xiao, Wei-min</creator><creator>Shi, Yong-zhong</creator><creator>Liu, Mei-dong</creator><creator>Xiao, Xian-zhong</creator><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>7X8</scope></search><sort><creationdate>200502</creationdate><title>HSP70 inhibits smac release from the mitochondria and protects against H2O2-induced apoptosis in C2C12 myogenic cells</title><author>Jiang, Bi-mei ; Xiao, Wei-min ; Shi, Yong-zhong ; Liu, Mei-dong ; Xiao, Xian-zhong</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-p124t-34a0bcd5cfec372d49968315fb5d3365492564fa926dd399c0216b4dd16b5c413</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>chi</language><creationdate>2005</creationdate><topic>Apoptosis - drug effects</topic><topic>Cells, Cultured</topic><topic>HSP70 Heat-Shock Proteins - pharmacology</topic><topic>Humans</topic><topic>Hydrogen Peroxide</topic><topic>Intracellular Signaling Peptides and Proteins - metabolism</topic><topic>Mitochondria, Heart - drug effects</topic><topic>Mitochondria, Heart - metabolism</topic><topic>Mitochondrial Proteins - antagonists & inhibitors</topic><topic>Mitochondrial Proteins - metabolism</topic><topic>Myoblasts - metabolism</topic><topic>Myocytes, Cardiac - drug effects</topic><topic>Myocytes, Cardiac - metabolism</topic><toplevel>online_resources</toplevel><creatorcontrib>Jiang, Bi-mei</creatorcontrib><creatorcontrib>Xiao, Wei-min</creatorcontrib><creatorcontrib>Shi, Yong-zhong</creatorcontrib><creatorcontrib>Liu, Mei-dong</creatorcontrib><creatorcontrib>Xiao, Xian-zhong</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>MEDLINE - Academic</collection><jtitle>Zhong nan da xue xue bao. Journal of Central South University. Yi xue ban</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Jiang, Bi-mei</au><au>Xiao, Wei-min</au><au>Shi, Yong-zhong</au><au>Liu, Mei-dong</au><au>Xiao, Xian-zhong</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>HSP70 inhibits smac release from the mitochondria and protects against H2O2-induced apoptosis in C2C12 myogenic cells</atitle><jtitle>Zhong nan da xue xue bao. Journal of Central South University. Yi xue ban</jtitle><addtitle>Zhong Nan Da Xue Xue Bao Yi Xue Ban</addtitle><date>2005-02</date><risdate>2005</risdate><volume>30</volume><issue>1</issue><spage>32</spage><epage>37</epage><pages>32-37</pages><issn>1672-7347</issn><abstract>To observe whether HSP70 could protect against H2O2-induced apoptosis in C2C12 myogenic cells by inhibiting Smac release from the mitochondria.
HSP70 gene and full length Smac gene was transiently transfected in C2C12 myogenic cells by lipofectamine and the protein levels of HSP70 and Smac were analysed by Western blotting. Hoechst 33 258 staining was used to examine cell morphological changes and to calculate percentage of apoptotic nuclei. DNA ladder pattern on agarose gel electrophoresis was used to observe the DNA fragmentation. Activities of caspase-3 and caspase-9 were assayed with Western blotting. The release of Smac from the mitochondria to the cytoplasm was observed by immunofluorescence.
H2O2 ( 0.5 mmol/L ) activated caspase-3, caspase-9 8 h after the treatment and specific morphological changes of apoptosis 12 h after the treatment, and overexpression of Smac significantly promoted H2O2-induced activation of caspase-3, caspase-9 and apoptosis in C2C12 myogenic cells. HSP70 overexpression significa</abstract><cop>China</cop><pmid>15871184</pmid><tpages>6</tpages></addata></record> |
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| ispartof | Zhong nan da xue xue bao. Journal of Central South University. Yi xue ban, 2005-02, Vol.30 (1), p.32-37 |
| issn | 1672-7347 |
| language | chi |
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| source | MEDLINE; Alma/SFX Local Collection |
| subjects | Apoptosis - drug effects Cells, Cultured HSP70 Heat-Shock Proteins - pharmacology Humans Hydrogen Peroxide Intracellular Signaling Peptides and Proteins - metabolism Mitochondria, Heart - drug effects Mitochondria, Heart - metabolism Mitochondrial Proteins - antagonists & inhibitors Mitochondrial Proteins - metabolism Myoblasts - metabolism Myocytes, Cardiac - drug effects Myocytes, Cardiac - metabolism |
| title | HSP70 inhibits smac release from the mitochondria and protects against H2O2-induced apoptosis in C2C12 myogenic cells |
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