Iodine-131 induces apoptosis in human cardiac muscle cells through the p53/Bax/caspase-3 and PIDD/caspase-2/t-BID/cytochrome c/caspase-3 signaling pathway
The aim of this study was to elucidate the effects of iodine-131 on the induction of apoptosis in human cardiac muscle cells and the underlying molecular mechanisms. We found that iodine-131 reduced cell proliferation, induced apoptosis, induced p53, PIDD, t-BID (mitochondria) protein expression, su...
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| Veröffentlicht in: | Oncology reports 2017-09, Vol.38 (3), p.1579-1586 |
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| creator | Wang, Yansheng Liu, Changqing Wang, Jianchun Zhang, Yang Chen, Linlin |
| description | The aim of this study was to elucidate the effects of iodine-131 on the induction of apoptosis in human cardiac muscle cells and the underlying molecular mechanisms. We found that iodine-131 reduced cell proliferation, induced apoptosis, induced p53, PIDD, t-BID (mitochondria) protein expression, suppressed cytochrome c (mitochondria) protein expression, and increased Bax protein expression, and promoted caspase-2, −3 and −9 expression levels in human cardiac muscle cells. Meanwhile, si-p53 inhibited the effects of iodine-131 on the reduction in cell proliferation and induction of apoptosis in human cardiac muscle cells through regulation of Bax/cytochrome c/caspase-3 and PIDD/caspase-2/t-BID/cytochrome c/caspase-3 signaling pathway. After si-Bax reduced the effects of iodine-131, it reduced cell proliferation and induced apoptosis in human cardiac muscle cells through the cytochrome c/caspase-3 signaling pathway. However, si-caspase-2 also reduced the effects of iodine-131 on the reduction of cell proliferation and induction of apoptosis in human cardiac muscle cells through the t-BID/cytochrome c/caspase-3 signaling pathway. These findings demonstrated that iodine-131 induces apoptosis in human cardiac muscle cells through the p53/Bax/caspase-3 and PIDD/caspase-2/t-BID/cytochrome c/caspase-3 signaling pathway. |
| doi_str_mv | 10.3892/or.2017.5813 |
| format | Article |
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We found that iodine-131 reduced cell proliferation, induced apoptosis, induced p53, PIDD, t-BID (mitochondria) protein expression, suppressed cytochrome c (mitochondria) protein expression, and increased Bax protein expression, and promoted caspase-2, −3 and −9 expression levels in human cardiac muscle cells. Meanwhile, si-p53 inhibited the effects of iodine-131 on the reduction in cell proliferation and induction of apoptosis in human cardiac muscle cells through regulation of Bax/cytochrome c/caspase-3 and PIDD/caspase-2/t-BID/cytochrome c/caspase-3 signaling pathway. After si-Bax reduced the effects of iodine-131, it reduced cell proliferation and induced apoptosis in human cardiac muscle cells through the cytochrome c/caspase-3 signaling pathway. However, si-caspase-2 also reduced the effects of iodine-131 on the reduction of cell proliferation and induction of apoptosis in human cardiac muscle cells through the t-BID/cytochrome c/caspase-3 signaling pathway. These findings demonstrated that iodine-131 induces apoptosis in human cardiac muscle cells through the p53/Bax/caspase-3 and PIDD/caspase-2/t-BID/cytochrome c/caspase-3 signaling pathway.</description><identifier>ISSN: 1021-335X</identifier><identifier>EISSN: 1791-2431</identifier><identifier>DOI: 10.3892/or.2017.5813</identifier><identifier>PMID: 28714021</identifier><language>eng</language><publisher>Greece: D.A. Spandidos</publisher><subject>Apoptosis ; Apoptosis - drug effects ; Bax ; bcl-2-Associated X Protein - metabolism ; BH3 Interacting Domain Death Agonist Protein - metabolism ; caspase-3 ; Caspases - metabolism ; Cell growth ; Cell Line ; Cellular signal transduction ; Cytochrome ; Cytochromes c - metabolism ; Death Domain Receptor Signaling Adaptor Proteins - metabolism ; Flow cytometry ; Gangrene ; Gene expression ; Genetic aspects ; Health aspects ; Heart muscle ; human cardiac muscle cells ; Humans ; Hypoxia ; Iodine ; Iodine Radioisotopes - pharmacology ; iodine-131 ; Ischemia ; Isotopes ; Mitochondria ; Myocytes, Cardiac - drug effects ; Myocytes, Cardiac - metabolism ; p53 ; Protein expression ; Proteins ; Signal Transduction - drug effects ; Thyroid gland ; Tumor Suppressor Protein p53 - metabolism</subject><ispartof>Oncology reports, 2017-09, Vol.38 (3), p.1579-1586</ispartof><rights>Copyright © 2017, Spandidos Publications</rights><rights>COPYRIGHT 2017 Spandidos Publications</rights><rights>Copyright Spandidos Publications UK Ltd. 2017</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c486t-4916918c1623e5c81af622a0457dcb2e64e72ef211d6b27255afbcca021f0a793</citedby><cites>FETCH-LOGICAL-c486t-4916918c1623e5c81af622a0457dcb2e64e72ef211d6b27255afbcca021f0a793</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,776,780,27901,27902</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/28714021$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Wang, Yansheng</creatorcontrib><creatorcontrib>Liu, Changqing</creatorcontrib><creatorcontrib>Wang, Jianchun</creatorcontrib><creatorcontrib>Zhang, Yang</creatorcontrib><creatorcontrib>Chen, Linlin</creatorcontrib><title>Iodine-131 induces apoptosis in human cardiac muscle cells through the p53/Bax/caspase-3 and PIDD/caspase-2/t-BID/cytochrome c/caspase-3 signaling pathway</title><title>Oncology reports</title><addtitle>Oncol Rep</addtitle><description>The aim of this study was to elucidate the effects of iodine-131 on the induction of apoptosis in human cardiac muscle cells and the underlying molecular mechanisms. We found that iodine-131 reduced cell proliferation, induced apoptosis, induced p53, PIDD, t-BID (mitochondria) protein expression, suppressed cytochrome c (mitochondria) protein expression, and increased Bax protein expression, and promoted caspase-2, −3 and −9 expression levels in human cardiac muscle cells. Meanwhile, si-p53 inhibited the effects of iodine-131 on the reduction in cell proliferation and induction of apoptosis in human cardiac muscle cells through regulation of Bax/cytochrome c/caspase-3 and PIDD/caspase-2/t-BID/cytochrome c/caspase-3 signaling pathway. After si-Bax reduced the effects of iodine-131, it reduced cell proliferation and induced apoptosis in human cardiac muscle cells through the cytochrome c/caspase-3 signaling pathway. However, si-caspase-2 also reduced the effects of iodine-131 on the reduction of cell proliferation and induction of apoptosis in human cardiac muscle cells through the t-BID/cytochrome c/caspase-3 signaling pathway. These findings demonstrated that iodine-131 induces apoptosis in human cardiac muscle cells through the p53/Bax/caspase-3 and PIDD/caspase-2/t-BID/cytochrome c/caspase-3 signaling pathway.</description><subject>Apoptosis</subject><subject>Apoptosis - drug effects</subject><subject>Bax</subject><subject>bcl-2-Associated X Protein - metabolism</subject><subject>BH3 Interacting Domain Death Agonist Protein - metabolism</subject><subject>caspase-3</subject><subject>Caspases - metabolism</subject><subject>Cell growth</subject><subject>Cell Line</subject><subject>Cellular signal transduction</subject><subject>Cytochrome</subject><subject>Cytochromes c - metabolism</subject><subject>Death Domain Receptor Signaling Adaptor Proteins - metabolism</subject><subject>Flow cytometry</subject><subject>Gangrene</subject><subject>Gene expression</subject><subject>Genetic aspects</subject><subject>Health aspects</subject><subject>Heart muscle</subject><subject>human cardiac muscle cells</subject><subject>Humans</subject><subject>Hypoxia</subject><subject>Iodine</subject><subject>Iodine Radioisotopes - pharmacology</subject><subject>iodine-131</subject><subject>Ischemia</subject><subject>Isotopes</subject><subject>Mitochondria</subject><subject>Myocytes, Cardiac - drug effects</subject><subject>Myocytes, Cardiac - metabolism</subject><subject>p53</subject><subject>Protein expression</subject><subject>Proteins</subject><subject>Signal Transduction - drug effects</subject><subject>Thyroid gland</subject><subject>Tumor Suppressor Protein p53 - metabolism</subject><issn>1021-335X</issn><issn>1791-2431</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2017</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>BENPR</sourceid><recordid>eNptkkuLFDEQxxtR3IfePEtAkD2YmTw6_Tjuw8fAgh4UvIWaJD2dpTtpkzQ6X8VPa5pdZ3dFcqhU5VeVVOVfFK8oWfGmZWsfVozQeiUayp8Ux7RuKWYlp0_znjCKORffj4qTGG8IYTWp2ufFEWtqWubD4-L3xmvrDKacIuv0rExEMPkp-WhjjqB-HsEhBUFbUGicoxoMUmYYIkp98POuz9agSfD1BfxaK4gTRIM5AqfRl83V1SHE1glfbLK_T17l1DHXecBHu3MwWLdDE6T-J-xfFM86GKJ5eWdPi28f3n-9_ISvP3_cXJ5fY1U2VcJlS6uWNopWjBuhGgpdxRiQUtRabZmpSlMz0zFKdbVlNRMCuq1SkNvvCNQtPy3ObutOwf-YTUxytHHpEJzxc5S0zfNt88RIRt_8g974OeRnL1TJaNk0orqndjAYaV3nUwC1FJXngrRNJrnI1Oo_VF7ajFZ5Zzqb448S3j5I6A0MqY9-mJP1Lj4G392CKvgYg-nkFOwIYS8pkYtmpA9y0YxcNJPx13dNzdvR6AP8VyT3F-evctpqHw-MD5g3mHBMRZ7kH4vaxU4</recordid><startdate>20170901</startdate><enddate>20170901</enddate><creator>Wang, Yansheng</creator><creator>Liu, Changqing</creator><creator>Wang, Jianchun</creator><creator>Zhang, Yang</creator><creator>Chen, Linlin</creator><general>D.A. Spandidos</general><general>Spandidos Publications</general><general>Spandidos Publications UK Ltd</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>3V.</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AN0</scope><scope>BENPR</scope><scope>CCPQU</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>K9.</scope><scope>M0S</scope><scope>M1P</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>7X8</scope></search><sort><creationdate>20170901</creationdate><title>Iodine-131 induces apoptosis in human cardiac muscle cells through the p53/Bax/caspase-3 and PIDD/caspase-2/t-BID/cytochrome c/caspase-3 signaling pathway</title><author>Wang, Yansheng ; Liu, Changqing ; Wang, Jianchun ; Zhang, Yang ; Chen, Linlin</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c486t-4916918c1623e5c81af622a0457dcb2e64e72ef211d6b27255afbcca021f0a793</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2017</creationdate><topic>Apoptosis</topic><topic>Apoptosis - drug effects</topic><topic>Bax</topic><topic>bcl-2-Associated X Protein - metabolism</topic><topic>BH3 Interacting Domain Death Agonist Protein - metabolism</topic><topic>caspase-3</topic><topic>Caspases - metabolism</topic><topic>Cell growth</topic><topic>Cell Line</topic><topic>Cellular signal transduction</topic><topic>Cytochrome</topic><topic>Cytochromes c - metabolism</topic><topic>Death Domain Receptor Signaling Adaptor Proteins - metabolism</topic><topic>Flow cytometry</topic><topic>Gangrene</topic><topic>Gene expression</topic><topic>Genetic aspects</topic><topic>Health aspects</topic><topic>Heart muscle</topic><topic>human cardiac muscle cells</topic><topic>Humans</topic><topic>Hypoxia</topic><topic>Iodine</topic><topic>Iodine Radioisotopes - pharmacology</topic><topic>iodine-131</topic><topic>Ischemia</topic><topic>Isotopes</topic><topic>Mitochondria</topic><topic>Myocytes, Cardiac - drug effects</topic><topic>Myocytes, Cardiac - metabolism</topic><topic>p53</topic><topic>Protein expression</topic><topic>Proteins</topic><topic>Signal Transduction - drug effects</topic><topic>Thyroid gland</topic><topic>Tumor Suppressor Protein p53 - metabolism</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Wang, Yansheng</creatorcontrib><creatorcontrib>Liu, Changqing</creatorcontrib><creatorcontrib>Wang, Jianchun</creatorcontrib><creatorcontrib>Zhang, Yang</creatorcontrib><creatorcontrib>Chen, Linlin</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><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>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</collection><collection>ProQuest One Community College</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical 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><collection>MEDLINE - Academic</collection><jtitle>Oncology reports</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Wang, Yansheng</au><au>Liu, Changqing</au><au>Wang, Jianchun</au><au>Zhang, Yang</au><au>Chen, Linlin</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Iodine-131 induces apoptosis in human cardiac muscle cells through the p53/Bax/caspase-3 and PIDD/caspase-2/t-BID/cytochrome c/caspase-3 signaling pathway</atitle><jtitle>Oncology reports</jtitle><addtitle>Oncol Rep</addtitle><date>2017-09-01</date><risdate>2017</risdate><volume>38</volume><issue>3</issue><spage>1579</spage><epage>1586</epage><pages>1579-1586</pages><issn>1021-335X</issn><eissn>1791-2431</eissn><abstract>The aim of this study was to elucidate the effects of iodine-131 on the induction of apoptosis in human cardiac muscle cells and the underlying molecular mechanisms. We found that iodine-131 reduced cell proliferation, induced apoptosis, induced p53, PIDD, t-BID (mitochondria) protein expression, suppressed cytochrome c (mitochondria) protein expression, and increased Bax protein expression, and promoted caspase-2, −3 and −9 expression levels in human cardiac muscle cells. Meanwhile, si-p53 inhibited the effects of iodine-131 on the reduction in cell proliferation and induction of apoptosis in human cardiac muscle cells through regulation of Bax/cytochrome c/caspase-3 and PIDD/caspase-2/t-BID/cytochrome c/caspase-3 signaling pathway. After si-Bax reduced the effects of iodine-131, it reduced cell proliferation and induced apoptosis in human cardiac muscle cells through the cytochrome c/caspase-3 signaling pathway. However, si-caspase-2 also reduced the effects of iodine-131 on the reduction of cell proliferation and induction of apoptosis in human cardiac muscle cells through the t-BID/cytochrome c/caspase-3 signaling pathway. These findings demonstrated that iodine-131 induces apoptosis in human cardiac muscle cells through the p53/Bax/caspase-3 and PIDD/caspase-2/t-BID/cytochrome c/caspase-3 signaling pathway.</abstract><cop>Greece</cop><pub>D.A. Spandidos</pub><pmid>28714021</pmid><doi>10.3892/or.2017.5813</doi><tpages>8</tpages><oa>free_for_read</oa></addata></record> |
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| source | MEDLINE; Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals; Alma/SFX Local Collection |
| subjects | Apoptosis Apoptosis - drug effects Bax bcl-2-Associated X Protein - metabolism BH3 Interacting Domain Death Agonist Protein - metabolism caspase-3 Caspases - metabolism Cell growth Cell Line Cellular signal transduction Cytochrome Cytochromes c - metabolism Death Domain Receptor Signaling Adaptor Proteins - metabolism Flow cytometry Gangrene Gene expression Genetic aspects Health aspects Heart muscle human cardiac muscle cells Humans Hypoxia Iodine Iodine Radioisotopes - pharmacology iodine-131 Ischemia Isotopes Mitochondria Myocytes, Cardiac - drug effects Myocytes, Cardiac - metabolism p53 Protein expression Proteins Signal Transduction - drug effects Thyroid gland Tumor Suppressor Protein p53 - metabolism |
| title | Iodine-131 induces apoptosis in human cardiac muscle cells through the p53/Bax/caspase-3 and PIDD/caspase-2/t-BID/cytochrome c/caspase-3 signaling pathway |
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