Ionizing radiation accelerates Drp1-dependent mitochondrial fission, which involves delayed mitochondrial reactive oxygen species production in normal human fibroblast-like cells
► We report first time that ionizing radiation induces mitochondrial dynamic changes. ► Radiation-induced mitochondrial fission was caused by Drp1 localization. ► We found that radiation causes delayed ROS from mitochondria. ► Down regulation of Drp1 rescued mitochondrial dysfunction after radiation...
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| Veröffentlicht in: | Biochemical and biophysical research communications 2011-11, Vol.414 (4), p.795-800 |
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| creator | Kobashigawa, Shinko Suzuki, Keiji Yamashita, Shunichi |
| description | ► We report first time that ionizing radiation induces mitochondrial dynamic changes. ► Radiation-induced mitochondrial fission was caused by Drp1 localization. ► We found that radiation causes delayed ROS from mitochondria. ► Down regulation of Drp1 rescued mitochondrial dysfunction after radiation exposure.
Ionizing radiation is known to increase intracellular level of reactive oxygen species (ROS) through mitochondrial dysfunction. Although it has been as a basis of radiation-induced genetic instability, the mechanism involving mitochondrial dysfunction remains unclear. Here we studied the dynamics of mitochondrial structure in normal human fibroblast like cells exposed to ionizing radiation. Delayed mitochondrial O2- production was peaked 3days after irradiation, which was coupled with accelerated mitochondrial fission. We found that radiation exposure accumulated dynamin-related protein 1 (Drp1) to mitochondria. Knocking down of Drp1 expression prevented radiation induced acceleration of mitochondrial fission. Furthermore, knockdown of Drp1 significantly suppressed delayed production of mitochondrial O2-. Since the loss of mitochondrial membrane potential, which was induced by radiation was prevented in cells knocking down of Drp1 expression, indicating that the excessive mitochondrial fission was involved in delayed mitochondrial dysfunction after irradiation. |
| doi_str_mv | 10.1016/j.bbrc.2011.10.006 |
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Ionizing radiation is known to increase intracellular level of reactive oxygen species (ROS) through mitochondrial dysfunction. Although it has been as a basis of radiation-induced genetic instability, the mechanism involving mitochondrial dysfunction remains unclear. Here we studied the dynamics of mitochondrial structure in normal human fibroblast like cells exposed to ionizing radiation. Delayed mitochondrial O2- production was peaked 3days after irradiation, which was coupled with accelerated mitochondrial fission. We found that radiation exposure accumulated dynamin-related protein 1 (Drp1) to mitochondria. Knocking down of Drp1 expression prevented radiation induced acceleration of mitochondrial fission. Furthermore, knockdown of Drp1 significantly suppressed delayed production of mitochondrial O2-. Since the loss of mitochondrial membrane potential, which was induced by radiation was prevented in cells knocking down of Drp1 expression, indicating that the excessive mitochondrial fission was involved in delayed mitochondrial dysfunction after irradiation.</description><identifier>ISSN: 0006-291X</identifier><identifier>EISSN: 1090-2104</identifier><identifier>DOI: 10.1016/j.bbrc.2011.10.006</identifier><identifier>PMID: 22005465</identifier><language>eng</language><publisher>United States: Elsevier Inc</publisher><subject>BIOLOGICAL RADIATION EFFECTS ; Cells, Cultured ; Drp1 ; FIBROBLASTS ; Fibroblasts - metabolism ; Fibroblasts - radiation effects ; Fibroblasts - ultrastructure ; Gamma Rays ; GENE REGULATION ; GTP Phosphohydrolases - genetics ; GTP Phosphohydrolases - metabolism ; Humans ; Ionizing radiation ; IONIZING RADIATIONS ; IRRADIATION ; Microtubule-Associated Proteins - genetics ; Microtubule-Associated Proteins - metabolism ; MITOCHONDRIA ; Mitochondria - metabolism ; Mitochondria - radiation effects ; Mitochondrial fission ; Mitochondrial Proteins - genetics ; Mitochondrial Proteins - metabolism ; PROTEINS ; RADIATION, THERMAL, AND OTHER ENVIRONMENTAL POLLUTANT EFFECTS ON LIVING ORGANISMS AND BIOLOGICAL MATERIALS ; Reactive oxygen species ; Reactive Oxygen Species - metabolism ; Singlet Oxygen - metabolism</subject><ispartof>Biochemical and biophysical research communications, 2011-11, Vol.414 (4), p.795-800</ispartof><rights>2011 Elsevier Inc.</rights><rights>Copyright © 2011 Elsevier Inc. All rights reserved.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c449t-2f19ee216094f4298bfd6b5e992ca2e4ade9f2f5ee4616cb9dab2b2f591dcb853</citedby><cites>FETCH-LOGICAL-c449t-2f19ee216094f4298bfd6b5e992ca2e4ade9f2f5ee4616cb9dab2b2f591dcb853</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://dx.doi.org/10.1016/j.bbrc.2011.10.006$$EHTML$$P50$$Gelsevier$$H</linktohtml><link.rule.ids>230,315,781,785,886,3551,27928,27929,45999</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/22005465$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink><backlink>$$Uhttps://www.osti.gov/biblio/22207554$$D View this record in Osti.gov$$Hfree_for_read</backlink></links><search><creatorcontrib>Kobashigawa, Shinko</creatorcontrib><creatorcontrib>Suzuki, Keiji</creatorcontrib><creatorcontrib>Yamashita, Shunichi</creatorcontrib><title>Ionizing radiation accelerates Drp1-dependent mitochondrial fission, which involves delayed mitochondrial reactive oxygen species production in normal human fibroblast-like cells</title><title>Biochemical and biophysical research communications</title><addtitle>Biochem Biophys Res Commun</addtitle><description>► We report first time that ionizing radiation induces mitochondrial dynamic changes. ► Radiation-induced mitochondrial fission was caused by Drp1 localization. ► We found that radiation causes delayed ROS from mitochondria. ► Down regulation of Drp1 rescued mitochondrial dysfunction after radiation exposure.
Ionizing radiation is known to increase intracellular level of reactive oxygen species (ROS) through mitochondrial dysfunction. Although it has been as a basis of radiation-induced genetic instability, the mechanism involving mitochondrial dysfunction remains unclear. Here we studied the dynamics of mitochondrial structure in normal human fibroblast like cells exposed to ionizing radiation. Delayed mitochondrial O2- production was peaked 3days after irradiation, which was coupled with accelerated mitochondrial fission. We found that radiation exposure accumulated dynamin-related protein 1 (Drp1) to mitochondria. Knocking down of Drp1 expression prevented radiation induced acceleration of mitochondrial fission. Furthermore, knockdown of Drp1 significantly suppressed delayed production of mitochondrial O2-. Since the loss of mitochondrial membrane potential, which was induced by radiation was prevented in cells knocking down of Drp1 expression, indicating that the excessive mitochondrial fission was involved in delayed mitochondrial dysfunction after irradiation.</description><subject>BIOLOGICAL RADIATION EFFECTS</subject><subject>Cells, Cultured</subject><subject>Drp1</subject><subject>FIBROBLASTS</subject><subject>Fibroblasts - metabolism</subject><subject>Fibroblasts - radiation effects</subject><subject>Fibroblasts - ultrastructure</subject><subject>Gamma Rays</subject><subject>GENE REGULATION</subject><subject>GTP Phosphohydrolases - genetics</subject><subject>GTP Phosphohydrolases - metabolism</subject><subject>Humans</subject><subject>Ionizing radiation</subject><subject>IONIZING RADIATIONS</subject><subject>IRRADIATION</subject><subject>Microtubule-Associated Proteins - genetics</subject><subject>Microtubule-Associated Proteins - metabolism</subject><subject>MITOCHONDRIA</subject><subject>Mitochondria - metabolism</subject><subject>Mitochondria - radiation effects</subject><subject>Mitochondrial fission</subject><subject>Mitochondrial Proteins - genetics</subject><subject>Mitochondrial Proteins - metabolism</subject><subject>PROTEINS</subject><subject>RADIATION, THERMAL, AND OTHER ENVIRONMENTAL POLLUTANT EFFECTS ON LIVING ORGANISMS AND BIOLOGICAL MATERIALS</subject><subject>Reactive oxygen species</subject><subject>Reactive Oxygen Species - metabolism</subject><subject>Singlet Oxygen - metabolism</subject><issn>0006-291X</issn><issn>1090-2104</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2011</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp9kc1u1DAUhSMEokPhBVggSyzYkMF2HbeW2KDyV6kSG5DYWf65ae6Q2MF2BobH4glxmMKCBStLR9-59_iepnnM6JZRJl_sttYmt-WUsSpsKZV3mg2jiracUXG32dAqtVyxzyfNg5x3tIJCqvvNCeeUdkJ2m-bnVQz4A8MNScajKRgDMc7BCMkUyOR1mlnrYYbgIRQyYYluiMEnNCPpMedqeE6-DegGgmEfx301eRjNAfw_dALjCu6BxO-HGwgkz-Cw0nOKfnG_N2MgIaapwsMymVAX2BTtaHJpR_wCpOYa88PmXm_GDI9u39Pm09s3Hy_ft9cf3l1dvrpunRCqtLxnCoAzSZXoBVcXtvfSdqAUd4aDMB5Uz_sOQEgmnVXeWG6roJh39qI7O22eHufGXFBnhwXc4GII4Irm9YTnXScq9exI1W98XSAXPWFec5oAcclaUS7PpTpjleRH0qWYc4Jezwknkw6aUb0Wqnd6LVSvha5aba-antyOX-wE_q_lT4MVeHkEoJ5ij5DWpBAceExrUB_xf_N_ATfOt3g</recordid><startdate>20111104</startdate><enddate>20111104</enddate><creator>Kobashigawa, Shinko</creator><creator>Suzuki, Keiji</creator><creator>Yamashita, Shunichi</creator><general>Elsevier Inc</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>7X8</scope><scope>OTOTI</scope></search><sort><creationdate>20111104</creationdate><title>Ionizing radiation accelerates Drp1-dependent mitochondrial fission, which involves delayed mitochondrial reactive oxygen species production in normal human fibroblast-like cells</title><author>Kobashigawa, Shinko ; Suzuki, Keiji ; Yamashita, Shunichi</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c449t-2f19ee216094f4298bfd6b5e992ca2e4ade9f2f5ee4616cb9dab2b2f591dcb853</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2011</creationdate><topic>BIOLOGICAL RADIATION EFFECTS</topic><topic>Cells, Cultured</topic><topic>Drp1</topic><topic>FIBROBLASTS</topic><topic>Fibroblasts - metabolism</topic><topic>Fibroblasts - radiation effects</topic><topic>Fibroblasts - ultrastructure</topic><topic>Gamma Rays</topic><topic>GENE REGULATION</topic><topic>GTP Phosphohydrolases - genetics</topic><topic>GTP Phosphohydrolases - metabolism</topic><topic>Humans</topic><topic>Ionizing radiation</topic><topic>IONIZING RADIATIONS</topic><topic>IRRADIATION</topic><topic>Microtubule-Associated Proteins - genetics</topic><topic>Microtubule-Associated Proteins - metabolism</topic><topic>MITOCHONDRIA</topic><topic>Mitochondria - metabolism</topic><topic>Mitochondria - radiation effects</topic><topic>Mitochondrial fission</topic><topic>Mitochondrial Proteins - genetics</topic><topic>Mitochondrial Proteins - metabolism</topic><topic>PROTEINS</topic><topic>RADIATION, THERMAL, AND OTHER ENVIRONMENTAL POLLUTANT EFFECTS ON LIVING ORGANISMS AND BIOLOGICAL MATERIALS</topic><topic>Reactive oxygen species</topic><topic>Reactive Oxygen Species - metabolism</topic><topic>Singlet Oxygen - metabolism</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Kobashigawa, Shinko</creatorcontrib><creatorcontrib>Suzuki, Keiji</creatorcontrib><creatorcontrib>Yamashita, Shunichi</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>MEDLINE - Academic</collection><collection>OSTI.GOV</collection><jtitle>Biochemical and biophysical research communications</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Kobashigawa, Shinko</au><au>Suzuki, Keiji</au><au>Yamashita, Shunichi</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Ionizing radiation accelerates Drp1-dependent mitochondrial fission, which involves delayed mitochondrial reactive oxygen species production in normal human fibroblast-like cells</atitle><jtitle>Biochemical and biophysical research communications</jtitle><addtitle>Biochem Biophys Res Commun</addtitle><date>2011-11-04</date><risdate>2011</risdate><volume>414</volume><issue>4</issue><spage>795</spage><epage>800</epage><pages>795-800</pages><issn>0006-291X</issn><eissn>1090-2104</eissn><abstract>► We report first time that ionizing radiation induces mitochondrial dynamic changes. ► Radiation-induced mitochondrial fission was caused by Drp1 localization. ► We found that radiation causes delayed ROS from mitochondria. ► Down regulation of Drp1 rescued mitochondrial dysfunction after radiation exposure.
Ionizing radiation is known to increase intracellular level of reactive oxygen species (ROS) through mitochondrial dysfunction. Although it has been as a basis of radiation-induced genetic instability, the mechanism involving mitochondrial dysfunction remains unclear. Here we studied the dynamics of mitochondrial structure in normal human fibroblast like cells exposed to ionizing radiation. Delayed mitochondrial O2- production was peaked 3days after irradiation, which was coupled with accelerated mitochondrial fission. We found that radiation exposure accumulated dynamin-related protein 1 (Drp1) to mitochondria. Knocking down of Drp1 expression prevented radiation induced acceleration of mitochondrial fission. Furthermore, knockdown of Drp1 significantly suppressed delayed production of mitochondrial O2-. Since the loss of mitochondrial membrane potential, which was induced by radiation was prevented in cells knocking down of Drp1 expression, indicating that the excessive mitochondrial fission was involved in delayed mitochondrial dysfunction after irradiation.</abstract><cop>United States</cop><pub>Elsevier Inc</pub><pmid>22005465</pmid><doi>10.1016/j.bbrc.2011.10.006</doi><tpages>6</tpages></addata></record> |
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| subjects | BIOLOGICAL RADIATION EFFECTS Cells, Cultured Drp1 FIBROBLASTS Fibroblasts - metabolism Fibroblasts - radiation effects Fibroblasts - ultrastructure Gamma Rays GENE REGULATION GTP Phosphohydrolases - genetics GTP Phosphohydrolases - metabolism Humans Ionizing radiation IONIZING RADIATIONS IRRADIATION Microtubule-Associated Proteins - genetics Microtubule-Associated Proteins - metabolism MITOCHONDRIA Mitochondria - metabolism Mitochondria - radiation effects Mitochondrial fission Mitochondrial Proteins - genetics Mitochondrial Proteins - metabolism PROTEINS RADIATION, THERMAL, AND OTHER ENVIRONMENTAL POLLUTANT EFFECTS ON LIVING ORGANISMS AND BIOLOGICAL MATERIALS Reactive oxygen species Reactive Oxygen Species - metabolism Singlet Oxygen - metabolism |
| title | Ionizing radiation accelerates Drp1-dependent mitochondrial fission, which involves delayed mitochondrial reactive oxygen species production in normal human fibroblast-like cells |
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