Autophagic Cardiomyocyte Death in Cardiomyopathic Hamsters and Its Prevention by Granulocyte Colony-Stimulating Factor
In UM-X7.1 hamster model of human dilated cardiomyopathy, heart failure progressively develops and causes 50% mortality by 30 weeks of age. Through ultrastructural analysis, we found that many cardiomyocytes of this model contain typical autophagic vacuoles including degraded mitochondria, glycogen...
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| Veröffentlicht in: | The American journal of pathology 2006-02, Vol.168 (2), p.386-397 |
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| creator | Miyata, Shusaku Takemura, Genzou Kawase, Yukinori Li, Yiwen Okada, Hideshi Maruyama, Rumi Ushikoshi, Hiroaki Esaki, Masayasu Kanamori, Hiromitsu Li, Longhu Misao, Yu Tezuka, Asaki Toyo-Oka, Teruhiko Minatoguchi, Shinya Fujiwara, Takako Fujiwara, Hisayoshi |
| description | In UM-X7.1 hamster model of human dilated cardiomyopathy, heart failure progressively develops and causes 50% mortality by 30 weeks of age. Through ultrastructural analysis, we found that many cardiomyocytes of this model contain typical autophagic vacuoles including degraded mitochondria, glycogen granules, and myelin-like figures. In addition, ubiquitin, cathepsin D, and Rab7 were overexpressed as determined by immunoassays. Importantly, most cardiomyocytes with leaky plasma membranes were positive for cathepsin D, suggesting a direct link between autophagic degeneration and cell death. Meanwhile, cardiomyocyte apoptosis appeared insignificant. Granulocyte colony-stimulating factor (10 μg/kg/day), injected 5 days/week from 15 to 30 weeks of age, improved survival among 30-week-old hamsters (100% versus 53% in the untreated hamsters,
P
< 0.0001); ventricular function and remodeling, increased cardiomyocyte size, and reduced myocardial fibrosis followed by a dramatic reduction in the autophagic findings were also seen. Granulocyte colony-stimulating factor also down-regulated tumor necrosis factor-α and increased activities of Akt signal transducer and activator of transcription-3, and matrix metalloproteinases. However, there was no clear evidence of transdifferentiation from bone marrow cells into cardiomyocytes. In conclusion, autophagic death is important for cardiomyocyte loss in the cardiomyopathic hamster, and the beneficial effect of granulocyte colony-stimulating factor acts mainly via an anti-autophagic mechanism rather than anti-apo-ptosis or regeneration. |
| doi_str_mv | 10.2353/ajpath.2006.050137 |
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P
< 0.0001); ventricular function and remodeling, increased cardiomyocyte size, and reduced myocardial fibrosis followed by a dramatic reduction in the autophagic findings were also seen. Granulocyte colony-stimulating factor also down-regulated tumor necrosis factor-α and increased activities of Akt signal transducer and activator of transcription-3, and matrix metalloproteinases. However, there was no clear evidence of transdifferentiation from bone marrow cells into cardiomyocytes. In conclusion, autophagic death is important for cardiomyocyte loss in the cardiomyopathic hamster, and the beneficial effect of granulocyte colony-stimulating factor acts mainly via an anti-autophagic mechanism rather than anti-apo-ptosis or regeneration.</description><identifier>ISSN: 0002-9440</identifier><identifier>EISSN: 1525-2191</identifier><identifier>DOI: 10.2353/ajpath.2006.050137</identifier><identifier>PMID: 16436654</identifier><identifier>CODEN: AJPAA4</identifier><language>eng</language><publisher>Bethesda, MD: Elsevier Inc</publisher><subject>Animals ; Apoptosis ; Autophagy ; Biological and medical sciences ; Cardiomyopathy, Dilated - metabolism ; Cardiomyopathy, Dilated - prevention & control ; Cathepsin D - metabolism ; Cricetinae ; Fibrosis - metabolism ; Fibrosis - prevention & control ; Granulocyte Colony-Stimulating Factor - therapeutic use ; Investigative techniques, diagnostic techniques (general aspects) ; Male ; Medical sciences ; Mesocricetus ; Mitochondria - pathology ; Myelin Sheath ; Myocytes, Cardiac - metabolism ; Myocytes, Cardiac - pathology ; Original Research Paper ; Pathology. Cytology. Biochemistry. Spectrometry. Miscellaneous investigative techniques ; Proto-Oncogene Proteins c-akt - metabolism ; rab GTP-Binding Proteins - metabolism ; Recombinant Proteins ; STAT3 Transcription Factor - metabolism ; Survival Rate ; Tumor Necrosis Factor-alpha - metabolism ; Ubiquitin - metabolism ; Vacuoles</subject><ispartof>The American journal of pathology, 2006-02, Vol.168 (2), p.386-397</ispartof><rights>2006 American Society for Investigative Pathology</rights><rights>2006 INIST-CNRS</rights><rights>Copyright © American Society for Investigative Pathology 2006</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c612t-4f918a213d804936fed88c4679346b363ee2538179dda7b84dc6c9347b41d0dc3</citedby><cites>FETCH-LOGICAL-c612t-4f918a213d804936fed88c4679346b363ee2538179dda7b84dc6c9347b41d0dc3</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/PMC1606501/pdf/$$EPDF$$P50$$Gpubmedcentral$$H</linktopdf><linktohtml>$$Uhttps://www.sciencedirect.com/science/article/pii/S0002944010621001$$EHTML$$P50$$Gelsevier$$H</linktohtml><link.rule.ids>230,314,723,776,780,881,3537,27901,27902,53766,53768,65306</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=17448953$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/16436654$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Miyata, Shusaku</creatorcontrib><creatorcontrib>Takemura, Genzou</creatorcontrib><creatorcontrib>Kawase, Yukinori</creatorcontrib><creatorcontrib>Li, Yiwen</creatorcontrib><creatorcontrib>Okada, Hideshi</creatorcontrib><creatorcontrib>Maruyama, Rumi</creatorcontrib><creatorcontrib>Ushikoshi, Hiroaki</creatorcontrib><creatorcontrib>Esaki, Masayasu</creatorcontrib><creatorcontrib>Kanamori, Hiromitsu</creatorcontrib><creatorcontrib>Li, Longhu</creatorcontrib><creatorcontrib>Misao, Yu</creatorcontrib><creatorcontrib>Tezuka, Asaki</creatorcontrib><creatorcontrib>Toyo-Oka, Teruhiko</creatorcontrib><creatorcontrib>Minatoguchi, Shinya</creatorcontrib><creatorcontrib>Fujiwara, Takako</creatorcontrib><creatorcontrib>Fujiwara, Hisayoshi</creatorcontrib><title>Autophagic Cardiomyocyte Death in Cardiomyopathic Hamsters and Its Prevention by Granulocyte Colony-Stimulating Factor</title><title>The American journal of pathology</title><addtitle>Am J Pathol</addtitle><description>In UM-X7.1 hamster model of human dilated cardiomyopathy, heart failure progressively develops and causes 50% mortality by 30 weeks of age. Through ultrastructural analysis, we found that many cardiomyocytes of this model contain typical autophagic vacuoles including degraded mitochondria, glycogen granules, and myelin-like figures. In addition, ubiquitin, cathepsin D, and Rab7 were overexpressed as determined by immunoassays. Importantly, most cardiomyocytes with leaky plasma membranes were positive for cathepsin D, suggesting a direct link between autophagic degeneration and cell death. Meanwhile, cardiomyocyte apoptosis appeared insignificant. Granulocyte colony-stimulating factor (10 μg/kg/day), injected 5 days/week from 15 to 30 weeks of age, improved survival among 30-week-old hamsters (100% versus 53% in the untreated hamsters,
P
< 0.0001); ventricular function and remodeling, increased cardiomyocyte size, and reduced myocardial fibrosis followed by a dramatic reduction in the autophagic findings were also seen. Granulocyte colony-stimulating factor also down-regulated tumor necrosis factor-α and increased activities of Akt signal transducer and activator of transcription-3, and matrix metalloproteinases. However, there was no clear evidence of transdifferentiation from bone marrow cells into cardiomyocytes. 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Cytology. Biochemistry. Spectrometry. Miscellaneous investigative techniques</subject><subject>Proto-Oncogene Proteins c-akt - metabolism</subject><subject>rab GTP-Binding Proteins - metabolism</subject><subject>Recombinant Proteins</subject><subject>STAT3 Transcription Factor - metabolism</subject><subject>Survival Rate</subject><subject>Tumor Necrosis Factor-alpha - metabolism</subject><subject>Ubiquitin - metabolism</subject><subject>Vacuoles</subject><issn>0002-9440</issn><issn>1525-2191</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2006</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp9kV2L1DAUhoMo7uzoH_BCeqN71TFfTVMQYRndD1hQUK9DmqQzWdpkTNKR_ntTOjh6s1chOc95z3vyAvAGwQ0mFfkgHw8y7TcYQraBFUSkfgZWqMJViVGDnoMVhBCXDaXwAlzG-JivjHD4ElwgRgljFV2B4_WY_GEvd1YVWxm09cPk1ZRM8dlk8cK68_M8LWN3cojJhFhIp4v7FItvwRyNS9a7op2K2yDd2C8aW997N5Xfkx3GXibrdsWNVMmHV-BFJ_toXp_ONfh58-XH9q58-Hp7v71-KBVDOJW0axCXGBHNIW0I64zmXFFWN4SyljBiDK4IR3WjtaxbTrViKtfqliINtSJr8GnRPYztYLTKNoPsxSHYQYZJeGnF_xVn92LnjwIxyOYvXYOrk0Dwv0YTkxhsVKbvpTN-jKKuKGeMNU0m3z9NwhpVlMwgXkAVfIzBdH_tICjmYMUSrJiDFUuwuentv4ucW05JZuDdCZBRyb7LKSgbz1xNKW8qcra5t7v9bxuMiIPs-yyL5rmIcYEF4SyDHxfQ5HyO1gQRlTVOGZ2bVBLa26cM_wHfFdEf</recordid><startdate>20060201</startdate><enddate>20060201</enddate><creator>Miyata, Shusaku</creator><creator>Takemura, Genzou</creator><creator>Kawase, Yukinori</creator><creator>Li, Yiwen</creator><creator>Okada, Hideshi</creator><creator>Maruyama, Rumi</creator><creator>Ushikoshi, Hiroaki</creator><creator>Esaki, Masayasu</creator><creator>Kanamori, Hiromitsu</creator><creator>Li, Longhu</creator><creator>Misao, Yu</creator><creator>Tezuka, Asaki</creator><creator>Toyo-Oka, Teruhiko</creator><creator>Minatoguchi, Shinya</creator><creator>Fujiwara, Takako</creator><creator>Fujiwara, Hisayoshi</creator><general>Elsevier Inc</general><general>ASIP</general><general>American Society for Investigative Pathology</general><scope>IQODW</scope><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>7T5</scope><scope>H94</scope><scope>5PM</scope></search><sort><creationdate>20060201</creationdate><title>Autophagic Cardiomyocyte Death in Cardiomyopathic Hamsters and Its Prevention by Granulocyte Colony-Stimulating Factor</title><author>Miyata, Shusaku ; Takemura, Genzou ; Kawase, Yukinori ; Li, Yiwen ; Okada, Hideshi ; Maruyama, Rumi ; Ushikoshi, Hiroaki ; Esaki, Masayasu ; Kanamori, Hiromitsu ; Li, Longhu ; Misao, Yu ; Tezuka, Asaki ; Toyo-Oka, Teruhiko ; Minatoguchi, Shinya ; Fujiwara, Takako ; Fujiwara, Hisayoshi</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c612t-4f918a213d804936fed88c4679346b363ee2538179dda7b84dc6c9347b41d0dc3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2006</creationdate><topic>Animals</topic><topic>Apoptosis</topic><topic>Autophagy</topic><topic>Biological and medical sciences</topic><topic>Cardiomyopathy, Dilated - metabolism</topic><topic>Cardiomyopathy, Dilated - prevention & control</topic><topic>Cathepsin D - metabolism</topic><topic>Cricetinae</topic><topic>Fibrosis - metabolism</topic><topic>Fibrosis - prevention & control</topic><topic>Granulocyte Colony-Stimulating Factor - therapeutic use</topic><topic>Investigative techniques, diagnostic techniques (general aspects)</topic><topic>Male</topic><topic>Medical sciences</topic><topic>Mesocricetus</topic><topic>Mitochondria - pathology</topic><topic>Myelin Sheath</topic><topic>Myocytes, Cardiac - metabolism</topic><topic>Myocytes, Cardiac - pathology</topic><topic>Original Research Paper</topic><topic>Pathology. Cytology. Biochemistry. Spectrometry. 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Through ultrastructural analysis, we found that many cardiomyocytes of this model contain typical autophagic vacuoles including degraded mitochondria, glycogen granules, and myelin-like figures. In addition, ubiquitin, cathepsin D, and Rab7 were overexpressed as determined by immunoassays. Importantly, most cardiomyocytes with leaky plasma membranes were positive for cathepsin D, suggesting a direct link between autophagic degeneration and cell death. Meanwhile, cardiomyocyte apoptosis appeared insignificant. Granulocyte colony-stimulating factor (10 μg/kg/day), injected 5 days/week from 15 to 30 weeks of age, improved survival among 30-week-old hamsters (100% versus 53% in the untreated hamsters,
P
< 0.0001); ventricular function and remodeling, increased cardiomyocyte size, and reduced myocardial fibrosis followed by a dramatic reduction in the autophagic findings were also seen. Granulocyte colony-stimulating factor also down-regulated tumor necrosis factor-α and increased activities of Akt signal transducer and activator of transcription-3, and matrix metalloproteinases. However, there was no clear evidence of transdifferentiation from bone marrow cells into cardiomyocytes. In conclusion, autophagic death is important for cardiomyocyte loss in the cardiomyopathic hamster, and the beneficial effect of granulocyte colony-stimulating factor acts mainly via an anti-autophagic mechanism rather than anti-apo-ptosis or regeneration.</abstract><cop>Bethesda, MD</cop><pub>Elsevier Inc</pub><pmid>16436654</pmid><doi>10.2353/ajpath.2006.050137</doi><tpages>12</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | Animals Apoptosis Autophagy Biological and medical sciences Cardiomyopathy, Dilated - metabolism Cardiomyopathy, Dilated - prevention & control Cathepsin D - metabolism Cricetinae Fibrosis - metabolism Fibrosis - prevention & control Granulocyte Colony-Stimulating Factor - therapeutic use Investigative techniques, diagnostic techniques (general aspects) Male Medical sciences Mesocricetus Mitochondria - pathology Myelin Sheath Myocytes, Cardiac - metabolism Myocytes, Cardiac - pathology Original Research Paper Pathology. Cytology. Biochemistry. Spectrometry. Miscellaneous investigative techniques Proto-Oncogene Proteins c-akt - metabolism rab GTP-Binding Proteins - metabolism Recombinant Proteins STAT3 Transcription Factor - metabolism Survival Rate Tumor Necrosis Factor-alpha - metabolism Ubiquitin - metabolism Vacuoles |
| title | Autophagic Cardiomyocyte Death in Cardiomyopathic Hamsters and Its Prevention by Granulocyte Colony-Stimulating Factor |
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