Na+/Ca2+ exchanger-deficient mice have disorganized myofibrils and swollen mitochondria in cardiomyocytes
The Na(+)/Ca(2+) exchanger (NCX1) plays a key role in maintaining Ca(2+) homeostasis in cardiomyocytes. Disruption of Ncx1 gene in mice results in embryonic lethality between embryonic day 9 and 10, with the mice lacking spontaneous heartbeats. We examined the mechanism of lack of heartbeats in Ncx1...
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| Veröffentlicht in: | Comparative Biochemistry and Physiology Part B: Biochemistry and Molecular Biology 2003-05, Vol.135 (1), p.9-15 |
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| container_title | Comparative Biochemistry and Physiology Part B: Biochemistry and Molecular Biology |
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| creator | Wakimoto, Koji Fujimura, Hisako Iwamoto, Takahiro Oka, Toru Kobayashi, Kinji Kita, Satomi Kudoh, Sumiyo Kuro-o, Makoto Nabeshima, Yo ichi Shigekawa, Munekazu Imai, Yuji Komuro, Issei |
| description | The Na(+)/Ca(2+) exchanger (NCX1) plays a key role in maintaining Ca(2+) homeostasis in cardiomyocytes. Disruption of Ncx1 gene in mice results in embryonic lethality between embryonic day 9 and 10, with the mice lacking spontaneous heartbeats. We examined the mechanism of lack of heartbeats in Ncx1-deficient mice. Ultrastructual analysis demonstrated that Ncx1-deficient mice showed severe disorganization of myofibrils, a lack of Z-lines and swelling of mitochondria in cardiomyocytes. However, the expressions of cardiac-specific genes including transcription factor genes and contractile protein genes were not changed in Ncx1-deficient mice. Abnormal Ca(2+) handling itself or the lack of heartbeats due to the inactivation of Ncx1 gene may cause the disorganization of myofibrillogenesis. Although NCX1 protein levels were decreased in heterozygous mice, there were no changes in NCX2 and NCX3 protein levels between wild type and heterozygous mice. |
| doi_str_mv | 10.1016/s1096-4959(03)00057-5 |
| format | Article |
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Disruption of Ncx1 gene in mice results in embryonic lethality between embryonic day 9 and 10, with the mice lacking spontaneous heartbeats. We examined the mechanism of lack of heartbeats in Ncx1-deficient mice. Ultrastructual analysis demonstrated that Ncx1-deficient mice showed severe disorganization of myofibrils, a lack of Z-lines and swelling of mitochondria in cardiomyocytes. However, the expressions of cardiac-specific genes including transcription factor genes and contractile protein genes were not changed in Ncx1-deficient mice. Abnormal Ca(2+) handling itself or the lack of heartbeats due to the inactivation of Ncx1 gene may cause the disorganization of myofibrillogenesis. 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Disruption of Ncx1 gene in mice results in embryonic lethality between embryonic day 9 and 10, with the mice lacking spontaneous heartbeats. We examined the mechanism of lack of heartbeats in Ncx1-deficient mice. Ultrastructual analysis demonstrated that Ncx1-deficient mice showed severe disorganization of myofibrils, a lack of Z-lines and swelling of mitochondria in cardiomyocytes. However, the expressions of cardiac-specific genes including transcription factor genes and contractile protein genes were not changed in Ncx1-deficient mice. Abnormal Ca(2+) handling itself or the lack of heartbeats due to the inactivation of Ncx1 gene may cause the disorganization of myofibrillogenesis. Although NCX1 protein levels were decreased in heterozygous mice, there were no changes in NCX2 and NCX3 protein levels between wild type and heterozygous mice.</description><subject>Animals</subject><subject>Blotting, Western</subject><subject>Brain - metabolism</subject><subject>Cells, Cultured</subject><subject>Embryo, Mammalian</subject><subject>Gene Expression Regulation</subject><subject>Heart</subject><subject>Kidney - metabolism</subject><subject>Mice</subject><subject>Mice, Knockout</subject><subject>Mitochondria - metabolism</subject><subject>Mitochondria - ultrastructure</subject><subject>Myocytes, Cardiac - chemistry</subject><subject>Myocytes, Cardiac - metabolism</subject><subject>Myocytes, Cardiac - ultrastructure</subject><subject>Myofibrils - chemistry</subject><subject>Myofibrils - metabolism</subject><subject>Myofibrils - ultrastructure</subject><subject>Reverse Transcriptase Polymerase Chain Reaction</subject><subject>Sodium-Calcium Exchanger - analysis</subject><subject>Sodium-Calcium Exchanger - genetics</subject><subject>Sodium-Calcium Exchanger - physiology</subject><issn>1096-4959</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2003</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNpFkEtLAzEUhbNQbK3-BCUrUcrYZJJ5LaX4AtGFug53kjttZCapyVStv97WFl1dOHznXPgIOeHskjOeTyJnVZ7IKqvOmbhgjGVFku2R4V88IIcxvjEmSi74ARnwtCh5lZdDYh9hPJlCOqb4pefgZhgSg43VFl1PO6uRzuEDqbHRhxk4-42Gdivf2DrYNlJwhsZP37bo1nTv9dw7EyxQ66iGYKxfw3rVYzwi-w20EY93d0Reb65fpnfJw9Pt_fTqIdGCiT6pDa9qqaHOmGyKnGMhaki5yYVkmEKZYq5RooQ859JAaZqsELwsgVUMuKnFiJxtdxfBvy8x9qqzUWPbgkO_jKoQIuWVTNdgtgV18DEGbNQi2A7CSnGmNl7V80ag2ghUTKhfrypb9053D5Z1h-a_tZMqfgDBxHdx</recordid><startdate>200305</startdate><enddate>200305</enddate><creator>Wakimoto, Koji</creator><creator>Fujimura, Hisako</creator><creator>Iwamoto, Takahiro</creator><creator>Oka, Toru</creator><creator>Kobayashi, Kinji</creator><creator>Kita, Satomi</creator><creator>Kudoh, Sumiyo</creator><creator>Kuro-o, Makoto</creator><creator>Nabeshima, Yo ichi</creator><creator>Shigekawa, Munekazu</creator><creator>Imai, Yuji</creator><creator>Komuro, Issei</creator><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></search><sort><creationdate>200305</creationdate><title>Na+/Ca2+ exchanger-deficient mice have disorganized myofibrils and swollen mitochondria in cardiomyocytes</title><author>Wakimoto, Koji ; Fujimura, Hisako ; Iwamoto, Takahiro ; Oka, Toru ; Kobayashi, Kinji ; Kita, Satomi ; Kudoh, Sumiyo ; Kuro-o, Makoto ; Nabeshima, Yo ichi ; Shigekawa, Munekazu ; Imai, Yuji ; Komuro, Issei</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c303t-bd19b4cab504f761e73ba21d6340e2a82e6ce4e4a6614da8df573188a090a1db3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2003</creationdate><topic>Animals</topic><topic>Blotting, Western</topic><topic>Brain - metabolism</topic><topic>Cells, Cultured</topic><topic>Embryo, Mammalian</topic><topic>Gene Expression Regulation</topic><topic>Heart</topic><topic>Kidney - metabolism</topic><topic>Mice</topic><topic>Mice, Knockout</topic><topic>Mitochondria - metabolism</topic><topic>Mitochondria - ultrastructure</topic><topic>Myocytes, Cardiac - chemistry</topic><topic>Myocytes, Cardiac - metabolism</topic><topic>Myocytes, Cardiac - ultrastructure</topic><topic>Myofibrils - chemistry</topic><topic>Myofibrils - metabolism</topic><topic>Myofibrils - ultrastructure</topic><topic>Reverse Transcriptase Polymerase Chain Reaction</topic><topic>Sodium-Calcium Exchanger - analysis</topic><topic>Sodium-Calcium Exchanger - genetics</topic><topic>Sodium-Calcium Exchanger - physiology</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Wakimoto, Koji</creatorcontrib><creatorcontrib>Fujimura, Hisako</creatorcontrib><creatorcontrib>Iwamoto, Takahiro</creatorcontrib><creatorcontrib>Oka, Toru</creatorcontrib><creatorcontrib>Kobayashi, Kinji</creatorcontrib><creatorcontrib>Kita, Satomi</creatorcontrib><creatorcontrib>Kudoh, Sumiyo</creatorcontrib><creatorcontrib>Kuro-o, Makoto</creatorcontrib><creatorcontrib>Nabeshima, Yo ichi</creatorcontrib><creatorcontrib>Shigekawa, Munekazu</creatorcontrib><creatorcontrib>Imai, Yuji</creatorcontrib><creatorcontrib>Komuro, Issei</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><jtitle>Comparative Biochemistry and Physiology Part B: Biochemistry and Molecular Biology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Wakimoto, Koji</au><au>Fujimura, Hisako</au><au>Iwamoto, Takahiro</au><au>Oka, Toru</au><au>Kobayashi, Kinji</au><au>Kita, Satomi</au><au>Kudoh, Sumiyo</au><au>Kuro-o, Makoto</au><au>Nabeshima, Yo ichi</au><au>Shigekawa, Munekazu</au><au>Imai, Yuji</au><au>Komuro, Issei</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Na+/Ca2+ exchanger-deficient mice have disorganized myofibrils and swollen mitochondria in cardiomyocytes</atitle><jtitle>Comparative Biochemistry and Physiology Part B: Biochemistry and Molecular Biology</jtitle><addtitle>Comp Biochem Physiol B Biochem Mol Biol</addtitle><date>2003-05</date><risdate>2003</risdate><volume>135</volume><issue>1</issue><spage>9</spage><epage>15</epage><pages>9-15</pages><issn>1096-4959</issn><abstract>The Na(+)/Ca(2+) exchanger (NCX1) plays a key role in maintaining Ca(2+) homeostasis in cardiomyocytes. 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| subjects | Animals Blotting, Western Brain - metabolism Cells, Cultured Embryo, Mammalian Gene Expression Regulation Heart Kidney - metabolism Mice Mice, Knockout Mitochondria - metabolism Mitochondria - ultrastructure Myocytes, Cardiac - chemistry Myocytes, Cardiac - metabolism Myocytes, Cardiac - ultrastructure Myofibrils - chemistry Myofibrils - metabolism Myofibrils - ultrastructure Reverse Transcriptase Polymerase Chain Reaction Sodium-Calcium Exchanger - analysis Sodium-Calcium Exchanger - genetics Sodium-Calcium Exchanger - physiology |
| title | Na+/Ca2+ exchanger-deficient mice have disorganized myofibrils and swollen mitochondria in cardiomyocytes |
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