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G13-mediated signaling pathway is required for pressure overload-induced cardiac remodeling and heart failure
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| Veröffentlicht in: | Circulation 126(2012), 16, Seite 1972-1982 |
|---|---|
| Personen und Körperschaften: | , , , , , , , , |
| Titel: | G13-mediated signaling pathway is required for pressure overload-induced cardiac remodeling and heart failure/ Mikito Takefuji, MD, Angela Wirth, PhD, Martina Lukasova, PhD, Seiko Takefuji, MD, Thomas Boettger, PhD, Thomas Braun, MD, PhD, Till Althoff, MD, Stefan Offermanns, MD, Nina Wettschureck, MD |
| Format: | E-Book-Kapitel |
| Sprache: | Englisch |
| veröffentlicht: |
12 Sep 2012
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| Gesamtaufnahme: |
: Circulation, 126(2012), 16, Seite 1972-1982
, volume:126 |
| Schlagwörter: | |
| Quelle: | Verbunddaten SWB Lizenzfreie Online-Ressourcen |
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| 245 | 1 | 0 | |a G13-mediated signaling pathway is required for pressure overload-induced cardiac remodeling and heart failure |c Mikito Takefuji, MD, Angela Wirth, PhD, Martina Lukasova, PhD, Seiko Takefuji, MD, Thomas Boettger, PhD, Thomas Braun, MD, PhD, Till Althoff, MD, Stefan Offermanns, MD, Nina Wettschureck, MD |
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| 520 | |a Background—Cardiac remodeling in response to pressure or volume overload plays an important role in the pathogenesis of heart failure. Various mechanisms have been suggested to translate mechanical stress into structural changes, one of them being the release of humoral factors such as angiotensin II and endothelin-1, which in turn promote cardiac hypertrophy and fibrosis. A large body of evidence suggests that the prohypertrophic effects of these factors are mediated by receptors coupled to the Gq/11 family of heterotrimeric G proteins. Most Gq/11-coupled receptors, however, can also activate G proteins of the G12/13 family, but the role of G12/13 in cardiac remodeling is not understood. - Methods and Results—We use siRNA-mediated knockdown in vitro and conditional gene inactivation in vivo to study the role of the G12/13 family in pressure overload-induced cardiac remodeling. We show in detail that inducible cardiomyocyte-specific inactivation of the α subunit of G13, Gα13, does not affect basal heart function but protects mice from pressure overload-induced hypertrophy and fibrosis as efficiently as inactivation of Gαq/11. Furthermore, inactivation of Gα13 prevents the development of heart failure up to 1 year after overloading. On the molecular level, we show that Gα13, but not Gαq/11, controls agonist-induced expression of hypertrophy-specific genes through activation of the small GTPase RhoA and consecutive activation of myocardin-related transcription factors. - Conclusion—Our data show that the G12/13 family of heterotrimeric G proteins is centrally involved in pressure overload-induced cardiac remodeling and plays a central role in the transition to heart failure. | ||
| 650 | 4 | |a heart failure | |
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| author | Takefuji, Mikito, Wirth, Angela, Lukasova, Martina, Takefuji, Seiko, Böttger, Thomas, Braun, Thomas, Althoff, Till F., Offermanns, Stefan, Wettschureck, Nina |
| author_facet | Takefuji, Mikito, Wirth, Angela, Lukasova, Martina, Takefuji, Seiko, Böttger, Thomas, Braun, Thomas, Althoff, Till F., Offermanns, Stefan, Wettschureck, Nina |
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| contents | Background—Cardiac remodeling in response to pressure or volume overload plays an important role in the pathogenesis of heart failure. Various mechanisms have been suggested to translate mechanical stress into structural changes, one of them being the release of humoral factors such as angiotensin II and endothelin-1, which in turn promote cardiac hypertrophy and fibrosis. A large body of evidence suggests that the prohypertrophic effects of these factors are mediated by receptors coupled to the Gq/11 family of heterotrimeric G proteins. Most Gq/11-coupled receptors, however, can also activate G proteins of the G12/13 family, but the role of G12/13 in cardiac remodeling is not understood. - Methods and Results—We use siRNA-mediated knockdown in vitro and conditional gene inactivation in vivo to study the role of the G12/13 family in pressure overload-induced cardiac remodeling. We show in detail that inducible cardiomyocyte-specific inactivation of the α subunit of G13, Gα13, does not affect basal heart function but protects mice from pressure overload-induced hypertrophy and fibrosis as efficiently as inactivation of Gαq/11. Furthermore, inactivation of Gα13 prevents the development of heart failure up to 1 year after overloading. On the molecular level, we show that Gα13, but not Gαq/11, controls agonist-induced expression of hypertrophy-specific genes through activation of the small GTPase RhoA and consecutive activation of myocardin-related transcription factors. - Conclusion—Our data show that the G12/13 family of heterotrimeric G proteins is centrally involved in pressure overload-induced cardiac remodeling and plays a central role in the transition to heart failure. |
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| spelling | Takefuji, Mikito VerfasserIn (DE-588)1162204354 (DE-627)1025670949 (DE-576)507255844 aut, G13-mediated signaling pathway is required for pressure overload-induced cardiac remodeling and heart failure Mikito Takefuji, MD, Angela Wirth, PhD, Martina Lukasova, PhD, Seiko Takefuji, MD, Thomas Boettger, PhD, Thomas Braun, MD, PhD, Till Althoff, MD, Stefan Offermanns, MD, Nina Wettschureck, MD, 12 Sep 2012, 11, Text txt rdacontent, Computermedien c rdamedia, Online-Ressource cr rdacarrier, Im Titel ist die Zahl 13 tiefgestellt, Gesehen am 04.07.2018, Background—Cardiac remodeling in response to pressure or volume overload plays an important role in the pathogenesis of heart failure. Various mechanisms have been suggested to translate mechanical stress into structural changes, one of them being the release of humoral factors such as angiotensin II and endothelin-1, which in turn promote cardiac hypertrophy and fibrosis. A large body of evidence suggests that the prohypertrophic effects of these factors are mediated by receptors coupled to the Gq/11 family of heterotrimeric G proteins. Most Gq/11-coupled receptors, however, can also activate G proteins of the G12/13 family, but the role of G12/13 in cardiac remodeling is not understood. - Methods and Results—We use siRNA-mediated knockdown in vitro and conditional gene inactivation in vivo to study the role of the G12/13 family in pressure overload-induced cardiac remodeling. We show in detail that inducible cardiomyocyte-specific inactivation of the α subunit of G13, Gα13, does not affect basal heart function but protects mice from pressure overload-induced hypertrophy and fibrosis as efficiently as inactivation of Gαq/11. Furthermore, inactivation of Gα13 prevents the development of heart failure up to 1 year after overloading. On the molecular level, we show that Gα13, but not Gαq/11, controls agonist-induced expression of hypertrophy-specific genes through activation of the small GTPase RhoA and consecutive activation of myocardin-related transcription factors. - Conclusion—Our data show that the G12/13 family of heterotrimeric G proteins is centrally involved in pressure overload-induced cardiac remodeling and plays a central role in the transition to heart failure., heart failure, hypertrophy, left ventricular, mice, signal transduction, ventricular remodeling, Wirth, Angela VerfasserIn (DE-588)1158699085 (DE-627)1020779624 (DE-576)504337394 aut, Lukasova, Martina VerfasserIn (DE-588)131426621 (DE-627)509054021 (DE-576)298470284 aut, Takefuji, Seiko VerfasserIn (DE-588)1162205539 (DE-627)1025673190 (DE-576)507257863 aut, Böttger, Thomas 1974- VerfasserIn (DE-588)13178823X (DE-627)513955046 (DE-576)255012985 aut, Braun, Thomas 1961- VerfasserIn (DE-588)1162207310 (DE-627)1025677609 (DE-576)507263057 aut, Althoff, Till F. VerfasserIn (DE-588)1158699395 (DE-627)1020780398 (DE-576)504337742 aut, Offermanns, Stefan 1964- VerfasserIn (DE-588)113037279 (DE-627)584488734 (DE-576)289750113 aut, Wettschureck, Nina 1971- VerfasserIn (DE-588)120748630 (DE-627)080865828 (DE-576)182697207 aut, Enthalten in Circulation Philadelphia, Pa. : Lippincott, Williams & Wilkins, 1950 126(2012), 16, Seite 1972-1982 Online-Ressource (DE-627)265784670 (DE-600)1466401-X (DE-576)074891189 1524-4539 nnns, volume:126 year:2012 number:16 pages:1972-1982 extent:11, http://dx.doi.org/10.1161/CIRCULATIONAHA.112.109256 Verlag Resolving-System kostenfrei Volltext, http://circ.ahajournals.org/content/126/16/1972 Verlag kostenfrei Volltext, http://dx.doi.org/10.1161/CIRCULATIONAHA.112.109256 LFER, LFER 2018-07-10T00:00:00Z |
| spellingShingle | Takefuji, Mikito, Wirth, Angela, Lukasova, Martina, Takefuji, Seiko, Böttger, Thomas, Braun, Thomas, Althoff, Till F., Offermanns, Stefan, Wettschureck, Nina, G13-mediated signaling pathway is required for pressure overload-induced cardiac remodeling and heart failure, Background—Cardiac remodeling in response to pressure or volume overload plays an important role in the pathogenesis of heart failure. Various mechanisms have been suggested to translate mechanical stress into structural changes, one of them being the release of humoral factors such as angiotensin II and endothelin-1, which in turn promote cardiac hypertrophy and fibrosis. A large body of evidence suggests that the prohypertrophic effects of these factors are mediated by receptors coupled to the Gq/11 family of heterotrimeric G proteins. Most Gq/11-coupled receptors, however, can also activate G proteins of the G12/13 family, but the role of G12/13 in cardiac remodeling is not understood. - Methods and Results—We use siRNA-mediated knockdown in vitro and conditional gene inactivation in vivo to study the role of the G12/13 family in pressure overload-induced cardiac remodeling. We show in detail that inducible cardiomyocyte-specific inactivation of the α subunit of G13, Gα13, does not affect basal heart function but protects mice from pressure overload-induced hypertrophy and fibrosis as efficiently as inactivation of Gαq/11. Furthermore, inactivation of Gα13 prevents the development of heart failure up to 1 year after overloading. On the molecular level, we show that Gα13, but not Gαq/11, controls agonist-induced expression of hypertrophy-specific genes through activation of the small GTPase RhoA and consecutive activation of myocardin-related transcription factors. - Conclusion—Our data show that the G12/13 family of heterotrimeric G proteins is centrally involved in pressure overload-induced cardiac remodeling and plays a central role in the transition to heart failure., heart failure, hypertrophy, left ventricular, mice, signal transduction, ventricular remodeling |
| swb_id_str | 507290194 |
| title | G13-mediated signaling pathway is required for pressure overload-induced cardiac remodeling and heart failure |
| title_auth | G13-mediated signaling pathway is required for pressure overload-induced cardiac remodeling and heart failure |
| title_full | G13-mediated signaling pathway is required for pressure overload-induced cardiac remodeling and heart failure Mikito Takefuji, MD, Angela Wirth, PhD, Martina Lukasova, PhD, Seiko Takefuji, MD, Thomas Boettger, PhD, Thomas Braun, MD, PhD, Till Althoff, MD, Stefan Offermanns, MD, Nina Wettschureck, MD |
| title_fullStr | G13-mediated signaling pathway is required for pressure overload-induced cardiac remodeling and heart failure Mikito Takefuji, MD, Angela Wirth, PhD, Martina Lukasova, PhD, Seiko Takefuji, MD, Thomas Boettger, PhD, Thomas Braun, MD, PhD, Till Althoff, MD, Stefan Offermanns, MD, Nina Wettschureck, MD |
| title_full_unstemmed | G13-mediated signaling pathway is required for pressure overload-induced cardiac remodeling and heart failure Mikito Takefuji, MD, Angela Wirth, PhD, Martina Lukasova, PhD, Seiko Takefuji, MD, Thomas Boettger, PhD, Thomas Braun, MD, PhD, Till Althoff, MD, Stefan Offermanns, MD, Nina Wettschureck, MD |
| title_in_hierarchy | G13-mediated signaling pathway is required for pressure overload-induced cardiac remodeling and heart failure / Mikito Takefuji, MD, Angela Wirth, PhD, Martina Lukasova, PhD, Seiko Takefuji, MD, Thomas Boettger, PhD, Thomas Braun, MD, PhD, Till Althoff, MD, Stefan Offermanns, MD, Nina Wettschureck, MD, |
| title_short | G13-mediated signaling pathway is required for pressure overload-induced cardiac remodeling and heart failure |
| title_sort | g13 mediated signaling pathway is required for pressure overload induced cardiac remodeling and heart failure |
| topic | heart failure, hypertrophy, left ventricular, mice, signal transduction, ventricular remodeling |
| topic_facet | heart failure, hypertrophy, left ventricular, mice, signal transduction, ventricular remodeling |
| url | http://dx.doi.org/10.1161/CIRCULATIONAHA.112.109256, http://circ.ahajournals.org/content/126/16/1972 |