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dc.contributor.authorRamos-Kuri, Manuel
dc.contributor.otherCampus Ciudad de Méxicoes
dc.identifier.citationRamos-Kuri, M., Rapti, K., Mehel, H., Zhang, S., Dhandapany, P. S., Liang, L. … y Chemaly, E. R. (2015). Dominant negative Ras attenuates pathological ventricular remodeling in pressure overload cardiac hypertrophy. Biochimica et Biophysica Acta - Molecular Cell Research, 1853, (11), 2870-2884. DOI:
dc.description.abstractThe importance of the oncogene Ras in cardiac hypertrophy is well appreciated. The hypertrophic effects of the constitutively active mutant Ras-Val12 are revealed by clinical syndromes due to the Ras mutations and experimental studies. We examined the possible anti-hypertrophic effect of Ras inhibition in vitro using rat neonatal cardiomyocytes (NRCM) and in vivo in the setting of pressure-overload left ventricular (LV) hypertrophy (POH) in rats. Ras functions were modulated via adenovirus directed gene transfer of active mutant Ras-Val12 or dominant negative mutant N17-DN-Ras (DN-Ras). Ras-Val12 expression in vitro activates NFAT resulting in pro-hypertrophic and cardio-toxic effects on NRCM beating and Z-line organization. In contrast, the DN-Ras was antihypertrophic on NRCM, inhibited NFAT and exerted cardio-protective effects attested by preserved NRCM beating and Z line structure. Additional experiments with silencing H-Ras gene strategy corroborated the antihypertrophic effects of siRNA-H-Ras on NRCM. In vivo, with the POH model, both Ras mutants were associated with similar hypertrophy two weeks after simultaneous induction of POH and Ras-mutant gene transfer. However, LV diameters were higher and LV fractional shortening lower in the Ras-Val12 group compared to control and DN-Ras. Moreover, DN-Ras reduced the cross-sectional area of cardiomyocytes in vivo, and decreased the expression of markers of pathologic cardiac hypertrophy. In isolated adult cardiomyocytes after 2. weeks of POH and Ras-mutant gene transfer, DN-Ras improved sarcomere shortening and calcium transients compared to Ras-Val12. Overall, DN-Ras promotes a more physiological form of hypertrophy, suggesting an interesting therapeutic target for pathological cardiac hypertrophy. © 2015 Elsevier B.V.en
dc.publisherElsevier B.V.en
dc.relation.ispartofREPOSITORIO SCRIPTAes
dc.rightsAcceso Abiertoes
dc.sourceBiochimica et Biophysica Acta - Molecular Cell Researchen
dc.sourceBiochimica et Biophysica Acta - Molecular Cell Researchen
dc.subjectCardiac hypertrophyen
dc.subjectHeart failureen
dc.subjectPathological hypertrophyen
dc.subjectPhysiological hypertrophyen
dc.subjectRas inhibitionen
dc.subjectRas oncogeneen
dc.subjectAdenovirus vectoren
dc.subjectRas proteinen
dc.subjectSmall interfering RNAen
dc.subjectTranscription factor NFATen
dc.subjectProtein p21en
dc.subjectAnimal cellen
dc.subjectAnimal experimenten
dc.subjectAnimal modelen
dc.subjectAnimal tissueen
dc.subjectSprague Dawley raten
dc.subjectAmino Acid Substitutionen
dc.subjectMutation, Missenseen
dc.subjectMyocytes, Cardiacen
dc.subjectProto-Oncogene Proteins p21(ras)en
dc.subjectVentricular Remodelingen
dc.subject.classificationMEDICINA Y CIENCIAS DE LA SALUDes
dc.subject.classificationCiencias de la Saludes
dc.titleDominant negative Ras attenuates pathological ventricular remodeling in pressure overload cardiac hypertrophyen
dc.title.alternativeCorrigendum to "Dominant negative Ras attenuates pathological ventricular remodeling in pressure overload cardiac hypertrophy"en
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