Feature ArticleCardiac-specific overexpression of Gαq alters excitation–contraction coupling in isolated cardiac myocytes
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Cited by (35)
The atypical 'b' splice variant of phospholipase Cβ1 promotes cardiac contractile dysfunction
2015, Journal of Molecular and Cellular CardiologyCitation Excerpt :Conditional overexpression in adult hearts of GαqQ209L, like Gαq-WT, does not result in hypertrophy, but instead initiates a rapid loss of contractility, along with chamber dilatation and subsequent heart failure [43]. The reduced contractility, associated with depressed SR Ca2 + cycling [44] is reminiscent of responses to PLCβ1b, although the phenotype is more complex and more severe following conditional expression of GαqQ029L. Significantly, all of these responses to GαqQ209L appeared to require PLCβ activation, because a GαqQ209L mutant unable to activate PLCβ subtypes (GαqQ209LAA) did not cause any of these changes.
Cardiac-directed expression of adenylyl cyclase reverses electrical remodeling in cardiomyopathy
2006, Journal of Molecular and Cellular CardiologyDown regulation of the L-type Ca<sup>2+</sup> channel, GRK2, and phosphorylated phospholamban: protective mechanisms for the denervated failing heart
2006, Journal of Molecular and Cellular CardiologyCitation Excerpt :Myocardial cells were filtered through a 200 μm nylon mesh and stored in Krebs–Henseleit solution containing 1 mmol/l Ca2+. Myocyte contraction and relaxation functions were measured using a video motion edge detector at 32 °C, as previously described in [30,31]. Whole-cell ICa were characterized using patch-clamp techniques at room temperature (22–23 °C), as previously described in [32,33].
Mechanism of Enhanced Cardiac Function in Mice with Hypertrophy Induced by Overexpressed Akt
2003, Journal of Biological ChemistryCitation Excerpt :The inactivation kinetics of ICa at +10 mV was significantly faster in TG myocytes compared with WT myocytes (Fig. 2B). In mouse ventricular myocytes, ICa inactivation is controlled by Ca2+ in the sarcolemmal subspace (19, 23, 24). To examine whether the difference in ICa inactivation rate between WT and TG myocytes was due to the contribution of Ca2+ released from the SR, the SR Ca2+ content was depleted by ryanodine (10 μm).
Ventricular remodeling in heart failure
2002, Journal of Cardiac FailurePhysiological determinants of contractile force generation and calcium handling in mouse myocardium
2002, Journal of Molecular and Cellular Cardiology
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Please address all correspondence to: Dr Atsuko Yatani, Department of Pharmacology and Cell Biophysics, University of Cincinnati College of Medicine, Cincinnati, OH 45267-0575. E-mail: [email protected]