Adult Mouse Heart

Iwatate, M., Gu, Y., Dieterle, T. et al. (2003). In vivo high-efficiency transcoronary gene delivery and Cre-LoxP gene switching in the adult mouse heart. Gene Ther. 10(21), 1814-1820. 

Zhou YY, Wang SQ, Zhu WZ, et al. Culture and adenoviral infection of adult mouse cardiac myocytes methods for cellular genetic physiology. Am J Physiol Heart Circ Physiol 2000 279 H429-H436. 

Figure 6.8 Nine views of 3-D chemimages based on the amide I peak, showing different protein concentrations within the adult mouse heart, (a) Full longitudinal section image (abbreviations LV = left ventricle, RV = right ventricle, LA = left atrium, RA= right atrium.

D. Eckardt, M. Theis, J. Degen, T. Ott, H.V. van Rijen, S. Kirchhofif, J.S. Kim, J.M. de Bakker, K. Willecke, Functional role of connexin43 gap junction channels in adult mouse heart assessed by inducible gene deletion, J Mol Cell Cardiol 36 (2004) 101-110. 

M. Frank, A. Wirth, R.P. Andrie, M.M. Kreuzberg, R. Dobrowolski, G. Seifert, S. Offermanns, G. Nickenig, K. Willecke, J.W. Schrickel, Connexin45 provides optimal atrioventricular nodal conduction in the adult mouse heart, Circ Res 111 (2012) 1528-1538. 

RNA genome codes for four proteins. Three of these proteins are virus capsule proteins (they coat the RNA), and one of these proteins is a viral protease. The virus can cause temporary fever and sore throats in children however, about 5% of infections in adults and children result in damage to the heart, It is thought that Keshan disease In China, which is associated with selenium-deficient populations, is due to some influence of the selenium deficiency on the activation of coxsackievirus Studies with nrtice have revealed an interesting phenomenon. One particular strain of coxsackievirus can infect mice, but does not result in much hann to the mice. However, when the mice arc raised on an Sc-deficient diet, the virus acquires mutations in its genome and produces damage to the mouse s heart (Beck t ai., 1995). 

PrARs couple to the stimulatory Gs protein in both adult and neonatal myocytes, which leads to activation of adenylyl cyclase and production of cAMP (Fig. 1). In adult myocytes, the cAMP-dependent PKA phosphorylates various substrates, including the L-type Ca2+ channel, which increases Ca2+ entry into cells. PKA-mediated phosphorylation of phospholamban accelerates Ca2+ sequestration into the sarcoplasmic reticulum, resulting in accelerated cardiac relaxation (17). PKA-mediated phosphorylation of troponin I and C proteins reduces myofilament sensitivity to Ca2+ (17). The ryanodine receptor is also a substrate for PKA ryanodine receptor hyperphosphorylation has been observed in the failing human heart and in animal models of heart failure (58,59). Both in vivo and in vitro assays showed that the prAR plays the predominant role in modulating the rate and force of myocyte contraction in the mouse (24,30,55). 

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