Adenovirus-mediated expression of a voltage-gated potassium channel in vitro (rat cardiac myocytes) and in vivo (rat liver). A novel strategy for modifying excitability.
نویسندگان
چکیده
Excitability is governed primarily by the complement of ion channels in the cell membrane that shape the contour of the action potential. To modify excitability by gene transfer, we created a recombinant adenovirus designed to overexpress a Drosophila Shaker potassium channel (AdShK). In vitro, a variety of mammalian cell types infected with AdShK demonstrated robust expression of the exogenous channel. Spontaneous action potentials recorded from cardiac myocytes in primary culture were abbreviated compared with noninfected myocytes. Intravascular infusion of AdShK in neonatal rats induced Shaker potassium channel mRNA expression in the liver, and large potassium currents could be recorded from explanted hepatocytes. Thus, recombinant adenovirus technology has been used for in vitro and in vivo gene transfer of ion channel genes designed to modify cellular action potentials. With appropriate targeting, such a strategy may be useful in gene therapy of arrhythmias, seizure disorders, and myotonic muscle diseases.
منابع مشابه
Photocontrol of Voltage-Gated Ion Channel Activity by Azobenzene Trimethylammonium Bromide in Neonatal Rat Cardiomyocytes
The ability of azobenzene trimethylammonium bromide (azoTAB) to sensitize cardiac tissue excitability to light was recently reported. The dark, thermally relaxed trans- isomer of azoTAB suppressed spontaneous activity and excitation propagation speed, whereas the cis- isomer had no detectable effect on the electrical properties of cardiomyocyte monolayers. As the membrane potential of cardiac c...
متن کاملElectrophysiological modulation of cardiomyocytic tissue by transfected fibroblasts expressing potassium channels: a novel strategy to manipulate excitability.
BACKGROUND Traditional pharmacological therapies aiming to modify the abnormal electrophysiological substrate underlying cardiac arrhythmias may be limited by their relatively low efficacy, global cardiac activity, and significant proarrhythmic effects. We suggest a new approach, in which transfected cellular grafts expressing various ionic channels may be used to manipulate the local electroph...
متن کاملDesign of Novel Drugs (P3TZ, H2P3TZ, M2P3TZ, H4P3TZ and M4P3TZ) Based on Zonisamide for Autism Treatment by Binding to Potassium Voltage-gated Channel Subfamily D Member 2 (Kv4.2)
The present research article relates to the discovery of the novel drugs based on Zonisamide to treatment of autism disease. In first step, the electronic properties, reactivity and stability of the said compound are discussed. To attain these properties, the said molecular structure is optimized using B3LYP/6-311++G(d,p) level of theory at room temperature. The frontier molecular orbitals (FMO...
متن کاملGlucocorticoid induction of Kv1.5 K+ channel gene expression in ventricle of rat heart.
Multiple voltage-gated K+ channels contribute to the repolarization phases of the cardiac action potential and are targets of several antiarrhythmic drugs. The Kv1.5 K+ channel gene is expressed in the heart, and heterologous expression of this gene generates a slowly inactivating K+ current. Previously, we found that glucocorticoids specifically upregulate pituitary Kv1.5 gene expression. To t...
متن کاملEvidences on the existence of a new potassium channel in the rough endoplasmic reticulum (RER) of rat hepatocytes
Introduction: we have recently reported the presence of two potassium currents with 598 and 368 pS conductance in the rough endoplasmic reticulum (RER) membrane. The 598 pS channel was voltage dependent and ATP sensitive. However, the 368 pS channel was rarely observed and its identity remained obscure. Since cationic channels in intracellular organelles such as mitochondria and RER play imp...
متن کاملذخیره در منابع من
با ذخیره ی این منبع در منابع من، دسترسی به آن را برای استفاده های بعدی آسان تر کنید
عنوان ژورنال:
- The Journal of clinical investigation
دوره 96 2 شماره
صفحات -
تاریخ انتشار 1995