Key result
The KV2.1 gene product underlies the predominant voltage-gated outward K+ current in H9c2 myoblasts, which is suppressed by tetraethylammonium and quinidine with IC50s of 3.7 mM and 11.6 μM, respectively.
The study identifies the K(V)2.1 channel as the primary molecular basis for the major voltage-gated outward K+ current in H9c2 myoblasts.
No immediate clinical implications from rat myoblasts; leaves open KV2.1 relevance to human cardiac electrophysiology.
The H9c2 clonal cell line derived from embryonic rat ventricle is an in vitro model system for cardiac and skeletal myocytes. We used the whole-cell patch clamp technique to characterize the electrophysiological and pharmacological properties of an outward K+ current (IK(V)) and determined its molecular correlate in H9c2 myoblasts. IK(V) was activated by threshold depolarization to -30 mV, and its current amplitude and rate of activation increased with further depolarizations. IK(V) inactivated slowly with a time constant of 1-2 s, and the V(0.5) for steady-state inactivation was -37.9 +/- 4.6 mV (n = 10). Tetraethylammonium and quinidine suppressed IK(V) with IC(50)'s of 3.7 mM and 11.6 microM, respectively. Using RT-PCR analysis we found that the K(V )2.1 gene is the most abundantly expressed among genes for K(V)1.2, 1.4, 1.5, 2.1, 4.2, and 4.3, and by Western blotting we confirmed the synthesis of the K(V)2.1 alpha-subunit protein. We conclude that IK(V), the predominant voltage-gated outward current in H9c2 myoblasts, flows through the channels comprised of the K(V)2.1-subunit gene product.
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Wang et al. (2002) studied In vitro H9c2 myoblast model. Tetraethylammonium and quinidine vs. Control conditions was evaluated on IC50 for IKV suppression. The KV2.1 gene product underlies the predominant voltage-gated outward K+ current in H9c2 myoblasts, which is suppressed by tetraethylammonium and quinidine with IC50s of 3.7 mM and 11.6 μM, respectively.
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