| 20130208 |
Han Y, Chen JD, Liu ZM, Zhou Y, Xia JH, Du X, Jin MW: Functional ion channels in mouse cardiac c-kit+ cells. Am J Physiol Cell Physiol. 2010 Feb 3.
Cardiac c-kit (+) cells are generally believed to be the major population of stem/progenitor cells in the heart and can be used as a cell source for cardiomyoplasty; however, the cellular electrophysiological properties are not understood in this type of cells. The present study was to investigate functional ion channels in undifferentiated mouse cardiac c-kit (+) cells using approaches of whole-cell patch voltage clamp, RT-PCR, and cell proliferation assay. It was found that three types of ionic currents were present in mouse cardiac c-kit (+) cells, including a delayed rectifier K (+) current (IK (DR)) inhibited by 4-aminopyridine (4-AP), an inward rectifier K (+) current (I (Kir)) decreased by Ba (2+), and a volume-sensitive chloride current (I (Cl.vol)) inhibited by 5-nitro-1-(3-phenylpropylamino) benzoic acid (NPPB). RT-PCR revealed that the corresponding ion channel genes, Kv1.1, Kv1.2, and Kv1.6 (for IK (DR)), Kir.1.1, Kir2.1 and Kir2.2 (likely responsible for I (Kir)), and Clcn3 (for I (Cl.vol)) were significant in mouse cardiac c-kit (+) cells. The inhibition of I (Cl.vol) with NPPB and niflumic acid, but not IKDR with 4-AP and TEA, reduced cell proliferation, and accumulated the cell progression at G0/G1 phase in mouse cardiac c-kit (+) cells. Our results demonstrate that three types of functional ion channel currents (i.e., IK (DR), I (Kir), and I (Cl.vol)) are present in mouse cardiac c-kit (+) cells, and I (Cl.vol) participates in regulating cell proliferation. |
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