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Differential regulation of potassium currents by FGF‐1 and FGF‐2 in embryonic Xenopus laevis myocytes
Author(s) -
ChauhanPatel R.,
Spruce A. E.
Publication year - 1998
Publication title -
the journal of physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.802
H-Index - 240
eISSN - 1469-7793
pISSN - 0022-3751
DOI - 10.1111/j.1469-7793.1998.109bf.x
Subject(s) - xenopus , fibroblast growth factor , myocyte , microbiology and biotechnology , endocrinology , medicine , chemistry , tyrosine kinase , biology , embryonic stem cell , biophysics , signal transduction , receptor , biochemistry , gene
1 Fibroblast growth factors (FGFs) are involved in the regulation of many aspects of muscle development. This study investigated their role in regulating voltage‐dependent K + currents in differentiating Xenopus laevis myocytes. Both FGF‐1 and FGF‐2 are expressed by developing muscle cells, so their actions were compared. Experiments were performed on cultured myocytes isolated from stage 15 embryos. 2 Long‐term exposure of the embryonic myocytes to FGF‐1 downregulated inward rectifier K + current ( I K(IR) ) density as well as both sustained and inactivating voltage‐dependent outward K + currents ( I K,S and I K,I , respectively) and their densities. In contrast, FGF‐2 upregulated these currents, although, because of an increase in capacitance caused by FGF‐2, current density did not change with this factor. 3 The regulation of I K(IR) by FGF‐1 was prevented by the cytoplasmic tyrosine kinase inhibitor herbimycin A, but that of I K,S and I K,I was unaffected, indicating that FGF‐1 achieves its regulatory effects on electrical development via separate signalling pathways. The receptor tyrosine kinase inhibitor genistein in isolation suppressed K + currents, but this may have occurred through a channel‐blocking mechanism. 4 In many cells, I K,S was found to be composed of two components with differing voltage dependencies of activation. The FGFs brought about an alteration in the amount of total I K,S by equal effects on each component. Conversely, herbimycin A increased the proportion of low voltage‐activated current without affecting total current amplitude. Therefore, we suggest that a single species of channel whose voltage dependence is shifted by tyrosine phosphorylation generates I K,S . 5 In summary, FGF‐1 and FGF‐2 exert opposite effects on voltage‐dependent K + currents in embryonic myocytes and, furthermore, FGF‐1 achieves its effects on different K + currents via separate second messenger pathways.