Calcium-gated K+ channels of the KCa1.1 and KCa3.1 types couple intracellular Ca2+ signals to membrane hyperpolarization in mesenchymal stromal cells from the human adipose tissueстатья

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1. Полный текст Calcium-gated_K_channels2016.pdf 1,4 МБ 27 января 2017 [SysoevaVeronikaYu]

[1] Calcium-gated k+ channels of the kca1.1 and kca3.1 types couple intracellular ca2+ signals to membrane hyperpolarization in mesenchymal stromal cells from the human adipose tissue / M. V. Tarasov, M. F. Bystrova, P. D. Kotova et al. // European Journal of Physiology – Pflügers Archiv. — 2017. — Vol. 469, no. 2. — P. 349–362. Electrogenesis in mesenchymal stromal cells (MSCs) remains poorly understood, particularly, little is known about ion channels active in resting MSCs and activated upon MSC stimulation. Reportedly, certain GPCR agonists mobilize Ca2+ in the MSC cytoplasm. These Ca2+ signals may be coupled to MSC polarization by a variety of Ca2+-gated ion channels. Here we studied MSCs derived from the human adipose tissue and found that in cells, which generated Ca2+ responses to purinergic agonists or exhibited spontaneous Ca2+ oscillations, Ca2+ transients were associated with cell hypolarization mediated by Ca2+-gated K+ channels. The expression analysis revealed transcripts for KCNMA1 (KCa1.1) and KCNN4 (KCa3.1) genes encoding for Ca2+-activated K+ channels of large (BK) and intermediate (IK) conductance, respectively. Intracellular Ca2+ stimulated K+ channels virtually in each cell tested. In the majority of them, Ca2+-gated K+ currents strongly depended on membrane voltage and were completely blockable with iberiotoxin, a specific inhibitor of BK channels. In a small MSC subpopulation, iberiotoxin diminished a Ca2+-gated K+ current only partly, and a remaining unblocked component was inhibited by the specific KCa3.1 channel blocker TRAM 34, suggesting functional co-expression of BK and IK channels in such cells. Thus, BK channels represent the dominant type of Ca2+-activated K+ channels that can serve as an effector downstream of GPCR-mediated Ca2+ signaling. [ DOI ]

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