Calcium-gated K + channels of the K Ca 1.1- and K Ca 3.1-type couple intracellular Ca 2+ signals to membrane hyperpolarization in mesenchymal stromal cells from the human adipose tissue.
Tarasov MV., Bystrova MF., Kotova PD., Rogachevskaja OA., Sysoeva VY., Kolesnikov SS.
Laboratory Study, published in Pflugers Arch (2016) — summary generated from the PubMed abstract.
Evidence from laboratory and animal studies provides groundwork for understanding mechanisms and potential before human studies continue.
- Level A · Stronger Clinical Evidence
- Level B · Emerging clinical evidence with positive signals
- Level C · Early human research exploring benefits
- Level D · Scientific groundwork from lab and animal studies
- Emerging · Emerging topic under active research
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- Study type
- Laboratory Study
- Journal
- Pflugers Arch (2016)
- Country
- Germany
- Reported sample size
- —
- Source database
- PubMed
- PMID
- 28028617
- DOI
- 10.1007/s00424-016-1932-4
Abstract (original English)
Electrogenesis in mesenchymal stromal cells (MSCs) remains poorly understood. Little is known about ion channels active in resting MSCs and activated upon MSC stimulation, particularly, by agonists mobilizing Ca 2+ in the MSC cytoplasm. A variety of Ca 2+ -gated ion channels may couple Ca 2+ signals to polarization of the plasma membrane. Here, we studied MSCs from the human adipose tissue and found that in cells responsive to ATP and adenosine with Ca 2+ transients or exhibiting spontaneous Ca 2+ oscillations, Ca 2+ bursts were associated with hyperpolarization mediated by Ca 2+ -gated K + channels. The expression analysis revealed transcripts for KCNMA1 and KCNN4 genes encoding for Ca 2+ -activated K + channels of large (K Ca 1.1) and intermediate (K Ca 3.1) conductance, respectively. Moreover, transcripts for the Ca 2+ -gated cation channel TRPM4 and anion channels Ano1, Ano2, and bestrophin-1, bestrophin-3, and bestrophin-4 were revealed. In all assayed MSCs, a rise in cytosolic Ca 2+ stimulated K + currents that were inhibited with iberiotoxin. This suggested that K Ca 1.1 channels are invariably expressed in MSCs. In ATP- and adenosine-responsive cells, iberiotoxin and TRAM-34 diminished electrical responses, implicating both K Ca 1.1 and K Ca 3.1 channels in coupling agonist-dependent Ca 2+ signals to membrane voltage. Functional tests pointed at the existence of two sep
What this study does not prove
- • This study does not prove SVF is an approved treatment or a replacement for standard care.
- • This is preclinical work; animal or laboratory results cannot be applied to humans.
Evidence level
Evidence from laboratory and animal studies provides groundwork for understanding mechanisms and potential before human studies continue.
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