Beating under pressure
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《细胞学杂志》
Using patch-clamp electrical recordings on freshly dissociated cells, the team saw that increasing the viscosity of the medium on the cell surface caused an influx of calcium. The influx was blocked by the addition of an antibody against the TRPV4 channel. Furthermore, activation of the TRPV4 channel with a drug also induced a calcium influx and increased the ciliary beat frequency. Significantly, inhibition of phospholipase A2 blocked ciliary beat frequency changes in response to increased viscosity. Drug-induced activation of TRPV4 was not, however, affected by inhibition of phospholipase A2.
The team concludes that the TRPV4 channel is not the mechanosensor itself, but that something upstream in the phospholipase A2 pathway detects a compression force of the medium on the cell, triggering activation of phospholipase A2 and TRPV4. Just what the mechanosensor is remains a key question.(Ciliary beat frequencies in the respirat)
The team concludes that the TRPV4 channel is not the mechanosensor itself, but that something upstream in the phospholipase A2 pathway detects a compression force of the medium on the cell, triggering activation of phospholipase A2 and TRPV4. Just what the mechanosensor is remains a key question.(Ciliary beat frequencies in the respirat)