Abstract
In order to elucidate signal transduction mechanism on how cells sense mechanical deformation, cytosolic Ca transients, by poking with a heat-blunted glass micropipette, were directly observed in human microvascular endothelial cell (HMEC). Cytosolic Ca transients were observed in almost all the HMECs poked with a micropipette. The transients started at the point of poking, and propagated at the peripheral regions of the poked cell. Those transients were also observed to propagate to the adjacent cells. Neither transient of poked cells nor propagation to adjacent cells was detected under the condition of depletion of extracellular Ca or intracellular Ca stores. Either stretch-activated channel or voltage-sensitive ion channel blockage inhibited significantly Ca transients. Phospholipase C inhibition, resulting in inhibition of inositol 1,4,5-triphosphate (IP 3) production, caused no Ca transient by poking. The results suggested that Ca influx might be a trigger for Ca release from intracellular Ca stores by IP 3 in the case of HMEC poking experiments.
Sign-in/Register to access full text options 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a call
