Ll. Demer et al., MECHANICAL STIMULATION INDUCES INTERCELLULAR CALCIUM SIGNALING IN BOVINE AORTIC ENDOTHELIAL-CELLS, The American journal of physiology, 264(6), 1993, pp. 2094-2102
To study the mechanism by which endothelial cells respond to mechanica
l forces, we used digital fluorescence microscopy to measure changes i
n intracellular Ca2+ concentration ([Ca2+]i) in primary cultures of bo
vine aortic endothelial cells in response to mechanical stimulation. B
efore stimulation, [Ca2+]i was stable (approximately 50-75 nM). When a
n individual cell within the monolayer was mechanically stimulated wit
h a microprobe, [Ca2+]i increased in the stimulated cell and spread in
the form of a wave from the site of contact to the cell edges. After
a delay of approximately 1 s, nonstimulated adjacent cells showed a si
milar spreading rise in [Ca2+]i. This outwardly radiating [Ca2+]i wave
involved progressively more distal cells to a radius of 4-6 cells. Th
e time delay before the wave appeared in adjacent cells increased, and
peak [Ca2+]i in each cell decreased with distance from the stimulated
cell. In the absence of extracellular Ca2+, there was no increase in
[Ca2+]i in the stimulated cell, yet a wave of increased [Ca2+]i occurr
ed in neighboring cells as if communicated from the stimulated cell. T
hese results indicate that endothelial cell mechanosensitivity results
in increases in [Ca2+]i and that the temporospatial dynamics of inter
cellular Ca2+ signaling are mediated by a diffusible substance other t
han Ca2+.