Evidence for signaling via gap junctions from smooth muscle to endothelial cells in rat mesenteric arteries:: possible implication of a second messenger
Evidence for signaling via gap junctions from smooth muscle to endothelial cells in rat mesenteric arteries:: possible implication of a second messenger
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DOI:
10.1016/j.ceca.2004.11.004
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发表时间:
2005-04-01
期刊:
影响因子:
4
通讯作者:
Meister, JJ
中科院分区:
文献类型:
--
作者:
Lamboley, M;Pittet, P;Meister, JJ
We investigated heterocellular communication in rat mesenteric arterial strips at the cellular level using confocal microscopy. To visualize Ca2+ changes in different cell populations, smooth muscle cells (SMCs) were loaded with Fluo-4 and endothelial cells (ECs) with Fura red. SMC contraction was stimulated using high K+ solution and Phenylephrine. Depending on vasoconstrictor concentration, intracellular Ca2+ concentration ([Ca2+](i)) increased in a subpopulation of ECs 5-11 s after a [Ca2+](i) rise was observed in adjacent SMCs. This time interval suggests chemical coupling between SMCs and ECs via gap junctions. As potential chemical mediators we investigated Ca2+ or inositol 1,4,5-trisphosphate (IP3). First, phospholipase C inhibitor U-73122 was added to prevent IP3 production in response to the [Ca2+](i) increase in SMCs. In high K+ solution, all SMCs presented global and synchronous [Ca2+](i) increase, but no [Ca2+](i) variations were detected in ECs. Second, 2-aminoethoxydiphenylborate, an inhibitor of IP3-induced Ca2+ release, reduced the number of flashing ECs by 75 +/- 3% (n = 6). The number of flashing ECs was similarly reduced by adding the gap junction uncoupler palmitoleic acid. Thus, our results suggest a heterocellular communication through gap junctions from SMCs to ECs by diffusion, probably of IP3. (C) 2004 Elsevier Ltd. All rights reserved.