Intracellular calcium ([Ca2+]i) was measured in FURA 2-loaded endothelial cells plated on fibronectin or vitronectin. Average values for [Ca2+]i increased to approximately twofold above basal levels by approximately 1 h after plating, and then declined. The increase in [Ca2+]i required extracellular calcium. Substituting potassium for sodium in the medium reduced the elevation of [Ca2+]i, a result that rules out the involvement of Na-Ca exchangers or voltage-dependent calcium channels, but that is consistent with the involvement of voltage-independent calcium channels. Plating cells on an anti-integrin beta 1 subunit antibody gave a similar [Ca2+]i response, but clustering beta 1 integrins with the same antibody, or occupying integrins with RGD (arg-gly-asp) peptides had no effect. Time course measurements on single cells revealed that in each cell [Ca2+]i rose abruptly at some point during spreading, from the basal level to a higher steady-state level that was maintained for some time. The elevated [Ca2+]i was unrelated to previously observed changes in intracellular pH, because chelating the Ca2+ in the medium failed to inhibit the elevation of pHi that occurred during cell spreading. In conclusion, these results show that integrin-mediated cell spreading can regulate [Ca2+]i, and the pathways involved are distinct from those that regulate intracellular pH.
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Article| February 15 1993
Spreading of human endothelial cells on fibronectin or vitronectin triggers elevation of intracellular free calcium.
M A Schwartz
Scripps Research Institute Committee on Vascular Biology, La Jolla, California 92037.
Online Issn: 1540-8140
Print Issn: 0021-9525
J Cell Biol (1993) 120 (4): 1003–1010.
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M A Schwartz; Spreading of human endothelial cells on fibronectin or vitronectin triggers elevation of intracellular free calcium.. J Cell Biol 15 February 1993; 120 (4): 1003–1010. doi: https://doi.org/10.1083/jcb.120.4.1003
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