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Possible involvement of a chloride-bicarbonate exchanger in apoptosis of endothelial cells and cardiomyocytes.
Cell Biol Int. 1999; 23(4):241-9.CB

Abstract

We examined the role of ion movement in staurosporine-induced apoptosis of vascular endothelial cells. Cultured vascular endothelial cells from bovine carotid arteries were used. Apoptosis was determined by propidium iodide assay. Treatment of the endothelial cells with staurosporine (10 nmol/l-1 micromol/l) for 6 h induced nuclear fragmentation in a dose-dependent manner. Staurosporine (1 micromol/l) elicited apoptosis in 70.5+/-1.5% of cells. Concomitant treatment of endothelial cells with 1 mmol/l of 4, 4-diisothiocyanatostilbene-2,2-disulfonic acid (DIDS), a chloride-bicarbonate exchange blocker, completely inhibited staurosporine-induced apoptosis. Other ion transporter inhibitors such as dimethyl amiloride and anthracene-9 carboxylic acid were less effective inhibitors of staurosporine-induced apoptosis of endothelial cells. DIDS prevented staurosporine-induced apoptosis of endothelial cells as well as cardiomyocytes. Next, we determined whether chloride ions or bicarbonate are involved in apoptosis. Incubation with a chloride ion removal buffer did not inhibit staurosporine-induced apoptosis of endothelial cells. However, endothelial cell apoptosis was completely suppressed by an inhibitor of caspase, benzyloxycarbonyl-Asp-CH(2)-O(C)O-dichlorobenzene (zD-dcb, 50 micromol/l). Staurosporine (1 micromol/l) increased the intracellular pH of endothelial cells, and DIDS (1 mmol/l), but not a caspase inhibitor, inhibited this increase in pH caused by staurosporine. Our findings suggest that endothelial cell apoptosis induced by staurosporine may be associated with the Cl(-)and bicarbonate (HCO-3) ions. Thus, Cl(-)efflux from cells or HCO-3 influx to cells (which increases pH) may play an important role in signal transduction leading events such as activation of caspase in staurosporine-induced apoptosis.

Authors+Show Affiliations

Second Department of Internal Medicine, Kyorin University School of Medicine, 6-20-2, Shinkawa, Mitaka, Tokyo, 181, Japan.No affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article

Language

eng

PubMed ID

10600233

Citation

Fujita, H, et al. "Possible Involvement of a Chloride-bicarbonate Exchanger in Apoptosis of Endothelial Cells and Cardiomyocytes." Cell Biology International, vol. 23, no. 4, 1999, pp. 241-9.
Fujita H, Ishizaki Y, Yanagisawa A, et al. Possible involvement of a chloride-bicarbonate exchanger in apoptosis of endothelial cells and cardiomyocytes. Cell Biol Int. 1999;23(4):241-9.
Fujita, H., Ishizaki, Y., Yanagisawa, A., Morita, I., Murota, S. I., & Ishikawa, K. (1999). Possible involvement of a chloride-bicarbonate exchanger in apoptosis of endothelial cells and cardiomyocytes. Cell Biology International, 23(4), 241-9.
Fujita H, et al. Possible Involvement of a Chloride-bicarbonate Exchanger in Apoptosis of Endothelial Cells and Cardiomyocytes. Cell Biol Int. 1999;23(4):241-9. PubMed PMID: 10600233.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Possible involvement of a chloride-bicarbonate exchanger in apoptosis of endothelial cells and cardiomyocytes. AU - Fujita,H, AU - Ishizaki,Y, AU - Yanagisawa,A, AU - Morita,I, AU - Murota,S I, AU - Ishikawa,K, PY - 1999/12/22/pubmed PY - 1999/12/22/medline PY - 1999/12/22/entrez SP - 241 EP - 9 JF - Cell biology international JO - Cell Biol Int VL - 23 IS - 4 N2 - We examined the role of ion movement in staurosporine-induced apoptosis of vascular endothelial cells. Cultured vascular endothelial cells from bovine carotid arteries were used. Apoptosis was determined by propidium iodide assay. Treatment of the endothelial cells with staurosporine (10 nmol/l-1 micromol/l) for 6 h induced nuclear fragmentation in a dose-dependent manner. Staurosporine (1 micromol/l) elicited apoptosis in 70.5+/-1.5% of cells. Concomitant treatment of endothelial cells with 1 mmol/l of 4, 4-diisothiocyanatostilbene-2,2-disulfonic acid (DIDS), a chloride-bicarbonate exchange blocker, completely inhibited staurosporine-induced apoptosis. Other ion transporter inhibitors such as dimethyl amiloride and anthracene-9 carboxylic acid were less effective inhibitors of staurosporine-induced apoptosis of endothelial cells. DIDS prevented staurosporine-induced apoptosis of endothelial cells as well as cardiomyocytes. Next, we determined whether chloride ions or bicarbonate are involved in apoptosis. Incubation with a chloride ion removal buffer did not inhibit staurosporine-induced apoptosis of endothelial cells. However, endothelial cell apoptosis was completely suppressed by an inhibitor of caspase, benzyloxycarbonyl-Asp-CH(2)-O(C)O-dichlorobenzene (zD-dcb, 50 micromol/l). Staurosporine (1 micromol/l) increased the intracellular pH of endothelial cells, and DIDS (1 mmol/l), but not a caspase inhibitor, inhibited this increase in pH caused by staurosporine. Our findings suggest that endothelial cell apoptosis induced by staurosporine may be associated with the Cl(-)and bicarbonate (HCO-3) ions. Thus, Cl(-)efflux from cells or HCO-3 influx to cells (which increases pH) may play an important role in signal transduction leading events such as activation of caspase in staurosporine-induced apoptosis. SN - 1065-6995 UR - https://www.unboundmedicine.com/medline/citation/10600233/Possible_involvement_of_a_chloride_bicarbonate_exchanger_in_apoptosis_of_endothelial_cells_and_cardiomyocytes_ L2 - https://doi.org/10.1006/cbir.1999.0342 DB - PRIME DP - Unbound Medicine ER -