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Mitochondrial dysfunction is related to necrosis-like programmed cell death induced by A23187 in CEM cells.
Eur J Pharmacol. 2005 Jun 15; 516(3):187-96.EJ

Abstract

We have previously reported that calcium ionophore A23187 differentially induces necrosis in CEM cells, a T-lymphoblastic leukemia cell line, and apoptosis in HL60 cells, a promyelocytic leukemia cell line. Stimulation with VP16, however, induces typical apoptosis in both cell lines. Necrosis in CEM cells, characterized by cell shrinkage and clustering, began within 5 min of treatment. Swelling of the mitochondria, lumpy chromatin condensation and intact plasma membranes were evident by electron microscopy. These A23187-mediated changes in CEM cells were suppressed by clonazepam or CGP37157, inhibitors of the mitochondrial Na(+)/Ca(2+) exchanger. The changes, however, were not affected by cyclosporin A, an inhibitor of the mitochondrial permeability transition pore. In both CEM and HL60 cells, intra-cellular calcium increased with similar amplitude within 1 min of treatment with 2 microM A23187. Intra-mitochondrial calcium increased with clonazepam pre-treatment alone in both CEM and HL60 cells. However, intra-mitochondrial calcium did not change drastically in response to A23187 in CEM or HL60 cells, either untreated or pre-treated with clonazepam. A23187 induces necrosis in CEM cells concurrent with mitochondrial dysfunction, which is independent of the mitochondrial permeability transition, but affected by intra-mitochondrial calcium, while HL60 cells lack these early changes. Differences in the responses to A23187 between these two cell lines might derive from differences in the susceptibility of the mitochondrial membrane to rapid increases in intra-cellular calcium.

Authors+Show Affiliations

Department of Pediatrics, Graduate School of Medicine, Kyoto University, 54 Kawahara-cho, Shogoin, Sakyo-ku, Kyoto 606-8507, Japan.No affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article

Language

eng

PubMed ID

15963976

Citation

Hamahata, Keigo, et al. "Mitochondrial Dysfunction Is Related to Necrosis-like Programmed Cell Death Induced By A23187 in CEM Cells." European Journal of Pharmacology, vol. 516, no. 3, 2005, pp. 187-96.
Hamahata K, Adachi S, Matsubara H, et al. Mitochondrial dysfunction is related to necrosis-like programmed cell death induced by A23187 in CEM cells. Eur J Pharmacol. 2005;516(3):187-96.
Hamahata, K., Adachi, S., Matsubara, H., Okada, M., Imai, T., Watanabe, K., Toyokuni, S. Y., Ueno, M., Wakabayashi, S., Katanosaka, Y., Akiba, S., Kubota, M., & Nakahata, T. (2005). Mitochondrial dysfunction is related to necrosis-like programmed cell death induced by A23187 in CEM cells. European Journal of Pharmacology, 516(3), 187-96.
Hamahata K, et al. Mitochondrial Dysfunction Is Related to Necrosis-like Programmed Cell Death Induced By A23187 in CEM Cells. Eur J Pharmacol. 2005 Jun 15;516(3):187-96. PubMed PMID: 15963976.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Mitochondrial dysfunction is related to necrosis-like programmed cell death induced by A23187 in CEM cells. AU - Hamahata,Keigo, AU - Adachi,Souichi, AU - Matsubara,Hiroshi, AU - Okada,Masayuki, AU - Imai,Tsuyoshi, AU - Watanabe,Ken-ichiro, AU - Toyokuni,Shin-ya, AU - Ueno,Masaki, AU - Wakabayashi,Shigeo, AU - Katanosaka,Yuki, AU - Akiba,Satoshi, AU - Kubota,Masaru, AU - Nakahata,Tatsutoshi, PY - 2005/04/05/received PY - 2005/04/11/accepted PY - 2005/6/21/pubmed PY - 2005/8/30/medline PY - 2005/6/21/entrez SP - 187 EP - 96 JF - European journal of pharmacology JO - Eur J Pharmacol VL - 516 IS - 3 N2 - We have previously reported that calcium ionophore A23187 differentially induces necrosis in CEM cells, a T-lymphoblastic leukemia cell line, and apoptosis in HL60 cells, a promyelocytic leukemia cell line. Stimulation with VP16, however, induces typical apoptosis in both cell lines. Necrosis in CEM cells, characterized by cell shrinkage and clustering, began within 5 min of treatment. Swelling of the mitochondria, lumpy chromatin condensation and intact plasma membranes were evident by electron microscopy. These A23187-mediated changes in CEM cells were suppressed by clonazepam or CGP37157, inhibitors of the mitochondrial Na(+)/Ca(2+) exchanger. The changes, however, were not affected by cyclosporin A, an inhibitor of the mitochondrial permeability transition pore. In both CEM and HL60 cells, intra-cellular calcium increased with similar amplitude within 1 min of treatment with 2 microM A23187. Intra-mitochondrial calcium increased with clonazepam pre-treatment alone in both CEM and HL60 cells. However, intra-mitochondrial calcium did not change drastically in response to A23187 in CEM or HL60 cells, either untreated or pre-treated with clonazepam. A23187 induces necrosis in CEM cells concurrent with mitochondrial dysfunction, which is independent of the mitochondrial permeability transition, but affected by intra-mitochondrial calcium, while HL60 cells lack these early changes. Differences in the responses to A23187 between these two cell lines might derive from differences in the susceptibility of the mitochondrial membrane to rapid increases in intra-cellular calcium. SN - 0014-2999 UR - https://www.unboundmedicine.com/medline/citation/15963976/Mitochondrial_dysfunction_is_related_to_necrosis_like_programmed_cell_death_induced_by_A23187_in_CEM_cells_ L2 - https://linkinghub.elsevier.com/retrieve/pii/S0014-2999(05)00415-2 DB - PRIME DP - Unbound Medicine ER -