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Titolo:
Thymidine-dependent attenuation of the mitochondrial apoptotic pathway in adenosine-induced apoptosis of HL-60 cells
Autore:
Kang, CM; Suh, Y; Jang, IS; Park, SC;
Indirizzi:
Seoul Natl Univ, Coll Med,Aging & Phys Culture Res Inst, Lab Aging Res & Metab Engn, Dept Biochem & Mol Biol, Seoul 110799, South Korea Seoul Natl Univ Seoul South Korea 110799 Biol, Seoul 110799, South Korea
Titolo Testata:
JOURNAL OF CANCER RESEARCH AND CLINICAL ONCOLOGY
fascicolo: 9, volume: 127, anno: 2001,
pagine: 570 - 576
SICI:
0171-5216(200109)127:9<570:TAOTMA>2.0.ZU;2-N
Fonte:
ISI
Lingua:
ENG
Soggetto:
CYTOCHROME-C RELEASE; PERMEABILITY TRANSITION PORE; BCL-2 FAMILY PROTEINS; CASPASE ACTIVATION; BAX; CHANNEL; INHIBITION; MEMBRANE; BCL-X(L); PROTEASE;
Keywords:
adenosine; thymidine; mitochondria; Bax translocation; cytochrome c; apoptosis;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
43
Recensione:
Indirizzi per estratti:
Indirizzo: Park, SC Seoul Natl Univ, Coll Med,Aging & Phys Culture Res Inst, Lab Aging Res & Metab Engn, Dept Biochem & Mol Biol, Seoul 110799, South Korea Seoul Natl Univ Seoul South Korea 110799 ul 110799, South Korea
Citazione:
C.M. Kang et al., "Thymidine-dependent attenuation of the mitochondrial apoptotic pathway in adenosine-induced apoptosis of HL-60 cells", J CANC RES, 127(9), 2001, pp. 570-576

Abstract

Objective: We previously reported that adenosine-induced apoptosis in HL-60 cells was attenuated by cotreating the cells with pyrimidine nucleosides. The mechanism involved in this adenosine-induced apoptosis by the differential supply of nucleosides is studied here with a particular focus on the regulation of apoptosis-associated mitochondrial events. Methods: Time-dependent changes in the mitochondrial membrane potential (MMP) after treatment with adenosine and/or thymidine were monitored. Results: The cells did not show any decrease of MMP level up to 2.5 h after 1 mM adenosine exposure, whereas cytochrome c release. caspase-9 and caspase-3 activity, and DNA fragmentation were already activated, suggesting that mitochondrial depolarization is not a prerequisite of other apoptosis-related mitochondrial events. In contrast, the translocation of Bax to mitochondria and the release of cytochrome c began within the first hour of adenosine treatment. Conclusion: Thus, it is believed that adenosine-induced apoptosis is mediated by the activation of the caspase cascade by cytochrome c release with concomitant increase of Bax in the mitochondria. which implies that the translocation of Bax might be a leading event in the adenosine-induced apoptosis. Moreover, we found that most of the apoptotic parameters in adenosine-induced cellular changes, such as translocation of Bax. the release of cytochrome c, and the consequent activation of caspase-9 and caspase-3, were attenuated by thymidine supplement, thus indicating that the sensing of a nucleoside or nucleotide balance might be an upstream event of cytochrome c release. Therefore, it can be concluded that thymidine can attenuate adenosine-induced apoptosis by modulating the earliest stage of the mitochondrial apoptotic pathway.

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Documento generato il 21/09/20 alle ore 12:56:28