Thymidine-dependent attenuation of the mitochondrial apoptotic pathway in adenosine-induced apoptosis of HL-60 cells View Full Text


Ontology type: schema:ScholarlyArticle     


Article Info

DATE

2001-07-06

AUTHORS

Chang-Mo Kang, Yousin Suh, Ik-Soon Jang, Sang Park

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. More... »

PAGES

570-576

Identifiers

URI

http://scigraph.springernature.com/pub.10.1007/s004320100264

DOI

http://dx.doi.org/10.1007/s004320100264

DIMENSIONS

https://app.dimensions.ai/details/publication/pub.1043376862

PUBMED

https://www.ncbi.nlm.nih.gov/pubmed/11570579


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