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PubMed · 15314282

Apoptotic volume decrease, pH acidification and chloride channel activation during apoptosis requires CD45 expression in HPB-ALL T cells.

G Dupéré-Minier·C Hamelin·P Desharnais·J Bernier
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Abstract

Mitochondrial-perturbating agents such as toxic coumponds induce apoptosis. We note that the loss of CD45 expression in the lymphoblastic leukemia cell line HPB-ALL (HPB45.0) leads to an inhibition of nuclear apoptosis. Our hypothesis is that the absence of CD45 disturbs protein function regulated by a proto-oncogene of the Src family playing a significant role in nuclear apoptosis. In this work we explore the importance of a chloride efflux on DNA fragmentation. The role of tyrosine kinase in the function and regulation of the chloride channels was determined. Our results showed a disturbance of ionic homeostasis in CD45 deficient lymphocytes (CD45-) in contrast to normal lymphocytes (CD45+). The phosphorylation levels of the chloride channels are considerably inhibited in CD45-, while the expression levels of these channels are similar in the two types of cells. A hypertonic medium inhibits DNA fragmentation in CD45+ while a hypotonic medium increases DNA fragmentation in CD45-. Thus CD45 plays a significant role in nuclear apoptosis by the regulation of the chloride channels responsible for ionic homeostasis of the cell essential for the DFF40 activation.

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Antigens, CDApoptosisCell Line, TumorCell NucleusCell SizeChloride ChannelsHumansHydrogen-Ion ConcentrationLeukemia-Lymphoma, Adult T-CellLeukocyte Common AntigensPhosphatidylserinesProtein-Tyrosine KinasesProto-Oncogene MasJournal Article

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G Dupéré-Minier, C Hamelin, P Desharnais, J Bernier. 2004. Apoptotic volume decrease, pH acidification and chloride channel activation during apoptosis requires CD45 expression in HPB-ALL T cells.. https://doi.org/10.1023/b%3Aappt.0000038031.84705.84

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