Trichomonas vaginalis-induced apoptosis in RAW264.7 cells is regulated through Bcl-xL, but not Bcl-2

J. H. Chang, Y. S. Ryang, S. K. Kim, J. Y. Park

Research output: Contribution to journalArticle

8 Citations (Scopus)

Abstract

The purpose of this study was to determine whether anti-apoptotic proteins of the Bcl-2 family such as Bcl-2 and Bcl-xL, proteins that confer resistance to apoptotic death from some stimuli, block apoptotic cell death in RAW264.7 cells upon treatment with Trichomonas vaginalis. In this study, the expression level of Bcl-2 was unchanged throughout the course of apoptotic cell death, and overexpressed Bcl-2 did not prevent release of cytochrome c, the significant change of the membrane potential, activation of caspases, and PARP cleavage in T. vaginalis-treatedRAW264.7 cells. On the other hand, Bcl-x L expression was decreased after T. vaginalis treatment accompanied with Bax activation. Furthermore, we showed that release of mitochondrial cytochrome c, cleavage of caspase-9 and PARP during apoptosis in T. vaginalis-treated RAW264.7 cells were considerably diminished by transfection with overexpressed Bcl-xL, and overexpressed Bcl-xL could inhibit T. vaginalis-induced apoptosis in RAW264.7 cells. In addition, interestingly, pre-treatment with caspase inhibitors, Boc-D-FMK and Z-DEVD-FMK, significantly abolished T. vaginalis-induced down-regulation of Bcl-x L, suggesting that caspase-3 may play a pivotal role in the process of apoptosis as well as the down-regulation of Bcl-xL by T. vaginalis. Therefore, these results suggest that T. vaginalis-induced apoptosis in RAW264.7 cells can occur via a Bcl-xL-dependent apoptotic mechanism.

Original languageEnglish
Pages (from-to)141-150
Number of pages10
JournalParasite Immunology
Volume26
Issue number3
DOIs
Publication statusPublished - 2004 Mar 1

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Trichomonas vaginalis
Apoptosis
Cytochromes c
Cell Death
Down-Regulation
Apoptosis Regulatory Proteins
Caspase Inhibitors
Caspase 9
Caspases
Caspase 3
Membrane Potentials
Transfection

All Science Journal Classification (ASJC) codes

  • Parasitology
  • Immunology

Cite this

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title = "Trichomonas vaginalis-induced apoptosis in RAW264.7 cells is regulated through Bcl-xL, but not Bcl-2",
abstract = "The purpose of this study was to determine whether anti-apoptotic proteins of the Bcl-2 family such as Bcl-2 and Bcl-xL, proteins that confer resistance to apoptotic death from some stimuli, block apoptotic cell death in RAW264.7 cells upon treatment with Trichomonas vaginalis. In this study, the expression level of Bcl-2 was unchanged throughout the course of apoptotic cell death, and overexpressed Bcl-2 did not prevent release of cytochrome c, the significant change of the membrane potential, activation of caspases, and PARP cleavage in T. vaginalis-treatedRAW264.7 cells. On the other hand, Bcl-x L expression was decreased after T. vaginalis treatment accompanied with Bax activation. Furthermore, we showed that release of mitochondrial cytochrome c, cleavage of caspase-9 and PARP during apoptosis in T. vaginalis-treated RAW264.7 cells were considerably diminished by transfection with overexpressed Bcl-xL, and overexpressed Bcl-xL could inhibit T. vaginalis-induced apoptosis in RAW264.7 cells. In addition, interestingly, pre-treatment with caspase inhibitors, Boc-D-FMK and Z-DEVD-FMK, significantly abolished T. vaginalis-induced down-regulation of Bcl-x L, suggesting that caspase-3 may play a pivotal role in the process of apoptosis as well as the down-regulation of Bcl-xL by T. vaginalis. Therefore, these results suggest that T. vaginalis-induced apoptosis in RAW264.7 cells can occur via a Bcl-xL-dependent apoptotic mechanism.",
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Trichomonas vaginalis-induced apoptosis in RAW264.7 cells is regulated through Bcl-xL, but not Bcl-2. / Chang, J. H.; Ryang, Y. S.; Kim, S. K.; Park, J. Y.

In: Parasite Immunology, Vol. 26, No. 3, 01.03.2004, p. 141-150.

Research output: Contribution to journalArticle

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T1 - Trichomonas vaginalis-induced apoptosis in RAW264.7 cells is regulated through Bcl-xL, but not Bcl-2

AU - Chang, J. H.

AU - Ryang, Y. S.

AU - Kim, S. K.

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