LPS/IFN-'gama'-mediated protection of J774 macrophages from teniposide-induced apoptosis is associated with repression of pro-apoptotic BCL-2 members (2006)
- Authors:
- Autor USP: MENDES, JOAO GUSTAVO PESSINI AMARANTE - ICB
- Unidade: ICB
- Assunto: IMUNOLOGIA
- Language: Inglês
- Abstract: Introduction and Objectives: Macrophages are central components of the innate immunity and also play a major role in initiating the adaptive immunity. In both cases its immune function can be achieved by contact with others cells, cytokines and a variety of components of foreign organisms. In many cases contact with pathogens interferes with the apoptotic machinery. Herein, we evaluated the effect of LPS, I FN ã and its combination in cytokine production by macrophage cell line and if this combination could protect these cells against apoptosis induced by Teniposide. Methods and Results: J774 macrophage cell line were treated or not with LPS, IFN ã or both and then submitted to apoptogenic stimuli for 18h. Apoptosis was assessed by flow cytometry/cell cycle analysis of total DNA content. T he mRNA expression levels of some cytokines and Bcl-2, Bcl-XL, A1 (anti-apoptotic genes), BAK, BAX, PUMA and NOXA (proapoptotic genes) were performing by quantitative real-time PCR (qPCR) using Platinum SYBR Green qPCR Supermix-UDG (Invitrogen).The data obtained by flow cytometry revealed that only the treatment with the association of LPS + IFNã protected J774 cells from teniposideinduced apoptosis. Through the analysis the mRNA levels of some of the Bcl-2 family members, we observed that teniposide induced an upregulation of BAX, and NOXA, but did not interfere with the expression of BAK. Moreover, teniposide induced a downregulation of theantiapoptotic members Bcl-2, A1 and Bcl- XL. Pre-treatment with LPS + IFNã did not rescue the downregulation of these anti-apoptotic Bcl-2 members. However and importantly, LPS + IFNã prevented teniposide-induced upregulation of BAX and NOXA. Finally, although BAK mRNA level was not modified by teniposide, LPS + IFN ã -treated J774 cells displayed a lower BAK mRNA level, compared to untreated control. Conclusion: These preliminary data suggest that the treatment with LPS + I FN ã protects J774 cells from further apoptogenic insult by modulating the teniposide-induced upregulation of certain pro-apoptotic Bcl-2 family members.
- Imprenta:
- Source:
- Título do periódico: Abstracts
- Conference titles: Meeting of the Brazilian Society for Immunology
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ABNT
MARÇAL, M S et al. LPS/IFN-'gama'-mediated protection of J774 macrophages from teniposide-induced apoptosis is associated with repression of pro-apoptotic BCL-2 members. 2006, Anais.. São Paulo: Instituto de Ciências Biomédicas, Universidade de São Paulo, 2006. . Acesso em: 19 abr. 2024. -
APA
Marçal, M. S., Carneiro, P. S., De Franco, M., & Amarante-Mendes, J. G. P. (2006). LPS/IFN-'gama'-mediated protection of J774 macrophages from teniposide-induced apoptosis is associated with repression of pro-apoptotic BCL-2 members. In Abstracts. São Paulo: Instituto de Ciências Biomédicas, Universidade de São Paulo. -
NLM
Marçal MS, Carneiro PS, De Franco M, Amarante-Mendes JGP. LPS/IFN-'gama'-mediated protection of J774 macrophages from teniposide-induced apoptosis is associated with repression of pro-apoptotic BCL-2 members. Abstracts. 2006 ;[citado 2024 abr. 19 ] -
Vancouver
Marçal MS, Carneiro PS, De Franco M, Amarante-Mendes JGP. LPS/IFN-'gama'-mediated protection of J774 macrophages from teniposide-induced apoptosis is associated with repression of pro-apoptotic BCL-2 members. Abstracts. 2006 ;[citado 2024 abr. 19 ] - Pomolic acid triggers mitochondria-dependent apoptotic cell death in leukemia cell line
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