Osmotic stress sensitizes naturally resistant cells to TNF-α-induced apoptosis

Most cells are naturally resistant to TNF-α-induced cell death and become sensitized when NF-κB transactivation is blocked or in the presence of protein synthesis inhibitors that prevent the expression of anti-apoptotic genes. In this report we analyzed the role of osmotic stress on TNIF-α-induced c...

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Autores principales: Franco, D.L., Nojek, I.M., Molinero, L., Coso, O.A., Costas, M.A.
Formato: JOUR
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Acceso en línea:http://hdl.handle.net/20.500.12110/paper_13509047_v9_n10_p1090_Franco
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spelling todo:paper_13509047_v9_n10_p1090_Franco2023-10-03T16:10:04Z Osmotic stress sensitizes naturally resistant cells to TNF-α-induced apoptosis Franco, D.L. Nojek, I.M. Molinero, L. Coso, O.A. Costas, M.A. Apoptosis MAP kinases NF-κB TNF-α immunoglobulin enhancer binding protein phosphotransferase protein bcl 2 protein synthesis inhibitor synaptophysin tumor necrosis factor alpha apoptosis article cell death controlled study enzyme activity enzyme inhibition gene activity gene expression HeLa cell human human cell osmotic stress priority journal protein synthesis inhibition sensitization transactivation Apoptosis Dose-Response Relationship, Drug Enzyme Inhibitors Eukaryotic Cells Hela Cells Humans MAP Kinase Signaling System Mitogen-Activated Protein Kinase 12 Mitogen-Activated Protein Kinase 8 Mitogen-Activated Protein Kinases NF-kappa B Osmotic Pressure p38 Mitogen-Activated Protein Kinases Proto-Oncogene Proteins c-bcl-2 Saline Solution, Hypertonic Stress Sulfasalazine Transcription Factor RelA Tumor Necrosis Factor-alpha Most cells are naturally resistant to TNF-α-induced cell death and become sensitized when NF-κB transactivation is blocked or in the presence of protein synthesis inhibitors that prevent the expression of anti-apoptotic genes. In this report we analyzed the role of osmotic stress on TNIF-α-induced cell death. We found that it sensitizes the naturally resistant HeLa cells to TNF-α-induced apoptosis, with the involvement of an increase in the activity of several kinases, the inhibition of Bcl-2 expression, and a late increase on NF-κB activation. Cell death occurs regardless of the enhanced NF-κB activity, whose inhibition produces an increase in apoptosis. The inhibition of p38 kinase, also involved in NF-κB activation, significantly increases the effect of osmotic stress on TNF-α-induced cell death. Fil:Franco, D.L. Universidad de Buenos Aires. Facultad de Ciencias Exactas y Naturales; Argentina. Fil:Nojek, I.M. Universidad de Buenos Aires. Facultad de Ciencias Exactas y Naturales; Argentina. Fil:Molinero, L. Universidad de Buenos Aires. Facultad de Ciencias Exactas y Naturales; Argentina. Fil:Coso, O.A. Universidad de Buenos Aires. Facultad de Ciencias Exactas y Naturales; Argentina. Fil:Costas, M.A. Universidad de Buenos Aires. Facultad de Ciencias Exactas y Naturales; Argentina. JOUR info:eu-repo/semantics/openAccess http://creativecommons.org/licenses/by/2.5/ar http://hdl.handle.net/20.500.12110/paper_13509047_v9_n10_p1090_Franco
institution Universidad de Buenos Aires
institution_str I-28
repository_str R-134
collection Biblioteca Digital - Facultad de Ciencias Exactas y Naturales (UBA)
topic Apoptosis
MAP kinases
NF-κB
TNF-α
immunoglobulin enhancer binding protein
phosphotransferase
protein bcl 2
protein synthesis inhibitor
synaptophysin
tumor necrosis factor alpha
apoptosis
article
cell death
controlled study
enzyme activity
enzyme inhibition
gene activity
gene expression
HeLa cell
human
human cell
osmotic stress
priority journal
protein synthesis inhibition
sensitization
transactivation
Apoptosis
Dose-Response Relationship, Drug
Enzyme Inhibitors
Eukaryotic Cells
Hela Cells
Humans
MAP Kinase Signaling System
Mitogen-Activated Protein Kinase 12
Mitogen-Activated Protein Kinase 8
Mitogen-Activated Protein Kinases
NF-kappa B
Osmotic Pressure
p38 Mitogen-Activated Protein Kinases
Proto-Oncogene Proteins c-bcl-2
Saline Solution, Hypertonic
Stress
Sulfasalazine
Transcription Factor RelA
Tumor Necrosis Factor-alpha
spellingShingle Apoptosis
MAP kinases
NF-κB
TNF-α
immunoglobulin enhancer binding protein
phosphotransferase
protein bcl 2
protein synthesis inhibitor
synaptophysin
tumor necrosis factor alpha
apoptosis
article
cell death
controlled study
enzyme activity
enzyme inhibition
gene activity
gene expression
HeLa cell
human
human cell
osmotic stress
priority journal
protein synthesis inhibition
sensitization
transactivation
Apoptosis
Dose-Response Relationship, Drug
Enzyme Inhibitors
Eukaryotic Cells
Hela Cells
Humans
MAP Kinase Signaling System
Mitogen-Activated Protein Kinase 12
Mitogen-Activated Protein Kinase 8
Mitogen-Activated Protein Kinases
NF-kappa B
Osmotic Pressure
p38 Mitogen-Activated Protein Kinases
Proto-Oncogene Proteins c-bcl-2
Saline Solution, Hypertonic
Stress
Sulfasalazine
Transcription Factor RelA
Tumor Necrosis Factor-alpha
Franco, D.L.
Nojek, I.M.
Molinero, L.
Coso, O.A.
Costas, M.A.
Osmotic stress sensitizes naturally resistant cells to TNF-α-induced apoptosis
topic_facet Apoptosis
MAP kinases
NF-κB
TNF-α
immunoglobulin enhancer binding protein
phosphotransferase
protein bcl 2
protein synthesis inhibitor
synaptophysin
tumor necrosis factor alpha
apoptosis
article
cell death
controlled study
enzyme activity
enzyme inhibition
gene activity
gene expression
HeLa cell
human
human cell
osmotic stress
priority journal
protein synthesis inhibition
sensitization
transactivation
Apoptosis
Dose-Response Relationship, Drug
Enzyme Inhibitors
Eukaryotic Cells
Hela Cells
Humans
MAP Kinase Signaling System
Mitogen-Activated Protein Kinase 12
Mitogen-Activated Protein Kinase 8
Mitogen-Activated Protein Kinases
NF-kappa B
Osmotic Pressure
p38 Mitogen-Activated Protein Kinases
Proto-Oncogene Proteins c-bcl-2
Saline Solution, Hypertonic
Stress
Sulfasalazine
Transcription Factor RelA
Tumor Necrosis Factor-alpha
description Most cells are naturally resistant to TNF-α-induced cell death and become sensitized when NF-κB transactivation is blocked or in the presence of protein synthesis inhibitors that prevent the expression of anti-apoptotic genes. In this report we analyzed the role of osmotic stress on TNIF-α-induced cell death. We found that it sensitizes the naturally resistant HeLa cells to TNF-α-induced apoptosis, with the involvement of an increase in the activity of several kinases, the inhibition of Bcl-2 expression, and a late increase on NF-κB activation. Cell death occurs regardless of the enhanced NF-κB activity, whose inhibition produces an increase in apoptosis. The inhibition of p38 kinase, also involved in NF-κB activation, significantly increases the effect of osmotic stress on TNF-α-induced cell death.
format JOUR
author Franco, D.L.
Nojek, I.M.
Molinero, L.
Coso, O.A.
Costas, M.A.
author_facet Franco, D.L.
Nojek, I.M.
Molinero, L.
Coso, O.A.
Costas, M.A.
author_sort Franco, D.L.
title Osmotic stress sensitizes naturally resistant cells to TNF-α-induced apoptosis
title_short Osmotic stress sensitizes naturally resistant cells to TNF-α-induced apoptosis
title_full Osmotic stress sensitizes naturally resistant cells to TNF-α-induced apoptosis
title_fullStr Osmotic stress sensitizes naturally resistant cells to TNF-α-induced apoptosis
title_full_unstemmed Osmotic stress sensitizes naturally resistant cells to TNF-α-induced apoptosis
title_sort osmotic stress sensitizes naturally resistant cells to tnf-α-induced apoptosis
url http://hdl.handle.net/20.500.12110/paper_13509047_v9_n10_p1090_Franco
work_keys_str_mv AT francodl osmoticstresssensitizesnaturallyresistantcellstotnfainducedapoptosis
AT nojekim osmoticstresssensitizesnaturallyresistantcellstotnfainducedapoptosis
AT molinerol osmoticstresssensitizesnaturallyresistantcellstotnfainducedapoptosis
AT cosooa osmoticstresssensitizesnaturallyresistantcellstotnfainducedapoptosis
AT costasma osmoticstresssensitizesnaturallyresistantcellstotnfainducedapoptosis
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