scholarly journals MAPK inhibitors enhance cell death in pyrogallol-treated human pulmonary fibroblast cells via increasing O2•− levels

2017 ◽  
Vol 14 (1) ◽  
pp. 1179-1185 ◽  
Author(s):  
Bo Ram Han ◽  
Woo Hyun Park
Keyword(s):  
Cell Death ◽  
Fibroblast Cells ◽  
Mapk Inhibitors ◽  
Pulmonary Fibroblast

Mitogen-activated protein kinase inhibitors differently affect the growth inhibition and death of a proteasome inhibitor, MG132-treated human pulmonary fibroblast cells

2011 ◽  
Vol 30 (12) ◽  
pp. 1945-1954 ◽  
Author(s):  
Woo Hyun Park
Keyword(s):  
Cell Death ◽  
Cell Growth ◽  
Growth Inhibition ◽  
Proteasome Inhibitor ◽  
Mitogen Activated Protein Kinase ◽  
Cell Growth Inhibition ◽  
P38 Inhibitor ◽  
Mitogen Activated Protein ◽  
Mapk Inhibitors ◽  
Pulmonary Fibroblast

Carbobenzoxy-Leu-Leu-leucinal (MG132) as a proteasome inhibitor can induce growth inhibition and death in lung cancer or normal cells. However, little is known about relationship between proteasome inhibition and mitogen-activated protein kinase (MAPK) signaling in normal lung cells. Thus, in the present study, we investigated the effects of MAPK inhibitors on MG132-treated human pulmonary fibroblast (HPF) cells in relation to cell growth inhibition, cell death, reactive oxygen species (ROS) and glutathione (GSH). Treatment with 15 μM MG132 increased ROS levels including mitochondrial O2•− and GSH depleted cell numbers in HPF cells at 24 hours. MAP kinase or ERK kinase (MEK) inhibitor did not significantly affect cell growth inhibition, cell death, the loss of mitochondrial membrane potential (MMP; Δ Ψm), ROS level and GSH depletion in MG132-treated HPF cells. c-Jun N-terminal kinase (JNK) inhibitor attenuated the growth inhibition and death by MG132. This inhibitor also significantly decreased O2•− level in MG132-treated HPF cells. Although p38 inhibitor slightly enhanced HPF cell growth inhibition by MG132, this inhibitor and siRNA prevented HPF cell death induced by MG132. p38 inhibitor also attenuated d O2•− level and GSH depletion. Moreover, extracellular signal regulated kinase (ERK), JNK or p38 siRNA did not strongly affect ROS levels in MG132-treated HPF cells. ERK and JNK siRNAs decreased anonymous ubiquitinated protein levels in MG132-treated HPF cells. In conclusion, MAPK inhibitors differently affected the growth inhibition and death of MG132-treated HPF cells. Especially, p38 inhibitor attenuated HPF cell death by MG132, which was in part related to changes in ROS and GSH levels.

New Multi-Walled Carbon Nanotube of industrial interest induce cell death in murine fibroblast cells

2021 ◽  
pp. 1-31
Author(s):  
Krissia Franco de Godoy ◽  
Joice Margareth de Almeida Rodolpho ◽  
Patrícia Brassolatti ◽  
Bruna Dias de Lima Fragelli ◽  
Cynthia Aparecida de Castro ◽  
...  
Keyword(s):  
Cell Death ◽  
Carbon Nanotube ◽  
Fibroblast Cells ◽  
Induce Cell Death ◽  
Multi Walled Carbon Nanotube ◽  
Murine Fibroblast

scholarly journals Inhibition of Fibroblast Apoptosis by Borrrelia afzelii, Coxiella burnetii and Bartonella henselae

2011 ◽  
Vol 60 (3) ◽  
pp. 269-272 ◽  
Author(s):  
TOMASZ CHMIELEWSKI ◽  
STANISŁAWA TYLEWSKA-WIERZBANOWSKA
Keyword(s):  
Cell Death ◽  
Chronic Disease ◽  
Coxiella Burnetii ◽  
Caspase 3 ◽  
Bartonella Henselae ◽  
Tissue Homeostasis ◽  
Host Cells ◽  
Fibroblast Cells ◽  
Human Fibroblast Cells ◽  
Long Time

Apoptosis is a genetically controlled mechanism of cell death involved in the regulation of tissue homeostasis. The aim of this study was to investigate the influence of Borrelia afzelii, Coxiella burnetii, and Bartonella henselae bacteria on apoptosis measured as the level of caspase 3 activity in human fibroblast cells HEL-299. Our findings show that C. burnetii bacteria may inhibit the process of apoptosis in the host cells for a long time. This can permit intracellular survival in the host and mediatingthe development of chronic disease.

scholarly journals Autoantibodies from SLE patients induce programmed cell death in murine fibroblast cells through interaction with TNFR1 receptor

2020 ◽  
Vol 10 (1) ◽  
Author(s):  
Tatiana N. Sharapova ◽  
Elena A. Romanova ◽  
Natalia V. Soshnikova ◽  
Alexey A. Belogurov ◽  
Yakov A. Lomakin ◽  
...  
Keyword(s):  
Cell Death ◽  
Programmed Cell Death ◽  
Fibroblast Cells ◽  
Murine Fibroblast ◽  
Tnfr1 Receptor

Enhancement of gallic acid-induced human pulmonary fibroblast cell death by N-acetyl cysteine and L-buthionine sulfoximine

2010 ◽  
Vol 30 (8) ◽  
pp. 992-999 ◽  
Author(s):  
Bo Ra You ◽  
Woo Hyun Park
Keyword(s):  
Cell Death ◽  
Growth Inhibition ◽  
Gallic Acid ◽  
Buthionine Sulfoximine ◽  
Fibroblast Cell ◽  
Biological Properties ◽  
Dependent Manner ◽  
Toxicological Effect ◽  
Acetyl Cysteine ◽  
Pulmonary Fibroblast

Gallic acid (GA) has various biological properties including anti-cancer effect. However, little is known about the toxicological effect of GA in primary normal cells. Here, we evaluated the effects of GA on human pulmonary fibroblast (HPF) cells in relation to reactive oxygen species (ROS) and glutathione (GSH). GA inhibited the growth of HPF cells at 24 hours in a dose-dependent manner. GA also induced HPF cell death, which was accompanied by the loss of mitochondrial membrane potential (MMP; ΔΨm). GA increased ROS levels including O2•- and GSH-depleted cell numbers in HPF cells at 24 hours. Treatment with 2 mM N-acetyl-cysteine (NAC) intensified growth inhibition and death in GA-treated HPF cells. NAC decreased ROS levels and increased GSH depletion in these cells. Treatment with 10 μM L-buthionine sulfoximine (BSO) also enhanced growth inhibition and death in GA-treated HPF cells. BSO increased ROS levels and GSH depletion in these cells. In conclusion, GA-induced HPF cell death was accompanied by ROS increase and GSH depletion. The changes of ROS and GSH levels by NAC and BSO appeared to affect cell growth and death in GA-treated HPF cells.

scholarly journals Withaferin A Induces Cell Death Selectively in Androgen-Independent Prostate Cancer Cells but Not in Normal Fibroblast Cells

PLoS ONE ◽  
2015 ◽  
Vol 10 (7) ◽  
pp. e0134137 ◽  
Author(s):  
Yukihiro Nishikawa ◽  
Daisuke Okuzaki ◽  
Kohshiro Fukushima ◽  
Satomi Mukai ◽  
Shouichi Ohno ◽  
...  
Keyword(s):  
Prostate Cancer ◽  
Cell Death ◽  
Cancer Cells ◽  
Withaferin A ◽  
Normal Fibroblast ◽  
Fibroblast Cells ◽  
Prostate Cancer Cells ◽  
Androgen Independent
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