scholarly journals Identification of NRF2, a member of the NF-E2 family of transcription factors, as a substrate for caspase-3(-like) proteases

1999 ◽  
Vol 6 (9) ◽  
pp. 865-872 ◽  
Author(s):  
Tsuguteru Ohtsubo ◽  
Shinji Kamada ◽  
Toshiyuki Mikami ◽  
Hiroko Murakami ◽  
Yoshihide Tsujimoto
Keyword(s):  
Transcription Factors ◽  
Caspase 3

scholarly journals Lugol Increases Lipolysis through Upregulation of PPAR-Gamma and Downregulation of C/EBP-Alpha in Mature 3T3-L1 Adipocytes

2020 ◽  
Vol 2020 ◽  
pp. 1-9
Author(s):  
Cuellar-Rufino Sergio ◽  
Zepeda Rossana Citlali ◽  
Flores-Muñoz Mónica ◽  
Santiago-Roque Isela ◽  
Arroyo-Helguera Omar
Keyword(s):  
Transcription Factors ◽  
Culture Medium ◽  
Caspase 3 ◽  
Lethal Dose ◽  
Molecular Iodine ◽  
Ppar Gamma ◽  
Overweight And Obesity ◽  
Intracellular Lipid ◽  
Lugol Solution ◽  
Release Of Glycerol

Overweight and obesity are defined as excessive and abnormal fat accumulation that is harmful to health. This study analyzes the effect of different concentrations of the lugol solution (molecular iodine dissolved in potassium iodide) on lipolysis in cultured 3T3-L1-differentiated adipocytes. The mature adipocytes were treated with doses from 1 to 100 µm of lugol for 0.5, 6, and 24 h. The results showed that mature adipocytes exposed to lugol decrease their viability and increase caspase-3 activity with a lethal dose (LD50) of 473 µm. In mature adipocytes, lugol decreased the total intracellular lipid content, being significant at doses of 10 and 100 µm after 6 and 24 h of treatment (P<0.01), and the accumulation of intracellular triglycerides decreased after 24 h of exposure to lugol (P<0.05). Lugol treatment significantly increases the release of glycerol to the culture medium (P<0.05). The levels of adipocyte-specific transcription factors C/EBP-α were downregulated and PPAR-γ upregulated after 30 min with lugol. These results indicate a lipolytic effect of lugol dependent on PPAR-γ and C/EBP-α expression in mature 3T3-L1 adipocytes.

185 Directed Differentiation of Porcine Induced Pluripotent Stem Cells into all Three Germ Layers via Embryoid Body Formation

2018 ◽  
Vol 30 (1) ◽  
pp. 232
Author(s):  
W. Chakritbudsabong ◽  
S. Pamonsupornvichit ◽  
L. Sariya ◽  
R. Pronarkngver ◽  
S. Chaiwattanarungruengpaisan ◽  
...  
Keyword(s):  
Stem Cells ◽  
Transcription Factors ◽  
Induced Pluripotent Stem Cells ◽  
Cell Lines ◽  
Pluripotent Stem Cells ◽  
Caspase 3 ◽  
Embryoid Body ◽  
Germ Layers ◽  
Significant Difference ◽  
Induced Pluripotent

Human induced pluripotent stem cells (iPSC) have been generated by reprogramming somatic cells using a cocktail of stem cell transcription factors but the application has been limited in transplantation therapies. The pig represents an ideal model for human clinical research, in part because of its similarity to human physiology and immunology but also because of its use in assessing side effects in long-term preclinical studies. Porcine induced pluripotent stem cells (piPSC) have been established in many studies but their differentiation pattern has not been reported. The aim of this study was to estimate the efficiency and pattern of differentiated piPSC into all 3 germ layers using embryoid body (EB) formation. Two piPSC lines (VSMUi001-A and VSMUi001-D) were induced from porcine embryonic fibroblasts by retroviral overexpression of 5 human reprogramming transcription factors (OCT4, SOX2, KLF4, c-MYC, and LIN28). For EB formation, the piPSC were harvested by treating with TrypLE™ Select (Thermo Fisher Scientific, Waltham, MA, USA) and the cells were cultured in nonadherent 96-well plates in piPSC media without growth factors. Data are expressed as mean ± SEM of at least 3 independent experiments. Statistical analyses were evaluated with Student t-tests for comparison between the 2 cell lines. Statistical significance was set at a P-value of < 0.05. The percentages of EB formation, which were calculated as the number of wells containing EB on Day 3 of differentiation, were 95.3 ± 3.42 and 89.1 ± 5.34 (VSMUi001-A and VSMUi001-D, respectively). However, there was no significant difference between the percentages of EB formation derived from the 2 cell lines. For EB size measurement, 20 EB per experiment were taken after incubation for 3, 7, 14, and 21 days. Both EB sizes increased over time (average diameter of 238.1 ± 6.18, 297.9 ± 4.10, 438.6 ± 13.33, and 728.8 ± 24.92 mm from VSMUi001-A, and 255.8 ± 5.12, 357.9 ± 3.94, 459.6 ± 11.88, and 439.4 ± 20.31 mm from VSMUi001-D). Moreover, both EB displayed homogeneity in size and shape (Day 3, 7), exhibited a cystic structure (Day 14), and a vesicular cavity was present (Day 21). For immunohistochemical analysis, both EB had lower levels of cleaved caspase 3, a marker of apoptotic cells, on Day 3 but higher levels of cleaved caspase 3 from Day 7 through 21. On the contrary, EB showed higher levels of Ki67, a marker of proliferating cells, on Day 3 but lower levels of Ki67 on Days 7, 14, and 21, respectively. In gene expression assessment, EB exhibited ectoderm gene (NeuroD1), mesoderm genes (TNNT2 and TNNI1), and endoderm genes (SOX17 and Endolase) at Day 7 and 21 by using RT-PCR. In conclusion, we report the successful in vitro formation of cystic EB from 2 piPSC lines, indicating that the piPSC could differentiate into 3 germ layers. This will allow researchers to unveil the roadmap of molecular cues needed for piPSC differentiation. This research project is supported by grants from the Mahidol University, Thailand.

Expression of transcription factors c-Fos, c-Jun, CREB-1 and ATF-2, and caspase-3 in relation with abnormal tau deposits in Pick’s disease

2006 ◽  
Vol 111 (4) ◽  
pp. 341-350 ◽  
Author(s):  
María Nieto-Bodelón ◽  
Gabriel Santpere ◽  
Benjamín Torrejón-Escribano ◽  
Berta Puig ◽  
Isidre Ferrer
Keyword(s):  
Transcription Factors ◽  
Caspase 3 ◽  
Pick's Disease ◽  
Pick’S Disease

Androstenediol inhibits the trauma-hemorrhage-induced increase in caspase-3 by downregulating the inducible nitric oxide synthase pathway

2007 ◽  
Vol 102 (3) ◽  
pp. 933-941 ◽  
Author(s):  
Juliann G. Kiang ◽  
Russell M. Peckham ◽  
Leah E. Duke ◽  
Tomoharu Shimizu ◽  
Irshad H. Chaudry ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Transcription Factors ◽  
Nitric Oxide Synthase ◽  
Inducible Nitric Oxide Synthase ◽  
Caspase 3 ◽  
Molecular Events ◽  
Tissue Trauma ◽  
Oxide Synthase ◽  
Interfering Rna ◽  
Inducible Nitric Oxide

Soft tissue trauma and hemorrhage (T-H) diminishes various aspects of liver function, while it increases hepatic nitrate/nitrite, inducible nitric oxide synthase (iNOS), and endothelin-1 levels. Treatment with androstenediol (AED) inhibits the T-H-induced alterations of the above parameters. We sought to identify the molecular events underlying the beneficial effect of AED. Exposure of rats to T-H significantly increased the caspase-3 activity and protein, whereas treatment with AED significantly limited these increases. AED treatment also suppressed the T-H-induced increase in iNOS by effectively altering the levels of key transcription factors involved in the regulation of iNOS expression. Immunoprecipitation and immunoblotting analyses indicate that T-H increased apoptosome formation, and AED treatment significantly decreased it. Modulating the iNOS protein by transfecting cells with iNOS gene or small interfering RNA further confirmed the correlation between iNOS and caspase-3. Our data indicate that AED limits caspase-3 expression by suppressing the expression of transcription factors involved in the production of iNOS, resulting in decreased apoptosome. AED can potentially be a useful adjuvant for limiting liver apoptosis following T-H shock.

scholarly journals Oxidative Stress Activates the Transcription Factors FoxO 1a and FoxO 3a in the Hippocampus of Rats Exposed to Low Doses of Ozone

2014 ◽  
Vol 2014 ◽  
pp. 1-8 ◽  
Author(s):  
Nancy P. Gómez-Crisóstomo ◽  
Erika Rodríguez Martínez ◽  
Selva Rivas-Arancibia
Keyword(s):  
Oxidative Stress ◽  
Cell Cycle ◽  
Transcription Factors ◽  
Caspase 3 ◽  
Low Doses ◽  
Cyclin D2 ◽  
Regulatory Pathways ◽  
Forkhead Box ◽  
Male Wistar Rats ◽  
Active Caspase

The exposure to low doses of ozone induces an oxidative stress state, which is involved in neurodegenerative diseases. Forkhead box O (FoxO) family of transcription factors are activated by oxidative signals and regulate cell proliferation and resistance to oxidative stress. Our aim was to study the effect of chronic exposure to ozone on the activation of FoxO 1a and FoxO 3a in the hippocampus of rats. Male Wistar rats were divided into six groups and exposed to 0.25 ppm of ozone for 0, 7, 15, 30, 60, and 90 days. After treatment, the groups were processed for western blotting and immunohistochemistry against FoxO 3a, Mn SOD, cyclin D2, FoxO 1a, and active caspase 3. We found that exposure to ozone increased the activation of FoxO 3a at 30 and 60 days and expression of Mn SOD at all treatment times. Additionally, increases in cyclin D2 from 7 to 90 days; FoxO 1a at 15, 30, and 60 days; and activate caspase 3 from 30 to 60 days of exposure were noted. The results indicate that ozone alters regulatory pathways related to both the antioxidant system and the cell cycle, inducing neuronal reentry into the cell cycle and apoptotic death.

Regulation of caspase-3 and -9 activation in oxidant stress to RTE by forkhead transcription factors, Bcl-2 proteins, and MAP kinases

2004 ◽  
Vol 287 (6) ◽  
pp. F1258-F1268 ◽  
Author(s):  
Gur P. Kaushal ◽  
Ling Liu ◽  
Varsha Kaushal ◽  
Xiaoman Hong ◽  
Oksana Melnyk ◽  
...  
Keyword(s):  
Cell Death ◽  
Transcription Factors ◽  
Family Member ◽  
Caspase 3 ◽  
Oxidant Stress ◽  
Caspase Activation ◽  
Oxidant Injury ◽  
Kinase Inhibition ◽  
Forkhead Transcription Factors ◽  
The Impact

Cytotoxicity to renal tubular epithelial cells (RTE) is dependent on the relative response of cell survival and cell death signals triggered by the injury. Forkhead transcription factors, Bcl-2 family member Bad, and mitogen-activated protein kinases are regulated by phosphorylation that plays crucial roles in determining cell fate. We examined the role of phosphorylation of these proteins in regulation of H2O2-induced caspase activation in RTE. The phosphorylation of FKHR, FKHRL, and Bcl-2 family member Bad was markedly increased in response to oxidant injury, and this increase was associated with elevated levels of basal phosphorylation of Akt/protein kinase B. Phosphoinositol (PI) 3-kinase inhibitors abolished this phosphorylation and also decreased expression of antiapoptotic proteins Bcl-2 and BclxL. Inhibition of phosphorylation of forkhead proteins resulted in a marked increase in the proapoptotic protein Bim. These downstream effects of PI 3-kinase inhibition promoted the oxidant-induced activation of caspase-3 and -9, but not caspase-8 and -1. The impact of enhanced activation of caspases by PI 3-kinase inhibition was reflected on accelerated oxidant-induced cell death. Oxidant stress also induced marked phosphorylation of ERK1/2, P38, and JNK kinases. Inhibition of ERK1/2 phosphorylation but not P38 and JNK kinase increased caspase-3 and -9 activation; however, this activation was far less than induced by inhibition of Akt phosphorylation. Thus the Akt-mediated phosphorylation pathway, ERK signaling, and the antiapoptotic Bcl-2 proteins distinctly regulate caspase activation during oxidant injury to RTE. These studies suggest that enhancing renal-specific survival signals may lead to preservation of renal function during oxidant injury.

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