scholarly journals Zinc finger protein 667 expression is upregulated by cerebral ischemic preconditioning and protects cells from oxidative stress

2013 ◽  
Vol 1 (4) ◽  
pp. 534-538 ◽  
Author(s):  
DUN YUAN ◽  
JUN HUANG ◽  
XIANRUI YUAN ◽  
JIE ZHAO ◽  
WEIXI JIANG
Keyword(s):  
Oxidative Stress ◽  
Zinc Finger ◽  
Ischemic Preconditioning ◽  
Zinc Finger Protein ◽  
Finger Protein ◽  
Cerebral Ischemic ◽  
Cerebral Ischemic Preconditioning

MCP-1 causes cardiomyoblast death via autophagy resulting from ER stress caused by oxidative stress generated by inducing a novel zinc-finger protein, MCPIP

2010 ◽  
Vol 426 (1) ◽  
pp. 43-53 ◽  
Author(s):  
Craig W. Younce ◽  
Pappachan E. Kolattukudy
Keyword(s):  
Oxidative Stress ◽  
Heart Failure ◽  
Cell Death ◽  
Er Stress ◽  
Zinc Finger ◽  
Zinc Finger Protein ◽  
Beclin 1 ◽  
Finger Protein ◽  
Caspase 2 ◽  
Specific Inhibitors

MCP-1 (monocyte chemotactic protein-1) plays a critical role in the development of heart failure that is known to involve apoptosis. How MCP-1 contributes to cell death involved in the development of heart disease is not understood. In the present study we show that MCP-1 causes death in cardiac myoblasts, H9c2 cells, by inducing oxidative stress which causes ER stress leading to autophagy via a novel zinc-finger protein, MCPIP (MCP-1-induced protein). MCPIP expression caused cell death, and knockdown of MCPIP attenuated MCP-1induced cell death. It caused induction of iNOS (inducible NO synthase), translocation of the NADPH oxidase subunit phox47 from the cytoplasm to the membrane, production of ROS (reactive oxygen species), and induction of ER (endoplasmic reticulum) stress markers HSP40 (heat-shock protein 40), PDI (protein disulfide-isomerase), GRP78 (guanine-nucleotide-releasing protein 78) and IRE1α (inositol-requiring enzyme 1α). It also caused autophagy, as indicated by beclin-1 induction, cleavage of LC3 (microtubule-associated protein 1 light chain 3) and autophagolysosome formation, and apoptosis, as indicated by caspase 3 activation and TUNEL (terminal deoxynucleotidyltransferase-mediated dUTP nick-end labelling) assay. Inhibitors of oxidative stress, including CeO2 nanoparticles, inhibited ROS formation, ER stress, autophagy and cell death. Specific inhibitors of ER stress inhibited autophagy and cell death as did knockdown of the ER stress signalling protein IRE1. Knockdown of beclin-1 and autophagy inhibitors prevented cell death. This cell death involved caspase 2 and caspase 12, as specific inhibitors of these caspases prevented MCPIP-induced cell death. Microarray analysis showed that MCPIP expression caused induction of a variety of genes known to be involved in cell death. MCPIP caused activation of JNK (c-Jun N-terminal kinase) and p38 and induction of p53 and PUMA (p53 up-regulated modulator of apoptosis). Taken together, these results suggest that MCPIP induces ROS/RNS (reactive nitrogen species) production that causes ER stress which leads to autophagy and apoptosis through caspase 2/12 and IRE1α–JNK/p38–p53–PUMA pathway. These results provide the first molecular insights into the mechanism by which elevated MCP-1 levels associated with chronic inflammation may contribute to the development of heart failure.

scholarly journals Roles of Zinc Finger Protein 423 in Proliferation and Invasion of Cholangiocarcinoma through Oxidative Stress

Biomolecules ◽  
2019 ◽  
Vol 9 (7) ◽  
pp. 263
Author(s):  
Timpika Chaiprasert ◽  
Napat Armartmuntree ◽  
Anchalee Techasen ◽  
Chadamas Sakonsinsiri ◽  
Somchai Pinlaor ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Cell Lines ◽  
Zinc Finger ◽  
Zinc Finger Protein ◽  
Expression Patterns ◽  
Immunohistochemical Analysis ◽  
Oxidative Stress Marker ◽  
Finger Protein ◽  
Hydrogen Peroxide Treatment ◽  
Proliferation And Invasion

Zinc finger protein 423 (ZNF423) is a transcriptional factor involved in the development and progression of cancers but has not yet been examined in cholangiocarcinoma (CCA), an oxidative stress-driven cancer of biliary epithelium. In this study, we hypothesized that oxidative stress mediated ZNF423 expression regulates its downstream genes resulting in CCA genesis. ZNF423 protein expression patterns and 8-oxodG (an oxidative stress marker) formation in CCA tissues were investigated using immunohistochemical analysis. The results showed that ZNF423 was overexpressed in CCA cells compared to normal bile duct cells adjacent of the tumor. Notably, ZNF423 expression was positively correlated with 8-oxodG formation. Moreover, ZNF423 expression in an immortalized cholangiocyte cell line (MMNK1) was increased by hydrogen peroxide-treatment, suggesting that oxidative stress induces ZNF423 expression. To investigate the roles of ZNF423 in CCA progression, ZNF423 mRNA was silenced using specific siRNA in CCA cell lines, KKU-100 and KKU-213. Silencing of ZNF423 significantly inhibits cell proliferation and invasion of both CCA cell lines. Taking all these results together, the present study denoted that ZNF423 is an oxidative stress-responsive gene with an oncogenic property contributing to the regulation of CCA genesis.

scholarly journals Specificity protein 1-zinc finger protein 179 pathway is involved in the attenuation of oxidative stress following brain injury

Redox Biology ◽  
2017 ◽  
Vol 11 ◽  
pp. 135-143 ◽  
Author(s):  
Jian-Ying Chuang ◽  
Tzu-Jen Kao ◽  
Shu-Hui Lin ◽  
An-Chih Wu ◽  
Pin-Tse Lee ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Brain Injury ◽  
Zinc Finger ◽  
Zinc Finger Protein ◽  
Specificity Protein 1 ◽  
Finger Protein ◽  
Specificity Protein

scholarly journals Lycopersicon Eculentum C2H2-type Zinc Finger Protein Induced by Oxidative Stress Especially

2007 ◽  
Vol 34 (3) ◽  
pp. 167-172 ◽  
Author(s):  
Eun-Soo Seong ◽  
Ji-Yeon Lee ◽  
Chang-Yeon Yu ◽  
Deok-Chun Yang ◽  
Seok-Hyun Eom ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Zinc Finger ◽  
Zinc Finger Protein ◽  
Finger Protein
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