Identification of an Apis cerana zinc finger protein 41 gene and its involvement in the oxidative stress response

2021 ◽  
Author(s):  
Hui‐juan Guo ◽  
Li‐jun Wang ◽  
Chen Wang ◽  
De‐zheng Guo ◽  
Bao‐hua Xu ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Stress Response ◽  
Zinc Finger ◽  
Zinc Finger Protein ◽  
Apis Cerana ◽  
Oxidative Stress Response ◽  
Finger Protein

scholarly journals Molecular cloning, expression and oxidative stress response of the vitellogenin Gene (AccVg) from Apis cerana cerana

Apidologie ◽  
2017 ◽  
Vol 48 (5) ◽  
pp. 599-611 ◽  
Author(s):  
Weixing Zhang ◽  
Zhenguo Liu ◽  
Ming Zhu ◽  
Lanting Ma ◽  
Ying Wang ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Stress Response ◽  
Molecular Cloning ◽  
Apis Cerana ◽  
Oxidative Stress Response ◽  
Apis Cerana Cerana ◽  
Vitellogenin Gene ◽  
And Oxidative Stress

A putative maize zinc-finger protein gene, ZmAN13, participates in abiotic stress response

2011 ◽  
Vol 107 (1) ◽  
pp. 101-112 ◽  
Author(s):  
Ning Xuan ◽  
Ying Jin ◽  
Hongwei Zhang ◽  
Yuanhong Xie ◽  
Yunjun Liu ◽  
...  
Keyword(s):  
Abiotic Stress ◽  
Stress Response ◽  
Zinc Finger ◽  
Protein Gene ◽  
Zinc Finger Protein ◽  
Abiotic Stress Response ◽  
Zinc Finger Protein Gene ◽  
Finger Protein

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.

Sign in / Sign up

Export Citation Format

Share Document