scholarly journals Expression of Endoplasmic Reticulum Stress-Related Factors in the Retinas of Diabetic Rats

2012 ◽  
Vol 2012 ◽  
pp. 1-11 ◽  
Author(s):  
Shu Yan ◽  
Cui Zheng ◽  
Zhi-qi Chen ◽  
Rong Liu ◽  
Gui-gang Li ◽  
...  
Keyword(s):  
Endoplasmic Reticulum ◽  
Endoplasmic Reticulum Stress ◽  
Western Blot ◽  
Er Stress ◽  
Diabetic Rats ◽  
Stress Factors ◽  
Diabetic Rat ◽  
Related Factors ◽  
Diabetes Model ◽  
Polymerase Chain

Recent reports show that ER stress plays an important role in diabetic retinopathy (DR), but ER stress is a complicated process involving a network of signaling pathways and hundreds of factors, What factors involved in DR are not yet understood. We selected 89 ER stress factors from more than 200, A rat diabetes model was established by intraperitoneal injection of streptozotocin (STZ). The expression of 89 ER stress-related factors was found in the retinas of diabetic rats, at both 1- and 3-months after development of diabetes, by quantitative real-time polymerase chain reaction arrays. There were significant changes in expression levels of 13 and 12 ER stress-related factors in the diabetic rat retinas in the first and third month after the development of diabetes, Based on the array results, homocysteine- inducible, endoplasmic reticulum stress-inducible, ubiquitin-like domain member 1(HERP), and synoviolin(HRD1) were studied further by immunofluorescence and Western blot. Immunofluorescence and Western blot analyses showed that the expression of HERP was reduced in the retinas of diabetic rats in first and third month. The expression of Hrd1 did not change significantly in the retinas of diabetic rats in the first month but was reduced in the third month.

Testicular Injury Attenuated by Rapamycin Through Induction of Autophagy and Inhibition of Endoplasmic Reticulum Stress in Streptozotocin- Induced Diabetic Rats

2019 ◽  
Vol 19 (5) ◽  
pp. 665-675 ◽  
Author(s):  
Wenjiao Shi ◽  
Zhixin Guo ◽  
Ruixia Yuan
Keyword(s):  
Oxidative Stress ◽  
Endoplasmic Reticulum ◽  
Endoplasmic Reticulum Stress ◽  
Protective Effect ◽  
Er Stress ◽  
B Cell Lymphoma ◽  
Diabetic Rats ◽  
Pathological Changes ◽  
Rapamycin Treatment ◽  
Related Proteins

Background and Objective: This study investigated whether rapamycin has a protective effect on the testis of diabetic rats by regulating autophagy, endoplasmic reticulum stress, and oxidative stress. Methods: Thirty male Sprague-Dawley rats were randomly divided into three groups: control, diabetic, and diabetic treated with rapamycin, which received gavage of rapamycin (2mg.kg-1.d-1) after induction of diabetes. Diabetic rats were induced by intraperitoneal injection of streptozotocin (STZ, 65mg.Kg-1). All rats were sacrificed at the termination after 8 weeks of rapamycin treatment. The testicular pathological changes were determined by hematoxylin and eosin staining. The protein or mRNA expression of autophagy-related proteins (Beclin1, microtubule-associated protein light chain 3 (LC3), p62), ER stress marked proteins (CCAAT/enhancer-binding protein (C/EBP) homologous protein (CHOP), caspase-12), oxidative stress-related proteins (p22phox, nuclear factor erythroid2-related factor 2 (Nrf2)) and apoptosis-related proteins (Bax, B cell lymphoma-2 (Bcl-2)) were assayed by western blot or real-time fluorescence quantitative PCR. Results: There were significant pathological changes in the testes of diabetic rats. The expression of Beclin1, LC3, Nrf2, Bcl-2 were significantly decreased and p62, CHOP, caspase12, p22phox, and Bax were notably increased in the testis of diabetic rats (P <0.05). However, rapamycin treatment for 8 weeks significantly reversed the above changes in the testis of diabetic rats (P <0.05). Conclusion: Rapamycin appears to produce a protective effect on the testes of diabetic rats by inducing the expression of autophagy and inhibiting the expression of ER-stress, oxidative stress, and apoptosis.

scholarly journals Exploring the Differential Gene of CHOP-Related Factors in Hepatocellular Injury Caused by Endoplasmic Reticulum Stress

2021 ◽  
Author(s):  
Leng-xin Duan ◽  
Man-lin Guo ◽  
Xiang-yu Ma ◽  
Yu-qing Gong ◽  
San-qiang Li
Keyword(s):  
Endoplasmic Reticulum ◽  
Endoplasmic Reticulum Stress ◽  
Er Stress ◽  
Cell Receptor ◽  
Differentially Expressed ◽  
Lipocalin 2 ◽  
Hepatocellular Injury ◽  
Chromosome 11 ◽  
Gamma Chain ◽  
Related Factors

Abstract Objective: CCAAT/enhancer-binding protein (C/EBP) homologous protein (CHOP/DDIT3) is a protein activated by endoplasmic reticulum stress (ERS). However, the downstream genes of CHOP on liver damage caused by ER-stress have been unclear. Herein, we investigated the potential downstream related factors of CHOP in L-02 cells.Methods and Material: Tunicamycin (TM) was used to induce ER-stress. Short hairpin RNA (shRNA) was used to knocked down CHOP, and the functions of differentially expressed genes (DEGs) were obtained from functional annotations. qRT-PCR was employed to validate the expression levels of candidate DEGs.Results: 633 genes were differentially expressed between ERS L-02 cells and normal L-02 cells，and 131 genes were differentially expressed between shRNA-CHOP and shRNA-NC in ERS L-02 cells. By analyze these results, we luckily found 8 genes including Interferon a-inducible protein 27 (IFI27), Lipocalin 2 (LCN2), Chromosome 11 Open Reading Frame 86 (C11orf86), Calmegin (CLGN), Kelch domain- containing 7B (KLHDC7B), Niban Apoptosis Regulator 1 (Niban), T-Cell Receptor Gamma- Chain Constant Region (TARP), Lysosome associated membrane protein 3 (LAMP3) were intimately related to chop. Conclusion: Our study might contribute to better understand how CHOP functions during ER-stress, and these results can expand databases of CHOP in GenBank or others.

scholarly journals SWCNH (Single walled carbon nanohorn) supervises ER (Endoplasmic reticulum) stress through triggering autophagy process of hepatocytes, especially in hepatoma cell line HepG2

2021 ◽  
Author(s):  
Jinling Dong ◽  
Ying Zhang ◽  
Zhihong Xie ◽  
Jie He ◽  
Tiantian Wu
Keyword(s):  
Endoplasmic Reticulum ◽  
Endoplasmic Reticulum Stress ◽  
Western Blot ◽  
Er Stress ◽  
Cell Line ◽  
Cell Apoptosis ◽  
Hepatoma Cell ◽  
Hepatoma Cell Line ◽  
Catabolic Pathway ◽  
Hepatoma Cell Line Hepg2

Abstract Backgrounds: The cellular homeostasis is major maintained by the catabolic pathway of autophagy. Our previous work indicated that SWCNH were associated with endoplasmic reticulum (ER) stress mediated by calcium flow and autophagic response. But, its mechanism was unclear. Methods: The regulation of SWCNH on the calcium flow then autophagy of liver cells were investigated through inducing ER stress with tunicamycin and SWCNH. The calcuim flow was determined using Fluo-3, then autophagy was examined with immunofluorescence or western blot for LC3, Beclin-1, ATG-5, and p62. Moreover, the apopototic protein of Bax and Bcl-2 was detected, too. Results: Tunicamycin-induced ER stress in hepatocytes was related to calcium flow, especially for hepatoma cell line HepG2. Moreover, SWCNH participated in the regulation of endoplasmic reticulum stress-related calcium flow. Besides, SWCNH induced hepatocyte autophagy and inhibited cell apoptosis, then mediated the process of hepatocyte autophagy. Conclusions: Tunicamycin-induced ER stress in hepatocytes was related to calcium flow. Moreover, SWCNH induced hepatocyte autophagy, inhibited cell apoptosis, and participated in the autophagy regulation of hepatocyte, especially for hepatoma cell line.

scholarly journals Effects of Apoptin-Induced Endoplasmic Reticulum Stress on Lipid Metabolism, Migration, and Invasion of HepG-2 Cells

2021 ◽  
Vol 11 ◽  
Author(s):  
Yilong Zhu ◽  
Yiquan Li ◽  
Bing Bai ◽  
Chao Shang ◽  
Jinbo Fang ◽  
...  
Keyword(s):  
Endoplasmic Reticulum ◽  
Lipid Metabolism ◽  
Endoplasmic Reticulum Stress ◽  
Western Blot ◽  
Er Stress ◽  
Blot Analysis ◽  
Western Blot Analysis ◽  
Migration And Invasion ◽  
Expression Levels

In this study, we investigated the effects of Apoptin-induced endoplasmic reticulum (ER) stress on lipid metabolism, migration and invasion of HepG-2 cells, and preliminarily explored the relationship between endoplasmic reticulum stress, lipid metabolism, migration, and invasion. The effects of Apoptin on ER function and structure in HepG-2 cells were determined by flow cytometry, fluorescence staining and western blotting by assessing the expression levels of ER stress related proteins. The effects of Apoptin on HepG-2 cells’ lipid metabolism were determined by western blot analysis of the expression levels of triglyceride, cholesterol, and lipid metabolism related enzymes. The effects of Apoptin on HepG-2 cells’ migration and invasion were studied using migration and invasion assays and by Western-blot analysis of the expression of proteins involved in migration and invasion. The in vivo effects of endoplasmic reticulum stress on lipid metabolism, migration and invasion of HepG-2 cells were also investigated by immunohistochemistry analysis of tumor tissues from HepG2 cells xenografted nude mice models. Both in vitro and in vivo experiments showed that Apoptin can cause a strong and lasting ER stress response, damage ER functional structure, significantly change the expression levels of lipid metabolism related enzymes and reduce the migration and invasion abilities of HepG-2 cells. Apoptin can also affect HepG-2 cells’ lipid metabolism through endoplasmic reticulum stress and the abnormal expression of enzymes closely related to tumor migration and invasion. These results also showed that lipid metabolism may be one of the main inducements that reduce HepG-2 cells’ migration and invasion abilities.

scholarly journals Endoplasmic reticulum stress is involved in myocardial apoptosis of streptozocin-induced diabetic rats

2007 ◽  
Vol 196 (3) ◽  
pp. 565-572 ◽  
Author(s):  
Zhenhua Li ◽  
Tao Zhang ◽  
Hongyan Dai ◽  
Guanghui Liu ◽  
Haibin Wang ◽  
...  
Keyword(s):  
Endoplasmic Reticulum ◽  
Endoplasmic Reticulum Stress ◽  
Diabetic Cardiomyopathy ◽  
Critical Role ◽  
Diabetic Rats ◽  
Diabetic Heart ◽  
Terminal Deoxynucleotidyl Transferase ◽  
Diabetic Rat ◽  
Mrna Levels ◽  
Diabetic Myocardium

Apoptosis plays a critical role in the diabetic cardiomyopathy, and endoplasmic reticulum stress (ERS) is one of the intrinsic apoptosis pathways. Previous studies have shown that the endoplasmic reticulum becomes swollen and dilated in diabetic myocardium, and ERS is involved in heart failure and diabetic kidney. This study is aimed to demonstrate whether ERS is induced in myocardium of streptozotocin (STZ)-induced diabetic rats. We established a type 1 diabetic rat model, used echocardiographic evaluation, hematoxylin–eosin staining, and the terminal deoxynucleotidyl transferase-mediated DNA nick-end labeling staining to identify the existence of diabetic cardiomyopathy and enhanced apoptosis in the diabetic heart. We performed immunohistochemistry, western blot, and real-time PCR to analyze the hallmarks of ERS that include glucose-regulated protein 78, CCAAT/enhancer-binding protein homologous protein (CHOP) and caspase12. We found these hallmarks to have enhanced expression in protein and mRNA levels in diabetic myocardium. Also, another pathway that can lead to cell death of ERS, c-Jun NH2-terminal kinase-dependent pathway, was also activated in diabetic heart. Those results suggested that ERS was induced in STZ-induced diabetic rats' myocardium, and ERS-associated apoptosis occurred in the pathophysiology of diabetic cardiomyopathy.

scholarly journals Different Expression of Mitochondrial and Endoplasmic Reticulum Stress Genes in Epicardial Adipose Tissue Depends on Coronary Atherosclerosis

2021 ◽  
Vol 22 (9) ◽  
pp. 4538
Author(s):  
Helena Kratochvílová ◽  
Miloš Mráz ◽  
Barbora J. Kasperová ◽  
Daniel Hlaváček ◽  
Jakub Mahrík ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Endoplasmic Reticulum ◽  
Adipose Tissue ◽  
Cardiac Surgery ◽  
Endoplasmic Reticulum Stress ◽  
Er Stress ◽  
Mrna Expression ◽  
Coronary Atherosclerosis ◽  
Stress Genes ◽  
Valvular Surgery

The aim of our study was to analyze mitochondrial and endoplasmic reticulum (ER) gene expression profiles in subcutaneous (SAT) and epicardial (EAT) adipose tissue, skeletal muscle, and myocardium in patients with and without CAD undergoing elective cardiac surgery. Thirty-eight patients, 27 with (CAD group) and 11 without CAD (noCAD group), undergoing coronary artery bypass grafting and/or valvular surgery were included in the study. EAT, SAT, intercostal skeletal muscle, and right atrium tissue and blood samples were collected at the start and end of surgery; mRNA expression of selected mitochondrial and ER stress genes was assessed using qRT-PCR. The presence of CAD was associated with decreased mRNA expression of most of the investigated mitochondrial respiratory chain genes in EAT, while no such changes were seen in SAT or other tissues. In contrast, the expression of ER stress genes did not differ between the CAD and noCAD groups in almost any tissue. Cardiac surgery further augmented mitochondrial dysfunction in EAT. In our study, CAD was associated with decreased expression of mitochondrial, but not endoplasmic reticulum stress genes in EAT. These changes may contribute to the acceleration of coronary atherosclerosis.

Phosphocreatine attenuates endoplasmic reticulum stress-mediated hepatocellular apoptosis ameliorates insulin resistance in diabetes model

2018 ◽  
Vol 506 (3) ◽  
pp. 611-618 ◽  
Author(s):  
Yazeed Jamalat ◽  
Yaser Gamallat ◽  
Pires Sanches Jaceline Gislaine ◽  
Abdo Meyiah ◽  
Abdullah Shopit ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Endoplasmic Reticulum ◽  
Endoplasmic Reticulum Stress ◽  
Diabetes Model ◽  
Hepatocellular Apoptosis

scholarly journals RHBDL4 protects against endoplasmic reticulum stress by regulating the morphology and distribution of ER sheets

2021 ◽  
Author(s):  
Viorica Liebe Lastun ◽  
Matthew Freeman
Keyword(s):  
Cell Cycle ◽  
Endoplasmic Reticulum ◽  
Endoplasmic Reticulum Stress ◽  
Er Stress ◽  
Liver Steatosis ◽  
Physiological Role ◽  
Cell Types ◽  
Rhomboid Protease ◽  
Rapid Changes

In metazoans, the architecture of the endoplasmic reticulum (ER) differs between cell types, and undergoes major changes through the cell cycle and according to physiological needs. Although much is known about how the different ER morphologies are generated and maintained, especially the ER tubules, how context dependent changes in ER shape and distribution are regulated and the factors involved are less characterized. Here, we show that RHBDL4, an ER-resident rhomboid protease, modulates the shape and distribution of the ER, especially under conditions that require rapid changes in the ER sheet distribution, including ER stress. RHBDL4 interacts with CLIMP-63, a protein involved in ER sheet stabilisation, and with the cytoskeleton. Mice lacking RHBDL4 are sensitive to ER stress and develop liver steatosis, a phenotype associated with unresolved ER stress. Our data introduce a new physiological role of RHBDL4 and also imply that this function does not require its enzymatic activity.

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