scholarly journals Sustained Endoplasmic Reticulum Stress as a Cofactor of Oxidative Stress in Decidual Cells from Patients with Early Pregnancy Loss

2011 ◽  
Vol 96 (3) ◽  
pp. E493-E497 ◽  
Author(s):  
Ai-Xia Liu ◽  
Wei-Hua He ◽  
Li-Jun Yin ◽  
Ping-Ping Lv ◽  
Yu Zhang ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Endoplasmic Reticulum ◽  
Er Stress ◽  
Early Pregnancy ◽  
Pregnancy Loss ◽  
Redox Status ◽  
Early Pregnancy Loss ◽  
Decidual Cells ◽  
Failed Induction ◽  
Induced Apoptosis

Background: Oxidative stress is a common pathological background for different etiologies of early pregnancy loss (EPL). It has been suggested that elevated reactive oxygen species trigger endoplasmic reticulum (ER) stress by influencing ER function. However, it is unclear whether ER stress is associated with EPL. Objectives: The aim of the study was to determine whether and how ER stress occurs during the development of EPL. Approaches: Proteomic analysis was performed on decidua from women with EPL, and then ER stress markers, redox status, apoptotic features, and cell viability were analyzed in EPL decidual cells (DCs). Results: EPL decidua were characterized by decreased levels of glucose-regulated protein 78 (GPR78) and valosin-containing protein and burdened with ubiquitinated proteins. Evidence of ER stress-induced apoptosis in EPL DCs was demonstrated by extensive dilation of ER, morphological features of apoptosis, and activation of caspase-4 and caspase-12. Furthermore, H2O2 reduced the viabilities in both EPL and control DCs, whereas EPL DCs were more vulnerable to additional OS challenge than the controls as a result of failed induction of GRP78 expression. The cell survival percentages of DCs were dose-dependently reduced by H2O2 and could be reversed in the presence of vitamin E. This effect was partly mediated by reducing the amount of misfolded proteins rather than regulating GRP78 expression. Conclusions: The sum of these observations demonstrate for the first time that sustained ER stress occurs in EPL DCs and the potentially vicious relationship between ER stress and oxidative stress is likely to play an important role in the development of EPL.

scholarly journals Sustained Endoplasmic Reticulum Stress as a Cofactor of Oxidative Stress in Decidual Cells from Patients with Early Pregnancy Loss

Endocrinology ◽  
2011 ◽  
Vol 152 (1) ◽  
pp. 333-333
Author(s):  
Ai-Xia Liu ◽  
Wei-Hua He ◽  
Li-Jun Yin ◽  
Ping-Ping Lv ◽  
Yu Zhang ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Endoplasmic Reticulum ◽  
Er Stress ◽  
Early Pregnancy ◽  
Pregnancy Loss ◽  
Redox Status ◽  
Early Pregnancy Loss ◽  
Decidual Cells ◽  
Failed Induction ◽  
Induced Apoptosis

Background: Oxidative stress (OS) is a common pathological background for different etiologies of early pregnancy loss (EPL). It has been suggested that elevated reactive oxygen species trigger endoplasmic reticulum (ER) stress by influencing ER function. However, it is unclear whether ER stress is associated with EPL. Objectives: The aim of the study was to determine whether and how ER stress occurs during the development of EPL. Approaches: Proteomic analysis was performed on decidua from women with EPL, and then ER stress markers, redox status, apoptotic features, and cell viability were analyzed in EPL decidual cells (DCs). Results: EPL decidua were characterized by decreased levels of glucose-regulated protein 78 (GPR78) and valosin-containing protein and burdened with ubiquitinated proteins. Evidence of ER stress-induced apoptosis in EPL DCs was demonstrated by extensive dilation of ER, morphological features of apoptosis, and activation of caspase-4 and caspase-12. Furthermore, H2O2 reduced the viabilities in both EPL and control DCs, whereas EPL DCs were more vulnerable to additional OS challenge than the controls as a result of failed induction of GRP78 expression. The cell survival percentages of DCs were dose-dependently reduced by H2O2 and could be reversed in the presence of vitamin E. This effect was partly mediated by reducing the amount of misfolded proteins rather than regulating GRP78 expression. Conclusions: The sum of these observations demonstrate for the first time that sustained ER stress occurs in EPL DCs and the potentially vicious relationship between ER stress and OS is likely to play an important role in the development of EPL.

Endoplasmic reticulum stress induced by oxidative stress in decidual cells: a possible mechanism of early pregnancy loss

2012 ◽  
Vol 39 (9) ◽  
pp. 9179-9186 ◽  
Author(s):  
Hui-Juan Gao ◽  
Yi-Min Zhu ◽  
Wei-Hua He ◽  
Ai-Xia Liu ◽  
Min-Yue Dong ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Endoplasmic Reticulum ◽  
Endoplasmic Reticulum Stress ◽  
Early Pregnancy ◽  
Pregnancy Loss ◽  
Early Pregnancy Loss ◽  
Decidual Cells

scholarly journals Sustained Endoplasmic Reticulum Stress as a Cofactor of Oxidative Stress in Decidual Cells from Patients with Early Pregnancy Loss

2011 ◽  
Vol 25 (1) ◽  
pp. 196-196
Author(s):  
Ai-Xia Liu ◽  
Wei-Hua He ◽  
Li-Jun Yin ◽  
Ping-Ping Lv ◽  
Yu Zhang ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Endoplasmic Reticulum ◽  
Endoplasmic Reticulum Stress ◽  
Early Pregnancy ◽  
Pregnancy Loss ◽  
Early Pregnancy Loss ◽  
Decidual Cells

scholarly journals Activation of endoplasmic reticulum stress mediates oxidative stress–induced apoptosis of granulosa cells in ovaries affected by endometrioma

2019 ◽  
Vol 26 (1) ◽  
pp. 40-52 ◽  
Author(s):  
Chisato Kunitomi ◽  
Miyuki Harada ◽  
Nozomi Takahashi ◽  
Jerilee M K Azhary ◽  
Akari Kusamoto ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Endoplasmic Reticulum ◽  
Er Stress ◽  
Granulosa Cells ◽  
Ovarian Function ◽  
Stress Sensor ◽  
Local Factor ◽  
High Oxidative Stress ◽  
Induced Apoptosis ◽  
Sensor Proteins

Abstract Endometriosis exerts detrimental effects on ovarian physiology and compromises follicular health. Granulosa cells from patients with endometriosis are characterized by increased apoptosis, as well as high oxidative stress. Endoplasmic reticulum (ER) stress, a local factor closely associated with oxidative stress, has emerged as a critical regulator of ovarian function. We hypothesized that ER stress is activated by high oxidative stress in granulosa cells in ovaries with endometrioma and that this mediates oxidative stress–induced apoptosis. Human granulosa-lutein cells (GLCs) from patients with endometrioma expressed high levels of mRNAs associated with the unfolded protein response (UPR). In addition, the levels of phosphorylated ER stress sensor proteins, inositol-requiring enzyme 1 (IRE1) and double-stranded RNA-activated protein kinase-like ER kinase (PERK), were elevated in granulosa cells from patients with endometrioma. Given that ER stress results in phosphorylation of ER stress sensor proteins and induces UPR factors, these findings indicate that these cells were under ER stress. H2O2, an inducer of oxidative stress, increased expression of UPR-associated mRNAs in cultured human GLCs, and this effect was abrogated by pretreatment with tauroursodeoxycholic acid (TUDCA), an ER stress inhibitor in clinical use. Treatment with H2O2 increased apoptosis and the activity of the pro-apoptotic factors caspase-8 and caspase-3, both of which were attenuated by TUDCA. Our findings suggest that activated ER stress induced by high oxidative stress in granulosa cells in ovaries with endometrioma mediates apoptosis of these cells, leading to ovarian dysfunction in patients with endometriosis.

scholarly journals Deltamethrin Induces Apoptosis in Cerebrum Neurons of Quail via Promoting Endoplasmic Reticulum Stress and Mitochondrial Dysfunction

2021 ◽  
Author(s):  
Pengfei Wu ◽  
Bing Han ◽  
Qingyue Yang ◽  
Siyu Li ◽  
Xiaoqiao Wang ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Endoplasmic Reticulum ◽  
Er Stress ◽  
Mitochondrial Dysfunction ◽  
Chronic Exposure ◽  
Molecular Mechanisms ◽  
Atp Content ◽  
Histological Changes ◽  
Real Time Quantitative Pcr ◽  
Induced Apoptosis

Abstract Deltamethrin (DLM) is a widely used and highly effective insecticide. DLM exposure is harmful to animal and human. Quail, as a bird model, has been widely used in the toxicology field. However, there is little information available in the literature about quail cerebrum damage caused by DLM. Here, we investigated the effect of DLM on quail cerebrum neurons. Four groups of healthy quails were assigned (10 quails in each group), respectively given 0, 15, 30, and 45 mg/kg DLM by gavage for 12 weeks. Through the measurements of quail cerebrum, it was found that DLM exposure induced obvious histological changes, oxidative stress, and neurons apoptosis. To further explore the possible molecular mechanisms, we performed real-time quantitative PCR to detect the expression of endoplasmic reticulum (ER) stress-related mRNA. In addition, we detected ATP content in quail cerebrum to evaluate the functional status of mitochondria. The study showed that DLM exposure significantly increased the expression of ER stress-related mRNA and decreased ATP content in quail cerebrum. These results suggest that chronic exposure to DLM induces apoptosis of quail cerebrum neurons via promoting ER stress and mitochondrial dysfunction. Furthermore, our results provide a novel explanation for DLM-induced apoptosis of avian cerebrum neurons.

The cellular immunity and oxidative stress markers in early pregnancy loss

2015 ◽  
pp. 1-4 ◽  
Author(s):  
Korkut Daglar ◽  
Ebru Biberoglu ◽  
Ayse Kirbas ◽  
Aylin Onder Dirican ◽  
Metin Genc ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Cellular Immunity ◽  
Early Pregnancy ◽  
Pregnancy Loss ◽  
Oxidative Stress Markers ◽  
Early Pregnancy Loss ◽  
Stress Markers ◽  
And Oxidative Stress

scholarly journals AβPP-induced UPR Transcriptomic Signature of Glial Cells to Oxidative Stress as an Adaptive Mechanism to Preserve Cell Function and Survival

2018 ◽  
Vol 15 (7) ◽  
pp. 643-654 ◽  
Author(s):  
Naima Chalour ◽  
Agathe Maoui ◽  
Patrice Rat ◽  
France Massicot ◽  
Melody Dutot ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Er Stress ◽  
Cell Function ◽  
Amyloid Β ◽  
Redox Status ◽  
Age Related Macular Degeneration ◽  
Amyloid Β Protein ◽  
Major Genes ◽  
Age Related ◽  
Induced Apoptosis

Background: Alzheimer's disease (AD) and age-related macular degeneration (AMD) present similarities, particularly with respect to oxidative stress, including production of 4-Hydroxy-2- nonenal (HNE). AMD has been named the AD in the eye. The Müller cells (MC) function as a principal glia of the retina and maintain water/potassium, glutamate homeostasis and redox status. Any MC dysfunction results in retinal neurodegeneration. Objectives: We investigated the effects of HNE in human MC. Results: HNE induced an increase of the reactive oxygen species associated with mitochondrial dysfunction and apoptosis. HNE induced endoplasmic reticulum (ER) stress (upregulation of GRP78/Bip, and the proapoptotic factor, CHOP). HNE also impaired expression of genes controlling potassium homeostasis (KCNJ10), glutamate detoxification (GS), and the visual cycle (RLBP1). MC adaptive response to HNE included upregulation of amyloid-β protein precursor (AβPP). To determine the role of AβPP, we overexpressed AβPP in MC. Overexpression of AβPP induced strong antioxidant and anti-ER stress (PERK downregulation and GADD34 upregulation) responses accompanied by activation of the prosurvival branch of the unfolded protein response. It was also associated with upregulation of major genes involved in MC-controlled retinal homeostasis (KCNJ10, GS, and RLBP1) and protection against HNE-induced apoptosis. Therefore, AβPP is an ER and oxidative stress responsive molecule, and is able to stimulate the transcription of major genes involved in MC functions impaired by HNE. Conclusion: Our study suggests that targeting oxidative and ER stress might be a potential therapeutic strategy against glia impairment in AMD and AD, in light of the common features between the two pathologies.

scholarly journals Oxidative Stress Markers in Early Pregnancy Loss: A Case-Control Study

2018 ◽  
Vol 7 (1) ◽  
pp. 61-66 ◽  
Author(s):  
Shahnaz Torkzahrani ◽  
Padideh Janati Ataei ◽  
Mehdi Hedayati ◽  
Soheila Khodakarim ◽  
Zohre Sheikhan ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Uric Acid ◽  
Pregnant Women ◽  
Spontaneous Abortion ◽  
Early Pregnancy ◽  
Pregnancy Loss ◽  
First Trimester ◽  
Demographic Characteristics ◽  
Early Pregnancy Loss ◽  
First Trimester Of Pregnancy

Objectives: Evidence suggests that oxidative stress (OS) plays a prominent role in the pathophysiology of pregnancy complications in women. The present study was conducted to determine the levels of OS markers in early pregnancy loss and to compare the results with those in healthy pregnant women. Materials and Methods: A total of 32 women with early pregnancy loss and 32 healthy women in the first trimester of pregnancy, with similar demographic characteristics entered this study as the cases and controls. Serum levels of malondialdehyde (MDA), total antioxidant capacity (TAC), uric acid, and bilirubin levels were determined in both groups. The data obtained were then analyzed and compared between the groups using the independent samples t test and Mann-Whitney U test. Results: The 2 groups matched in terms of personal-demographic characteristics including mother’s age, father’s age, gravidity, and body mass index (BMI). MDA levels increased significantly in the women with spontaneous abortion compared to the healthy pregnant women (4.35±1.47 vs. 3.42±1.68 µM/L; P=0.026) and TAC decreased significantly in the cases compared to the healthy controls (552.34±212.79 vs. 1003.23±1168.68 U/mL; P=0.040). Uric acid and bilirubin levels did not differ between the groups. Conclusions: The results of this study provides further evidence on the effect of increased OS on the incidence of early spontaneous abortion in the first trimester of pregnancy. High serum MDA levels and low TAC during pregnancy were 2 risk factors for spontaneous abortion. The present findings support the hypothesis that OS plays a key role in the etiopathogenesis of spontaneous abortion. Further studies are required for assessing the preventive role of antioxidant therapy in this complication.

scholarly journals NADPH oxidase links endoplasmic reticulum stress, oxidative stress, and PKR activation to induce apoptosis

2010 ◽  
Vol 191 (6) ◽  
pp. 1113-1125 ◽  
Author(s):  
Gang Li ◽  
Christopher Scull ◽  
Lale Ozcan ◽  
Ira Tabas
Keyword(s):  
Oxidative Stress ◽  
Endoplasmic Reticulum ◽  
Er Stress ◽  
Nicotinamide Adenine Dinucleotide Phosphate ◽  
Cellular Mechanisms ◽  
Apoptosis Pathway ◽  
Stress Oxidative ◽  
Induced Apoptosis ◽  
And Oxidative Stress

Endoplasmic reticulum (ER)–induced apoptosis and oxidative stress contribute to several chronic disease processes, yet molecular and cellular mechanisms linking ER stress and oxidative stress in the setting of apoptosis are poorly understood and infrequently explored in vivo. In this paper, we focus on a previously elucidated ER stress–apoptosis pathway whose molecular components have been identified and documented to cause apoptosis in vivo. We now show that nicotinamide adenine dinucleotide phosphate reduced oxidase (NOX) and NOX-mediated oxidative stress are induced by this pathway and that apoptosis is blocked by both genetic deletion of the NOX subunit NOX2 and by the antioxidant N-acetylcysteine. Unexpectedly, NOX and oxidative stress further amplify CCAAT/enhancer binding protein homologous protein (CHOP) induction through activation of the double-stranded RNA–dependent protein kinase (PKR). In vivo, NOX2 deficiency protects ER-stressed mice from renal cell CHOP induction and apoptosis and prevents renal dysfunction. These data provide new insight into how ER stress, oxidative stress, and PKR activation can be integrated to induce apoptosis in a pathophysiologically relevant manner.

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