scholarly journals HO-1 reduces heat stress-induced apoptosis in bovine granulosa cells by suppressing oxidative stress

Aging ◽  
2019 ◽  
Vol 11 (15) ◽  
pp. 5535-5547 ◽  
Author(s):  
Yiru Wang ◽  
Caixia Yang ◽  
Nahla Abdalla Hassan Elsheikh ◽  
Chengmin Li ◽  
Fangxiao Yang ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Heat Stress ◽  
Granulosa Cells ◽  
Induced Apoptosis

Encircling granulosa cells protects against di-(2-ethylhexyl)phthalate-induced apoptosis in rat oocytes cultured in vitro

Zygote ◽  
2019 ◽  
Vol 27 (4) ◽  
pp. 203-213 ◽  
Author(s):  
Anima Tripathi ◽  
Vivek Pandey ◽  
A.N. Sahu ◽  
Alok K. Singh ◽  
Pawan K. Dubey
Keyword(s):  
Oxidative Stress ◽  
Membrane Potential ◽  
Mitochondrial Membrane Potential ◽  
Granulosa Cells ◽  
Mitochondrial Membrane ◽  
Dependent Manner ◽  
Apoptotic Markers ◽  
Induced Apoptosis ◽  
Ethylhexyl Phthalate

SummaryThe present study investigated if the presence of encircling granulosa cells protected against di(2-ethylhexyl)phthalate (DEHP)-induced oxidative stress in rat oocytes cultured in vitro. Denuded oocytes and cumulus–oocyte complexes (COCs) were treated with or without various doses of DEHP (0.0, 25.0, 50.0, 100, 200, 400 and 800 μM) in vitro. Morphological apoptotic changes, levels of oxidative stress and reactive oxygen species (ROS), mitochondrial membrane potential, and expression levels of apoptotic markers (Bcl2, Bax, cytochrome c) were analyzed. Our results showed that DEHP induced morphological apoptotic changes in a dose-dependent manner in denuded oocytes cultured in vitro. The effective dose of DEHP (400 µg) significantly (P>0.05) increased oxidative stress by elevating ROS levels and the mitochondrial membrane potential with higher mRNA expression and protein levels of apoptotic markers (Bax, cytochrome c). Encircling granulosa cells protected oocytes from DEHP-induced morphological changes, increased oxidative stress and ROS levels, as well as increased expression of apoptotic markers. Taken together our data suggested that encircling granulosa cells protected oocytes against DEHP-induced apoptosis and that the presence of granulosa cells could act positively towards the survival of oocytes under in vitro culture conditions and may be helpful during assisted reproductive technique programmes.

Presence of encircling granulosa cells protects against oxidative stress-induced apoptosis in rat eggs cultured in vitro

APOPTOSIS ◽  
2016 ◽  
Vol 22 (1) ◽  
pp. 98-107 ◽  
Author(s):  
Meenakshi Tiwari ◽  
Anima Tripathi ◽  
Shail K. Chaube
Keyword(s):  
Oxidative Stress ◽  
Granulosa Cells ◽  
Rat Eggs ◽  
Induced Apoptosis

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.

MicroRNA-145 protects follicular granulosa cells against oxidative stress-induced apoptosis by targeting Krüppel-like factor 4

2017 ◽  
Vol 452 ◽  
pp. 138-147 ◽  
Author(s):  
Lu Xu ◽  
Haixiang Sun ◽  
Mei Zhang ◽  
Yue Jiang ◽  
Chunxue Zhang ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Granulosa Cells ◽  
Induced Apoptosis

scholarly journals Melatonin protects the mouse testis against heat-induced damage

2020 ◽  
Vol 26 (2) ◽  
pp. 65-79 ◽  
Author(s):  
Pengfei Zhang ◽  
Yi Zheng ◽  
Yinghua Lv ◽  
Fuyuan Li ◽  
Lihong Su ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Heat Stress ◽  
Male Fertility ◽  
Reactive Oxygen Species Generation ◽  
Free Radical Scavenger ◽  
Testicular Atrophy ◽  
Therapeutic Drug ◽  
Radical Scavenger ◽  
Induced Apoptosis ◽  
And Oxidative Stress

Abstract Spermatogenesis, an intricate process occurring in the testis, is responsible for ongoing production of spermatozoa and thus the cornerstone of lifelong male fertility. In the testis, spermatogenesis occurs optimally at a temperature 2–4°C lower than that of the core body. Increased scrotal temperature generates testicular heat stress and later causes testicular atrophy and spermatogenic arrest, resulting in a lower sperm yield and therefore impaired male fertility. Melatonin (N-acetyl-5-methoxytryptamine), a small neuro-hormone synthesized and secreted by the pineal gland and the testis, is widely known as a potent free-radical scavenger; it has been reported that melatonin protects the testis against inflammation and reactive oxygen species generation thereby playing anti-inflammatory, -oxidative and -apoptotic roles in the testis. Nevertheless, the role of melatonin in the testicular response to heat stress has not been studied. Here, by employing a mouse model of testicular hyperthermia, we systematically investigated the testicular response to heat stress as well as the occurrence of autophagy, apoptosis and oxidative stress in the testis. Importantly, we found that pre-treatment with melatonin attenuated heat-induced apoptosis and oxidative stress in the testis. Also, post-treatment with melatonin promoted recovery of the testes from heat-induced damage, probably by maintaining the integrity of the Sertoli cell tight-junction. Thus, we for the first time provide the proof of concept that melatonin can protect the testis against heat-induced damage, supporting the potential future use of melatonin as a therapeutic drug in men for sub/infertility incurred by various testicular hyperthermia factors.

scholarly journals RNAi-Mediated Silencing of Catalase Gene Promotes Apoptosis and Impairs Proliferation of Bovine Granulosa Cells under Heat Stress

Animals ◽  
2020 ◽  
Vol 10 (6) ◽  
pp. 1060
Author(s):  
Adnan Khan ◽  
Muhammad Zahoor Khan ◽  
Jinhuan Dou ◽  
Saqib Umer ◽  
Huitao Xu ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Heat Stress ◽  
Granulosa Cells ◽  
Ovarian Follicle ◽  
Regulatory Protein ◽  
Nuclear Antigen ◽  
Cellular Protection ◽  
Catalase Gene ◽  
Induced Apoptosis ◽  
Cytochrome P450 Family

Heat stress in dairy cattle is recognized to compromise fertility by altering the functions of ovarian follicle-enclosed cells, e.g., oocyte and granulosa cells (GCs). Catalase is an antioxidant enzyme that plays a significant role in cellular protection against oxidative damage by the degradation of hydrogen peroxide to oxygen and water. In this study, the role and mechanism of CAT on the heat stress (HS)-induced apoptosis and altered proliferation of bovine GCs were studied. The catalase gene was knocked-down successfully in bovine GCs at both the transcriptional and translational levels. After a successful knockdown using siRNA, GCs were divided into HS (40 °C + NC and 40 °C + CAT siRNA) and 38 °C + NC (NC) groups. The GCs were then examined for ROS, viability, mitochondrial membrane potential (MMP), cell cycle, and biosynthesis of progesterone (P4) and estrogen (E2) hormones. The results indicated that CAT silencing promoted ROS production and apoptosis by up-regulating the Bcl-2-associated X protein (BAX) and Caspase-3 genes both at the transcriptional and translational levels. Furthermore, the knockdown of CAT markedly disrupted the MMP, impaired the production of P4 and E2, altered the progression of the G1 phase of the cell cycle, and decreased the number of cells in the S phase. This was further verified by the down-regulation of proliferating cell nuclear antigen (PCNA), CyclinB1, steroidogenic acute regulatory protein (STAR), and cytochrome P450 family 11 subfamily A member 1 (Cyp11A1) genes. Our study presented a novel strategy to characterize how CAT can regulate cell proliferation and apoptosis in GCs under HS. We concluded that CAT is a broad regulatory marker in GCs by regulating apoptosis, cellular progression, and simultaneously by vital fluctuations in hormonal signaling. Our findings infer a crucial evidence of how to boost the fertility of heat-stressed cows.

PKCδ contributes to oxidative stress-induced apoptosis in porcine ovarian granulosa cells via activating JNK

2019 ◽  
Vol 131 ◽  
pp. 89-95 ◽  
Author(s):  
Shuo Liu ◽  
Ming Shen ◽  
Chengyu Li ◽  
Yinghui Wei ◽  
Xueqing Meng ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Granulosa Cells ◽  
Ovarian Granulosa Cells ◽  
Induced Apoptosis

scholarly journals MON-027 Activation of Endoplasmic Reticulum Stress Mediates Oxidative Stress-Induced Apoptosis of Granulosa Cells in Ovaries Affected by Endometrioma

2020 ◽  
Vol 4 (Supplement_1) ◽  
Author(s):  
Chisato Kunitomi ◽  
Miyuki Harada ◽  
Jerilee Mariam Khong Azahry
Keyword(s):  
Oxidative Stress ◽  
Er Stress ◽  
Granulosa Cells ◽  
Caspase 3 ◽  
Caspase 8 ◽  
Ovarian Dysfunction ◽  
High Oxidative Stress ◽  
Induced Apoptosis ◽  
Sensor Proteins ◽  
Apoptotic Factors

Abstract Endometriosis exerts detrimental effects on ovarian physiology and compromises follicular health. Granulosa cells of endometriosis patients are characterized by increased apoptosis, as well as high oxidative stress. Among several pathophysiologic factors associated with endometriosis, it is expected that oxidative stress contributes to the induction of apoptosis in granulosa cells, although the underlying mechanism remains unclear. 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 mediates oxidative stress-induced apoptosis. Ovaries from patients with endometrioma and control were collected to determine apoptosis, oxidative stress and ER stress by TUNEL, immunohistochemical staining of 8-OHdG and ER stress sensors, respectively. Human granulosa-lutein cells (GLCs) obtained from IVF patients were cultured with H2O2 (an oxidative stress inducer) or tauroursodeoxycholic acid (TUDCA, an ER stress inhibitor in clinical use) to assess apoptosis and ER stress by quantitative PCR and FACS. Activity of pro-apoptotic factors was determined by caspase-8 activity assay and western blotting for cleaved caspase-3. Human GLCs from patients with endometrioma expressed up to two times higher level of mRNAs associated with the unfolded protein response (UPR), including ATF4, ATF6, the spliced form of XBP1, HSPA5, and CHOP. In addition, the levels of phosphorylated ER stress sensor proteins, IRE1 and PERK, were elevated. 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 increased expression of UPR-associated mRNAs in cultured human GLCs, and this effect was abrogated by pre-treatment with TUDCA. Treatment with H2O2 increased apoptosis and the activity of 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 endometriosis patients. Targeting ER stress with currently clinically available ER stress inhibitors, or with these agents in combination with antioxidants, may serve as a novel strategy for rescuing endometriosis-associated ovarian dysfunction.

Autophagy Contributes to Oxidative Stress-Induced Apoptosis in Porcine Granulosa Cells

2020 ◽  
Author(s):  
Jia-Qing Zhang ◽  
Qiao-Ling Ren ◽  
Jun-Feng Chen ◽  
Bin-Wen Gao ◽  
Xian-Wei Wang ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Granulosa Cells ◽  
Porcine Granulosa Cells ◽  
Induced Apoptosis
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