scholarly journals Serum Deprivation-Induced Apoptosis in Cultured Porcine Granulosa Cells Is Characterized by Increased Expression of p53 Protein, Fas Antigen and Fas Ligand and by Decreased Expression of PCNA.

1998 ◽  
Vol 45 (2) ◽  
pp. 247-253 ◽  
Author(s):  
XINJIAN PENG ◽  
TAKESHI MARUO ◽  
HIROYA MATSUO ◽  
SHIGEKI TAKEKIDA ◽  
JUN DEGUCHI
Keyword(s):  
Granulosa Cells ◽  
Fas Ligand ◽  
P53 Protein ◽  
Serum Deprivation ◽  
Fas Antigen ◽  
Porcine Granulosa Cells ◽  
Induced Apoptosis

scholarly journals 2,3,7,8-Tetrachlorodibenzo-p-dioxin alters steroid secretion but does not affect cell viability and the incidence of apoptosis in porcine luteinised granulosa cells

2014 ◽  
Vol 62 (3) ◽  
pp. 408-421 ◽  
Author(s):  
Olga Jablonska ◽  
Joanna Piasecka-Srader ◽  
Anna Nynca ◽  
Agnieszka Kołomycka ◽  
Anna Robak ◽  
...  
Keyword(s):  
Cell Viability ◽  
Granulosa Cells ◽  
Steroid Hormone ◽  
Annexin V ◽  
Steroid Production ◽  
Steroid Secretion ◽  
Porcine Granulosa Cells ◽  
Affect Cell Viability ◽  
Preovulatory Follicles ◽  
Induced Apoptosis

The compound 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD), a by-product of human industrial activity, was found to affect ovarian steroidogenesis in animals, but the mechanism of its action is still unclear. The aims of the study were to examine the effect of TCDD on (1) progesterone (P4) and oestradiol (E2) production by granulosa cells isolated from medium (3–6 mm) and preovulatory (≥ 8 mm) porcine follicles, (2) the viability of the cells, and (3) the incidence of apoptosis. Porcine granulosa cells were cultured (48 h) with or without TCDD (100 pM, 100 nM). Steroid hormone concentrations in the medium were determined by radioimmunoassay. The viability of granulosa cells was tested spectrophotometrically (alamarBlue™ assay). Apoptosis was evaluated by flow cytometry using Annexin V and by TUNEL assay. The higher dose of TCDD (100 nM) significantly inhibited P4 and stimulated E2 production by luteinised granulosa cells isolated from medium follicles. The lower dose of TCDD (100 pM) significantly stimulated P4 and inhibited E2 secretion by the cells isolated from preovulatory follicles. None of the two TCDD doses affected cell viability or induced apoptosis in granulosa cells. In conclusion, TCDD directly affected steroid production by granulosa cells obtained from mature pigs, but the effect of TCDD was not due to its cytotoxicity.

scholarly journals Isorhamnetin Protects Zearalenone-induced Damage via the PI3K/Akt Signaling Pathway in Porcine Granulosa Cells

2021 ◽  
Author(s):  
Xiaoya Li ◽  
Huali Chen ◽  
Zelin Zhang ◽  
Xiaodi Li ◽  
Jiaxin Duan ◽  
...  
Keyword(s):  
Signaling Pathway ◽  
Granulosa Cells ◽  
Akt Signaling ◽  
Akt Signaling Pathway ◽  
Animal Reproduction ◽  
Bax Protein ◽  
Porcine Granulosa Cells ◽  
Cereal Grain ◽  
Induced Apoptosis ◽  
And Oxidative Stress

Abstract Background: Zearalenone (ZEA) is widely derived from moldy cereal grain, which has adverse effects on animal reproduction. In particular, pigs are more sensitive to ZEA-induced toxicity than other animals. Isorhamnetin, a flavonoid has extensive of pharmacological activities. However, little is known about the effects of isorhamnetin on reproduction. Thus, it would be interesting to clarify the effect and the underlying molecular mechanism of isorhamnetin involvement in ZEA-induced cytotoxicity in porcine granulosa cells.Results: Our findings showed that isorhamnetin suppressed ZEA-induced apoptosis by regulating Bcl-2 and Bax protein changes. Changes in intracellular Ca2+ levels and CHOP, ATF6, GRP78 indicated that isorhamnetin rescued ZEA-induced endoplasmic reticulum stress (ERS). Furthermore, isorhamnetin prevented ZEA-induced reactive oxygen species (ROS) via P38 signaling pathway. Mechanistically, isorhamnetin stimulated the expression of PCNA and CyclinD, thereby raising the ratio of S phases cells in response to ZEA-induced apoptosis via PI3K/Akt signaling pathway. Isorhamnetin also recovered ZEA-induced steroidogenesis disorder by regulating steroidogenic enzyme gene and proteins (FSH-R, CYP19A1). Conclusions: Collectively, these findings show that isorhamnetin protects granulosa cells from ZEA-induced damage via the PI3K/Akt signaling pathway, which promotes proliferation, alleviates steroidogenesis disorder, ERS and oxidative stress.

scholarly journals The susceptibility of granulosa cells to apoptosis is influenced by oestradiol and the cell cycle

2006 ◽  
Vol 189 (3) ◽  
pp. 441-453 ◽  
Author(s):  
Susan M Quirk ◽  
Robert G Cowan ◽  
Rebecca M Harman
Keyword(s):  
Cell Cycle ◽  
Granulosa Cells ◽  
Cell Cycle Progression ◽  
Fas Ligand ◽  
S Phase ◽  
G1 Phase ◽  
Cycle Progression ◽  
Induced Apoptosis ◽  
Cell Proliferation Marker ◽  
D2 Protein

Experiments were conducted to test whether oestradiol (E2) protects granulosa cells from Fas ligand (FasL)-induced apoptosis and whether protection involves modulation of the cell cycle of proliferation. Treatment of cultured bovine granulosa cells with E2 decreased susceptibility to FasL-induced apoptosis. The effects of E2 were mediated through oestrogen receptor and were not mediated by stimulation of IGF production. E2 also increased the percentage of cells progressing from G1 to S phase of the cell cycle, and increased expression of cyclin D2 protein and the cell proliferation marker Ki67. Progression from G1 to S phase of the cell cycle was necessary for the protective effect of E2; blocking progression from G1 to S phase with the cdk2 inhibitor roscovitine, or blocking cells in S phase with hydroxyurea, prevented protection by E2. The stages of the cell cycle during which granulosa cells are susceptible to apoptosis were assessed. First, treatment with the G1 phase blocker, mimosine, protected cells from FasL-induced apoptosis, indicating that cells in G0 or early- to mid-G1 phase are relatively resistant to apoptosis. Secondly, examination of recent DNA synthesis by cells that became apoptotic indicated that apoptosis did not occur in S, G2 or M phases. Taken together, the experiments indicate that cells may be most susceptible to apoptosis at the transition from G1 to S phase. E2 stimulates transition from G1 to S phase and protects against apoptosis only when cell cycle progression is unperturbed.

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

IGF-I Prevents Fas Ligand-Induced Apoptosis in Granulosa Cells of Buffalo (Bubalus bubalis) Ovarian Follicles In Vitro.

2011 ◽  
Vol 85 (Suppl_1) ◽  
pp. 657-657
Author(s):  
Ravindra P. Janivara ◽  
Sunil K. Patil ◽  
Jamuna V. Kolatalu ◽  
Dhanya Joseph ◽  
Raghavendra Subbarao ◽  
...  
Keyword(s):  
Granulosa Cells ◽  
Fas Ligand ◽  
Bubalus Bubalis ◽  
Ovarian Follicles ◽  
Igf I ◽  
Induced Apoptosis

FSH prevents porcine granulosa cells from hypoxia‐induced apoptosis via activating mitophagy through the HIF‐1α‐PINK1‐Parkin pathway

2020 ◽  
Vol 34 (3) ◽  
pp. 3631-3645 ◽  
Author(s):  
Chengyu Li ◽  
Jiaqi Zhou ◽  
Zhaojun Liu ◽  
Jilong Zhou ◽  
Wang Yao ◽  
...  
Keyword(s):  
Granulosa Cells ◽  
Porcine Granulosa Cells ◽  
Induced Apoptosis

scholarly journals Progesterone Receptor and the Cell Cycle Modulate Apoptosis in Granulosa Cells

Endocrinology ◽  
2004 ◽  
Vol 145 (11) ◽  
pp. 5033-5043 ◽  
Author(s):  
Susan M. Quirk ◽  
Robert G. Cowan ◽  
Rebecca M. Harman
Keyword(s):  
Cell Cycle ◽  
Progesterone Receptor ◽  
Granulosa Cells ◽  
Fas Ligand ◽  
Lh Surge ◽  
Theca Cells ◽  
Development Of Resistance ◽  
Preovulatory Follicles ◽  
Induced Apoptosis ◽  
Antagonist Ru486

Abstract Our previous studies showed that exposure of bovine preovulatory follicles to the LH surge-induced resistance of granulosa cells, but not theca cells, to apoptosis. Here, the temporal development of resistance to apoptosis and potential roles of progesterone receptor (PR) and alterations in the cell cycle in mediating this effect were examined. Injection of cows with GnRH induced an LH surge within 2 h. Granulosa cells isolated 0, 6, and 10 h after GnRH were sensitive to Fas ligand-induced apoptosis, but cells isolated at 14 h were resistant. PR was first detectable in granulosa cells at 10 and 14 h and was not detectable in theca. Treatment of granulosa cells isolated 14 h after GnRH with the PR antagonist, RU486, induced susceptibility to apoptosis, an effect mediated by PR and not glucocorticoid receptor. After GnRH treatment, granulosa cells, but not theca cells, exited the cell cycle, expression of cyclin D2 was reduced, and p27Kip1 was elevated. Treatment of granulosa cells isolated from small antral follicles with the G1 phase blocker, mimosine, reduced Fas ligand-induced killing, suggesting that nonproliferating cells are resistant to apoptosis. Treatment of granulosa cells isolated 14 h after GnRH with RU486 induced reentry of some cells into the cell cycle and reversed resistance to apoptosis, suggesting that cycling cells became susceptible to apoptosis. Treatment with mimosine prevented the ability of RU486 to promote susceptibility to apoptosis. In summary, the LH surge induces expression of PR by granulosa cells and withdrawal from the cell cycle, and these events promote resistance to apoptosis.

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