scholarly journals Apoptosis of bovine ovarian surface epithelial cells by Fas antigen/Fas ligand signaling

Reproduction ◽  
2005 ◽  
Vol 130 (5) ◽  
pp. 751-758 ◽  
Author(s):  
Kate A Margalit ◽  
Robert G Cowan ◽  
Rebecca M Harman ◽  
Susan M Quirk
Keyword(s):  
Cell Death ◽  
Epithelial Cells ◽  
Fas Ligand ◽  
Primary Cultures ◽  
Single Layer ◽  
Interferon Γ ◽  
Drug Induced ◽  
Fas Antigen ◽  
Ovarian Surface ◽  
Ovarian Surface Epithelial

Ovarian surface epithelial cells (OSEs), a single layer of cells that cover the surface of the ovary, undergo turnover at the site of follicular rupture at ovulation. Greater than 90% of ovarian cancers arise from the OSEs. The objective of this study was to determine whether OSEs have the capacity to regulate their own demise through expression of Fas antigen (Fas) and Fas ligand (FasL) and activation of Fas-mediated apoptosis. In initial experiments, primary cultures of bovine OSEs responded to treatment with recombinant FasL by undergoing apoptosis. The percentage of cell death was not affected by the presence or absence of serum in the media or by co-treatment with interferon-γ, a treatment shown to potentiate Fas-mediated apoptosis in a number of cell types. Subsequent experiments tested the ability of stress-inducing drugs, anisomycin and daunorubicin, to promote apoptosis by stimulating an endogenous Fas–FasL pathway in OSEs. Treatment with FasL, anisomycin or daunorubicin induced cell death and this was suppressed by co-treatment with a peptide inhibitor of caspases, ZVAD. Treatment with anisomycin or daunorubicin in the presence of ZVAD increased expression of FasL mRNA and protein but did not alter expression of Fas mRNA or protein. Treatment of OSEs with a recombinant protein that blocks interaction of FasL with Fas (Fas:Fc) reduced apoptosis in response to anisomycin and daunorubicin, indicating that drug-induced apoptosis was mediated at least partially through endogenous Fas–FasL interactions. In summary, OSEs undergo apoptosis in response to stress-inducing drugs through activation of an endogenous Fas pathway.

scholarly journals Fas Antigen-Mediated Apoptosis of Ovarian Surface Epithelial Cells*

Endocrinology ◽  
1997 ◽  
Vol 138 (11) ◽  
pp. 4558-4566 ◽  
Author(s):  
Susan M. Quirk ◽  
Robert G. Cowan ◽  
Sarah H. Huber
Keyword(s):  
Epithelial Cells ◽  
Fas Antigen ◽  
Ovarian Surface ◽  
Ovarian Surface Epithelial

Reciprocal Interactions between Human Ovarian Surface Epithelial Cells and Adjacent Extracellular Matrix

1994 ◽  
Vol 215 (1) ◽  
pp. 97-108 ◽  
Author(s):  
Patricia A. Kruk ◽  
Veli-Jukka Uitto ◽  
James D. Firth ◽  
Shoukat Dedhar ◽  
Nelly Auersperg
Keyword(s):  
Extracellular Matrix ◽  
Epithelial Cells ◽  
Reciprocal Interactions ◽  
Ovarian Surface ◽  
Ovarian Surface Epithelial

Microenvironmental Regulation of BRCA1 Gene Expression by c-Jun and Fra2 in Premalignant Human Ovarian Surface Epithelial Cells

2013 ◽  
Vol 11 (3) ◽  
pp. 272-281 ◽  
Author(s):  
Lixin Zhou ◽  
Marcia Graves ◽  
Gwen MacDonald ◽  
Jane Cipollone ◽  
Christopher R. Mueller ◽  
...  
Keyword(s):  
Gene Expression ◽  
Epithelial Cells ◽  
Brca1 Gene ◽  
Ovarian Surface ◽  
Ovarian Surface Epithelial

1092 Interferon-γ Acts Directly on Gastric Epithelial Cells by Regulating Cell Death

2016 ◽  
Vol 150 (4) ◽  
pp. S218
Author(s):  
Luciana H. Osaki ◽  
Kevin Bockerstett ◽  
Eric Ford ◽  
Richard DiPaolo ◽  
Jason Mills
Keyword(s):  
Cell Death ◽  
Epithelial Cells ◽  
Interferon Γ ◽  
Gastric Epithelial Cells

Nonrandom chromosomal imbalances in human ovarian surface epithelial cells immortalized by HPV16-E6E7 viral oncogenes

2001 ◽  
Vol 130 (2) ◽  
pp. 141-149 ◽  
Author(s):  
Sai Wah Tsao ◽  
Natalie Wong ◽  
Xianghong Wang ◽  
Yu Liu ◽  
Thomas Shek Kong Wan ◽  
...  
Keyword(s):  
Epithelial Cells ◽  
Chromosomal Imbalances ◽  
Viral Oncogenes ◽  
Ovarian Surface ◽  
Ovarian Surface Epithelial

Uterine epithelial expression of the tumor necrosis factor superfamily: a strategy for immune privilege during pregnancy in a true epitheliochorial placentation species

2020 ◽  
Vol 102 (4) ◽  
pp. 828-842 ◽  
Author(s):  
Inkyu Yoo ◽  
Yoon Chul Kye ◽  
Jisoo Han ◽  
Minjeong Kim ◽  
Soohyung Lee ◽  
...  
Keyword(s):  
Cell Death ◽  
Tumor Necrosis Factor ◽  
Epithelial Cells ◽  
Tumor Necrosis ◽  
Fas Ligand ◽  
Apoptotic Cell ◽  
Apoptotic Cell Death ◽  
Immune Privilege ◽  
Tumor Necrosis Factor Superfamily ◽  
Necrosis Factor

Abstract The maternal immune system tolerates semi-allogeneic placental tissues during pregnancy. Fas ligand (FASLG) and tumor necrosis factor superfamily 10 (TNFSF10) are known to be components of maternal immune tolerance in humans and mice. However, the role of FASLG and TNFSF10 in the tolerance process has not been studied in pigs, which form a true epitheliochorial type placenta. Thus, the present study examined the expression and function of FASLG and TNFSF10 and their receptors at the maternal-conceptus interface in pigs. The endometrium and conceptus tissues expressed FASLG and TNFSF10 and their receptor mRNAs during pregnancy in a stage-specific manner. During pregnancy, FASLG and TNFSF10 proteins were localized predominantly to endometrial luminal epithelial cells with strong signals on Day 30 to term and on Day 15, respectively, and receptors for TNFSF10 were localized to some stromal cells. Interferon-γ (IFNG) increased the expression of TNFSF10 and FAS in endometrial tissues. Co-culture of porcine endometrial epithelial cells over-expressing TNFSF10 with peripheral blood mononuclear cells yielded increased apoptotic cell death of lymphocytes and myeloid cells. In addition, many apoptotic T cells were found in the endometrium on Day 15 of pregnancy. The present study demonstrated that FASLG and TNFSF10 were expressed at the maternal-conceptus interface and conceptus-derived IFNG increased endometrial epithelial TNFSF10, which, in turn, induced apoptotic cell death of immune cells. These results suggest that endometrial epithelial FASLG and TNFSF10 may be critical for the formation of micro-environmental immune privilege at the maternal-conceptus interface for the establishment and maintenance of pregnancy in pigs.

Intermediate filaments in rat ovarian surface epithelial cells: changes with neoplastic progression in culture

1992 ◽  
Vol 70 (1) ◽  
pp. 16-25 ◽  
Author(s):  
Ann E. Hornby ◽  
Jie Pan ◽  
Nelly Auersperg
Keyword(s):  
Cell Density ◽  
Intermediate Filaments ◽  
Growth Pattern ◽  
Primary Cultures ◽  
Neoplastic Progression ◽  
Western Blots ◽  
Ovarian Surface ◽  
Keratin Expression ◽  
Keratin Filaments ◽  
Ovarian Surface Epithelial

Interrelationships between neoplastic progression and the expression of intermediate filaments were examined in primary cultures, immortal lines, and Kirsten murine sarcoma virus (KiMSV) transformed lines of rat ovarian surface epithelial (ROSE) cells. Immunofluorescence microscopy revealed abundant keratin filaments in all cells of primary cultures. In immortal, nontumorigenic lines, keratin filaments were detected in fewer cells, in smaller numbers, and in microscopically altered forms. The percentage of keratin-positive cells ranged from 4 to 54%. Its expression was inversely proportional to cell density. Keratin expression was similar in the two immortal lines, although one had retained a monolayered epithelial growth pattern resembling primary cultures, while in the other the growth pattern of the cells was more atypical. The two KiMSV-transformed lines were previously shown to produce tumors in vivo that resemble human ovarian endometrioid stromal sarcomas. In spite of this histologic appearance, the proportion of keratin-positive cells in these cells was increased over the immortal lines. Keratin expression was unrelated to cell density, and keratin in most virally transformed cells was limited to few, fine filaments. In thymidine-labelled immortal and virus-transformed cultures stained for keratin, no correlation was found between keratin expression and proliferative activity. The keratin profiles of primary and immortal cultures were identical on Western blots, with subtypes ranging from 52 to 66 kDa. The two virally transformed lines lacked some of the subtypes. Vimentin networks were faint or absent in primary cultures. In the immortal and the virus-transformed lines, neoplastic progression was associated with increasing vimentin expression but with no changes in filament morphology and distribution. The results show that the abnormalities in intermediate filament expression that accompany immortalization do not preclude the retention of a normal epithelial morphology and growth pattern in this cell type. Furthermore, the number of intermediate filaments and their intracellular distribution appear to be altered at an earlier stage in neoplastic progression than those mechanisms that select for specific keratin subtypes, or those that respond to regulation by cell density. Finally, the presence of keratin in the KiMSV-transformed lines examined in this study supports the hypothesis that human ovarian stromal sarcomas can arise in the OSE.Key words: neoplastic transformation, keratin, vimentin, cytoskeleton, ras oncogene, ovary, tissue culture.

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