Mechanisms of cytokine-induced death of cultured bovine luteal cells

Petroff, Margaret G.; Petroff, Brian K.; Pate, Joy L.

doi:10.1530/rep.0.1210753

Cited by 99 publications

(88 citation statements)

References 3 publications

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“…Gap junctions transfer regulatory molecules between adjacent cells and the response to chemical mediators in vitro is different between luteal slices and dissociated luteal cells [30]. Thus, NO may have different actions on the CL according to the culture system used, the estrous stage, or the species [5,8,[11][12][13][14]27]. However, overall findings suggest that although NO supports CL development and maintenance during the early luteal phase [14,24], it mediates luteolytic signals at the end of luteal phase [8,[12][13][14][15]31].…”

Section: Discussionmentioning

confidence: 99%

“…Three major pathways have been identified during apoptosis as follows: the death receptor pathway, mitochondrial pathway and nucleus pathway [2]. Many cytokine membrane receptors [5,18], second messengers, including calcium ions [Ca 2+ ]i [19], and regulatory proteins [20] are involved in apoptosis. F a s l i g a n d ( F a s L ) , a m e m b e r o f t h e T N F superfamily, primarily engages its receptors (Fas) to induce apoptosis [21].…”

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confidence: 99%

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Nitric Oxide Induces Apoptosis in Bovine Luteal Cells

Korzekwa

Okuda

Wocławek-Potocka

et al. 2006

Journal of Reproduction and Development

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Abstract. We previously showed in in vivo and in vitro studies that nitric oxide (NO) is engaged in luteolysis in cattle. Nitric oxide produced locally in the bovine corpus luteum (CL) inhibits progesterone (P4) synthesis and is suggested to be a component of the luteolytic cascade induced by uterine prostaglandin (PG) F2α. In the present study, the molecular mechanisms of NO action during structural luteolysis were studied in cultured bovine luteal cells (Days 15-17 of the estrous cycle). The effects of the NO donor (NONOate; 10 -4 M) on DNA fragmentation, cell viability, P4 production and caspase-3 activity were compared with those of PGF2α (10 -6 M). Moreover, mobilization of intracellular calcium [Ca 2+ ]i and gene expressions of Fas-L, Fas, bcl-2, bax, and caspase-3 in the cells were determined by semi-quantitative RT-PCR after NONOate treatment. Caspase-3 activity was examined calorimetrically. Contrary to PGF2α NONOate decreased cell viability. DNA fragmentation after NONOate treatment increased by more than with PGF22α. NONOate increased mobilization of [Ca 2+ ]i in the cells. Although the NO donor did not affect Fas-L and bcl-2 gene expression, it stimulated Fas and bax mRNA and caspase-3 expression. The ratio of bcl-2 to bax mRNA level decreased in the cells treated with NONOate. Moreover, NONOate stimulated caspase-3 activity more effectively than PGF2α. The overall results suggest that NO is a luteolytic factor that plays a crucial role in regulation of the estrous cycle in structural luteolysis by inducing apoptosis of luteal cells in cattle.

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Section: Discussionmentioning

confidence: 99%

mentioning

confidence: 99%

Nitric Oxide Induces Apoptosis in Bovine Luteal Cells

Korzekwa

Okuda

Wocławek-Potocka

et al. 2006

Journal of Reproduction and Development

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“…On the other hand, Petroff et al [37] reported that an NO synthase inhibitor did not inhibit cell death induced by TNF-α and IFN-γ in bovine mid-luteal cells in vitro. The sensitivity of bovine luteal cells to NO has been shown to increase dramatically from the early to late luteal phase [44,46].…”

Section: Nitric Oxidementioning

confidence: 99%

“…In addition, apoptosis is induced by a glutathione peroxidase inhibitor in cultured bovine luteal cells [36]. Apoptosis induced by TNF-α is inhibited by addition of antioxidants, superoxide dismutase (SOD) and catalase, suggesting that TNF-α induced luteal cell apoptosis is mediated by ROS [37]. PGF2α induces apoptosis by producing ROS via activation of protein kinase C and increased intracellular Ca 2+ [38].…”

Section: Bcl-2 Family and Reactive Oxygen Speciesmentioning

confidence: 99%

Species-Related Differences in the Mechanism of Apoptosis During Structural Luteolysis

Sugino

Okuda

2007

J. Reprod. Dev.

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Abstract. Luteolysis is defined as the loss of function and subsequent involution of the luteal structure. The luteolytic process is usually subdivided, whereby the decline in progesterone is described as functional luteolysis and the structural involution is described as structural luteolysis. After the corpus luteum ceases to produce progesterone, it decreases in size, experiences a loss of cellular integrity, and then disappears from the ovary as a result of apoptosis of luteal cells. However, the control mechanisms responsible for initiating and mediating apoptosis during structural luteolysis seem more complex than originally envisioned. Furthermore, efforts to elucidate the apoptotic mechanisms have been complicated by the fact that different mammalian species have different mechanisms for controlling luteal function. Therefore, it is of interest to know whether different mammalian species have different apoptotic mechanisms. The goal of this review was to focus on species-related differences in the mechanism of apoptosis during structural luteolysis in rodents, cattle and humans, the species that are used most for luteolysis research.

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“…Dispersed luteal cells (4!10 6 cells/flask) were cultured in serum-coated 25 cm 2 flasks in a total of 4 ml Hams F-12 containing insulin (5 mg/ml), transferrin (5 mg/ml), selenium (5 ng/ml), gentamicin (20 mg/ml), and LH (1 ng/ml). The cells were allowed to adhere overnight, medium was replaced, and the cultures were exposed to either 0 or 50 ng/ml TNF for 48 h, the latter concentration having been shown to affect function, viability, and gene expression in cultures of mixed bovine luteal cells (Townson & Pate 1994, Petroff et al 2001, Cannon & Pate 2003. Total RNA was extracted from the cells after 48 h of culture.…”

Section: Isolation and Culture Of Mixed Luteal Cells And Luteal Endotmentioning

confidence: 99%

The class II major histocompatibility complex molecule BoLA-DR is expressed by endothelial cells of the bovine corpus luteum

2007

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Cells expressing class II major histocompatibility complex (MHC) molecules are found within the corpus luteum (CL) of several species. Expression and localization of class II MHC molecules in the bovine CL were examined in the present study. Immunohistochemical evaluation revealed class II MHC molecules on single cells in early CL (days 4 and 5 post-estrus). Two class II MHC-expressing cell types were observed in midcycle CL (days 10-12 post-estrus), single cells similar to those observed in the early CL, and endothelial cells. Not all endothelial cells expressed class II MHC, and further investigation revealed expression of only one type of class II MHC molecule, DR, on endothelial cells. Class II MHC was also localized to endothelial cells in late CL (day 18 post-estrus). Steroidogenic luteal cells were negative for class II MHC throughout the estrous cycle. Quantitative RT-PCR revealed higher (P!0.05) concentrations of mRNA encoding the a-subunit of DR (DRA) in late CL when compared with those in the early CL. DRA mRNA abundance was also measured in cultures of mixed luteal and luteal endothelial (CLENDO) cells, in the presence or absence of tumor necrosis factor-a (TNF). No differences were found in the DRA mRNA concentration between mixed luteal and CLENDO cell cultures, and TNF had no effect on DRA mRNA concentration in both cell types. Expression of DR by endothelial cells of the midcycle CL may induce anergy of T lymphocytes, or stimulate them to secrete products that enhance normal luteal function.

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Mechanisms of cytokine-induced death of cultured bovine luteal cells

Cited by 99 publications

References 3 publications

Nitric Oxide Induces Apoptosis in Bovine Luteal Cells

Nitric Oxide Induces Apoptosis in Bovine Luteal Cells

Species-Related Differences in the Mechanism of Apoptosis During Structural Luteolysis

The class II major histocompatibility complex molecule BoLA-DR is expressed by endothelial cells of the bovine corpus luteum

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