The Experts below are selected from a list of 309 Experts worldwide ranked by ideXlab platform
Kiyoshi Okuda - One of the best experts on this subject based on the ideXlab platform.
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programmed necrosis a new mechanism of steroidogenic Luteal Cell death and elimination during luteolysis in cows
Scientific Reports, 2016Co-Authors: Takuo Hojo, K K Piotrowskatomala, A W Jonczyk, K. Lukasik, Marta J. Siemieniuch, Kiyoshi Okuda, Dariusz J SkarzynskiAbstract:Programmed necrosis (necroptosis) is an alternative form of programmed Cell death that is regulated by receptor-interacting protein kinase (RIPK) 1 and 3-dependent, but is a caspase (CASP)-independent pathway. In the present study, to determine if necroptosis participates in bovine structural luteolysis, we investigated RIPK1 and RIPK3 expression throughout the estrous cycle, during prostaglandin F2α (PGF)-induced luteolysis in the bovine corpus luteum (CL), and in cultured Luteal steroidogenic Cells (LSCs) after treatment with selected luteolytic factors. In addition, effects of a RIPK1 inhibitor (necrostatin-1, Nec-1; 50 μM) on Cell viability, progesterone secretion, apoptosis related factors and RIPKs expression, were evaluated. Expression of RIPK1 and RIPK3 increased in the CL tissue during both spontaneous and PGF-induced luteolysis (P < 0.05). In cultured LSCs, tumor necrosis factor α (TNF; 2.3 nM) in combination with interferon γ (IFNG; 2.5 nM) up-regulated RIPK1 mRNA and protein expression (P < 0.05). TNF + IFNG also up-regulated RIPK3 mRNA expression (P < 0.05), but not RIPK3 protein. Although Nec-1 prevented TNF + IFNG-induced Cell death (P < 0.05), it did not affect CASP3 and CASP8 expression. Nec-1 decreased both RIPK1 and RIPK3 protein expression (P < 0.05). These findings suggest that RIPKs-dependent necroptosis is a potent mechanism responsible for bovine structural luteolysis induced by pro-inflammatory cytokines.
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hypoxia promotes Luteal Cell death in bovine corpus luteum
Biology of Reproduction, 2008Co-Authors: Ryo Nishimura, Junichi Komiyama, Yukari Tasaki, Tomas J Acosta, Kiyoshi OkudaAbstract:Low oxygen caused by a decreasing blood supply is known to induce various responses of Cells, including apoptosis. The present study was conducted to examine whether low-oxygen conditions (hypoxia) induce Luteal Cell apoptosis in cattle. Bovine midLuteal Cells incubated under hypoxia (3% O(2)) showed significantly more Cell death than did those incubated under normoxia (20% O(2)) at 24 and 48 h of culture, and had significantly lower progesterone (P4) levels starting at 8 h. Characteristic features of apoptosis, such as shrunken nuclei and DNA fragmentation, were observed in Cells cultured under hypoxia for 48 h. Hypoxia increased the mRNA expressions of BNIP3 and caspase 3 at 24 and 48 h of culture. Hypoxia had no significant effect on the expressions of BCL2 and BAX mRNA. Hypoxia also increased BNIP3 protein, and activated caspase-3. Treatment of P4 attenuated Cell death, caspase-3 mRNA expression, and caspase-3 activity under hypoxia. Overall results of the present study indicate that hypoxia induces Luteal Cell apoptosis by enhancing the expression of proapoptotic protein, BNIP3, and by activating caspase-3, and that the induction of apoptosis by hypoxia is partially caused by a decrease in P4 production. Because hypoxia suppresses P4 synthesis in bovine Luteal Cells, we suggest that oxygen deficiency caused by a decreasing blood supply in bovine corpus luteum is one of the major factors contributing to both functional and structural luteolysis.
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fas fas ligand system mediates Luteal Cell death in bovine corpus luteum
Biology of Reproduction, 2002Co-Authors: Hiroaki Taniguchi, Yuichi Yokomizo, Kiyoshi OkudaAbstract:Fas antigen (Fas) is a Cell surface receptor that triggers apoptosis in sensitive Cells when bound to the Fas ligand (Fas L). The present study was undertaken to identify the presence of a Fas-Fas L system in bovine corpus luteum (CL) and to evaluate the regulation of Fas-mediated Luteal Cell death by leukocytederived cytokines. The reverse transcription-polymerase chain reaction showed higher levels of Fas mRNA expression in CL in the regressed Luteal stage (Days 19‐21) than in the other stages (P , 0.05). Bovine Luteal Cells from midcycle CL (Days 8‐12) were exposed for 24 h to interferon g (IFN; 50 ng/ml) and/or tumor necrosis factor a (TNF; 50 ng/ml). After 24 h of culture, the expression of Fas mRNA was detected in the cultured Cells and was increased by IFN. Moreover, TNF augmented the stimulatory action of IFN, whereas TNF alone did not affect the expression of Fas mRNA. The effects of IFN and TNF on Fas-mediated Cell death were also examined. Cells were exposed to IFN and/or TNF for 24 h and were further treated with IFN and/or TNF in the presence or absence of Fas L (100 ng/ml) for 24 h. Treatments of the Cells with IFN alone and in combination with TNF resulted in killing of 30% and 50% of the Cells (P , 0.05), respectively, whereas TNF alone did not have a cytotoxic effect on the Cells. On the other hand, Fas L killed 60% of the Cells treated with IFN (P , 0.01) and 85% of the Cells treated with the combination of TNF and IFN (P , 0.01), respectively, whereas Fas L showed no effect on the viability of the Luteal Cells treated with or without TNF. Furthermore, shrunken nuclei and apoptotic bodies were observed in the Cells treated with Fas L in the presence of TNF and IFN. The overall results suggest that a Fas-Fas L system is present in bovine CL and that leukocytederived TNF and IFN play important roles in Fas-mediated Luteal Cell death. apoptosis, corpus luteum, corpus luteum function, cytokines, ovary
Chih-hsien Chiu - One of the best experts on this subject based on the ideXlab platform.
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dynamic changes in mitochondrial 3d structure during folliculogenesis and Luteal formation in the goat large Luteal Cell lineage
Scientific Reports, 2021Co-Authors: Yifan Jiang, Yovita Permata Budi, Chih-hsien ChiuAbstract:In mammalian ovaries, mitochondria are integral sites of energy production and steroidogenesis. While shifts in Cellular activities and steroidogenesis are well characterized during the differentiation of large Luteal Cells in folliculogenesis and Luteal formation, mitochondrial dynamics during this process have not been previously evaluated. In this study, we collected ovaries containing primordial follicles, mature follicles, corpus hemorrhagicum, or corpus luteum from goats at specific times in the estrous cycle. Enzyme histochemistry, ultrastructural observations, and 3D structural analysis of serial sections of mitochondria revealed that branched mitochondrial networks were predominant in follicles, while spherical and tubular mitochondria were typical in large Luteal Cells. Furthermore, the average mitochondrial diameter and volume increased from folliculogenesis to Luteal formation. In primordial follicles, the signals of cytochrome c oxidase and ATP synthase were undetectable in most Cells, and the large Luteal Cells from the corpus hemorrhagicum also showed low enzyme signals and content when compared with granulosa Cells in mature follicles or large Luteal Cells from the corpus luteum. Our findings suggest that the mitochondrial enlargement could be an event during folliculogenesis and Luteal formation, while the modulation of mitochondrial morphology and respiratory enzyme expressions may be related to tissue remodeling during Luteal formation.
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Cantharidin and norcantharidin inhibit caprine Luteal Cell steroidogenesis in vitro.
Experimental and toxicologic pathology : official journal of the Gesellschaft fur Toxikologische Pathologie, 2010Co-Authors: Nae-fang Twu, Ramanujam Srinivasan, Chung-hsi Chou, Chih-hsien ChiuAbstract:Cantharidin and its analog norcantharidin are active constituents of Mylabris, have been demonstrated to ailments for a variety of cancers. But several reports of cantharidin's natural or accidental toxicoses in field animals and humans showed a strong connection between cantharidin and its abortifacient and aphrodisiac properties. However, their exact Cellular mechanisms in steroidogenesis remains poorly understood. Thus this study was aimed to explore the effects of cantharidin on Luteal Cell steroidogensis and to compare its effect with that of norcantharidin. For this purpose, Luteal Cells isolated from corpora lutea of native Taiwan goats were maintained in vitro and treated for 4 and 24 h with cantharidin and norcantharidin (0.1, 1.0, and 10 μg ml(-1)) to assess their steroidogenic effects. Progesterone (P(4)) levels and steroidogenic enzyme expression were assessed by enzyme immunoassay and Western blot methods, respectively. In caprine Luteal Cells, cantharidin and norcantharidin repressed basal P(4) production, as well as that mediated by ovine luteinizing hormone (oLH), 8-bromo-cyclic AMP (8-Br-cAMP), 22R-hydroxycholesterol (22R-OHC) and pregnenolone (P(5)). They also inhibited the expression of steroidogenic acute regulatory (StAR) protein, cytochrome P450 cholesterol side-chain cleavage (P450scc) enzyme, and 3β-hydroxysteroid dehydrogenase (3β-HSD) enzyme. Additionally, the greater inhibitory effect was detected using cantharidin, when it is compared with that of norcantharidin. Our results suggest that ingestion of cantharidin may decrease Luteal steroidogenesis, and the decline in Luteal P(4) levels may disrupt reproductive functions in humans as well as animals.
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Characterization of a stable steroidogenic caprine Luteal Cell line transformed by a temperature-sensitive simian virus 40.
The Chinese journal of physiology, 2008Co-Authors: Chih-hsien Chiu, Ing-chen Guo, Jen-hsou LinAbstract:A caprine Luteal Cell line (tsCLC-D) that synthesizes progesterone (P4) was established following by transformation with a temperature-sensitive A209 (tsA209) mutant of simian virus 40 (SV40). The transformed Cells have temperature-sensitive for morphology, Cell propagation and progesterone steroidogenesis. At the permissive temperature of 34℃, these Cells were spindle-shaped and grew with a similar rapidity as tumor Cells. However, at the nonpermissive temperature of 40℃, the Cells have exhibited a round shape and ceased to proliferate because the gene for maintenance of transformation was not expressed. The tsCLC-D Cell line responds to 8-Br-cyclic AMP, 22-hydroxycholesterol and pregnenolone treatment with an increase in progesterone biosynthesis. This Cell line still express StAR protein, 3β-HSD and P450scc enzyme of three kinds of steroidogenic protein and enzymes, this characteristic is similar to normal Luteal Cell. However, the addition of any doses oLH did not increase progesterone secretion. We speculate that tsCLC-D might lose the responsiveness to gonadotropins during the immortalization process, while retaining steroidogenic enzyme activity and progesterone production. To our knowledge, this is the first report of a stable Cell line derived from corpus luteum of ruminant. The tsCLC-D retains steroidogenic capacity, which will make this Cell line useful for the studies of regulation of steroidogenesis.
Geula Gibori - One of the best experts on this subject based on the ideXlab platform.
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mechanisms of Luteal Cell regulation by prolactin
2001Co-Authors: Michael Risk, Geula GiboriAbstract:The corpus luteum is an endocrine gland of limited lifespan formed from the remaining granulosa and theca Cells of the follicle following ovulation. The main function of this gland is the synthesis and secretion of progesterone. Progesterone is a steroid hormone required for preparing the endometrium for implantation, regulating pituitary gonadotropin secretion and, importantly, maintaining a quiescent uterus by inhibiting the contractile activity of the myometrium, thus preventing the onset of parturition. In some species, such as the rat and mouse, the corpus luteum is responsible for the secretion of progesterone throughout pregnancy and is necessary for the entire length of gestation. In other species, such as human, the placenta assumes the majority of progesterone secretion at some point in gestation. In all mammals, however, progesterone is required for pregnancy and during a portion of gestation it must come from the corpus luteum.
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Establishment and Characterization of a Simian Virus 40-Transformed Temperature-Sensitive Rat Luteal Cell Line
Endocrinology, 1998Co-Authors: N. Sugino, Carlos M. Telleria, M. Zilberstein, R. K. Srivastava, S E Nelson, Michael Risk, J. Y. Chou, Geula GiboriAbstract:The primary culture of rat Luteal Cells and their long-term maintenance have been difficult. Low Cellular yields have limited the possibility for the study of gene regulation in Luteal Cells. The goal of this study was to develop a Cell line to serve as a model by which to study the expression and regulation of various genes specific to Luteal Cells. We attempted to develop a Luteal Cell line by transformation of large Luteal Cells through infection with a temperature-sensitive simian virus (SV-40 tsA209) mutant that has a temperature-sensitive mutation required for the maintenance of Cell transformation. We report here the successful establishment of such a Cell line, designated GG-CL Cells. Large Luteal Cells were purified to homogeneity by flow cytometry from corpora lutea of day 14 pregnant rats, cultured for 24 h, and then infected with the SV-40 tsA209 mutant virus. Transformed Cells were maintained at the permissive temperature (33 C) until colonies were identified. Several colonies of transformed ...
Joy L Pate - One of the best experts on this subject based on the ideXlab platform.
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changes in microrna expression during maturation of the bovine corpus luteum regulation of Luteal Cell proliferation and function by microrna 34a
Biology of Reproduction, 2016Co-Authors: Samar W Maalouf, Courtney L Smith, Joy L PateAbstract:The corpus luteum (CL) develops from the remnants of the ovulatory follicle and produces progesterone, required for maintenance of pregnancy in mammals. The differentiation of granulosal and thecal Cells into Luteal Cells is accompanied by hypertrophy and hyperplasia of Cells. As the CL matures, growth ceases and in ruminants, the tissue acquires the ability to undergo regression in response to prostaglandin F2alpha. The regulators of this transition are poorly understood. MicroRNA, which are posttranscriptional regulators of tissue development and function, are expressed in the CL. However, the pattern of their expression and their function during the transition from developing to functional CL is not known. The objectives of this study were to profile the expression of miRNA in developing versus mature bovine CL and determine effects of miRNA on bovine Luteal Cell survival and function. Knockdown of Drosha in midcycle (MC) Luteal Cells decreased progesterone and increased Luteal Cell apoptosis in the presence or absence of proinflammatory cytokines. Microarray analysis demonstrated that a greater number of miRNA were expressed in MC compared to D4 CL. Ingenuity pathway analysis (IPA) predicted that D4-specific miRNA regulate pathways related to carbohydrate metabolism, while MC-specific miRNA regulate pathways related to Cell cycle and apoptosis signaling. Both predictions are consistent with a switch in the CL from a growing phase to a maintenance phase. One of the MC specific miRNA, miR-34a, was selected for further analysis. Increased concentrations of miR-34a in MC Luteal Cells resulted in decreased Luteal Cell proliferation, increased progesterone production, and inhibition of Notch1 and YY1 translation, but had no effect on Luteal Cell apoptosis. In conclusion, these data support a role for miRNA in general, and miR-34a in particular, in Luteal formation and function.
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tumor necrosis factor alpha alters bovine Luteal Cell synthetic capacity and viability
Endocrinology, 1992Co-Authors: Deborah Fairchild Benyo, Joy L PateAbstract:Tumor necrosis factor-alpha (TNF-alpha) is a macrophage-derived cytokine that is also reportedly produced by granulosal Cells and is localized in Luteal Cells. The present study employed serum-free culture of midcycle bovine Luteal Cells to investigate the effects of TNF-alpha, alone and with other cytokines, on Luteal function. TNF-alpha (1-1000 ng/ml) produced a dose-dependent increase in prostaglandin (PG)F2 alpha and 6-keto-PGF1 alpha synthesis on all days of culture, but had no effect on basal progesterone (P4) production. TNF-alpha, in combination with other known stimulators of Luteal PG synthesis, interleukin-1 beta (2.5 ng/ml) or interferon-gamma (IFN-gamma, 100 U/ml), had synergistic effects on PGF2 alpha production (greater than 50-fold above control, P less than 0.05) whereas interferon-alpha (1000 U/ml) significantly suppressed TNF-alpha-stimulated PGF2 alpha production. By day 7 of culture, TNF-alpha inhibited LH-stimulated P4 production (P less than 0.05). Luteal Cell numbers were significa...
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modulation of bovine Luteal Cell synthetic capacity by interferon gamma
Biology of Reproduction, 1991Co-Authors: D L Fairchild, Joy L PateAbstract:Previous work from our laboratory has demonstrated that major histocompatibility complex (MHC) antigens are expressed on cultured bovine Luteal Cells following exposure to the T lymphocyte-derived cytokine, interferon-gamma (IFN-gamma). In light of these actions of IFN-gamma, it was of interest to investigate the effects of this cytokine on other aspects of Luteal function. Therefore, bovine Luteal Cells were cultured for 7 days in the presence or absence of IFN-gamma, and Luteal progesterone (P4), prostaglandin F2 alpha (PGF2 alpha), and 6-keto-prostaglandin F1 alpha (6-keto-PGF1 alpha) production were evaluated. After a 24-h exposure to IFN-gamma (100 U), both PGF2 alpha and 6-keto-PGF1 alpha production were decreased approximately 50% (p less than 0.05). However, as time in culture progressed, IFN-gamma markedly increased the synthesis of both prostaglandins approximately 400% above controls (p less than 0.05). Stimulation of prostaglandin production by IFN-gamma was abrogated by the addition of exogenous P4. During the period of IFN-gamma-stimulated prostaglandin synthesis, LH-stimulated P4 production was inhibited by IFN-gamma treatment. However, the suppression of P4 production by IFN-gamma was not mediated by the increase in prostaglandins since concomitant treatment with indomethacin did not reverse the inhibition of steroidogenesis. These results suggest that IFN-gamma, in addition to an indirect role in promoting immune response mechanisms, may also directly affect Luteal function by enhancing Luteal prostaglandin synthesis and by inhibiting Luteal steroidogenesis.
Hajime Miyamoto - One of the best experts on this subject based on the ideXlab platform.
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soluble fas fasb regulates Luteal Cell apoptosis during luteolysis in murine ovaries
Molecular Reproduction and Development, 2003Co-Authors: Kohji Komatsu, Noboru Manabe, Minako Kiso, Munetake Shimabe, Hajime MiyamotoAbstract:During luteolysis, Luteal Cell apoptosis is induced by the Fas ligand (FasL)/Fas system. In murine Luteal bodies, we demonstrated the expression of mRNA of soluble form of Fas (FasB), which binds to FasL and prevents apoptosis induction. By in situ hybridization, strong expression of FasB mRNA was observed in normal Luteal bodies, in which no apoptotic Cells were detected, but negative/trace expression in regressing Luteal bodies, in which many apoptotic Cells were observed. Immunohistochemical staining revealed that Fas and TNF-alpha were localized in both normal and regressing Luteal bodies, but IFN-gamma was localized only in regressing Luteal bodies. Apoptosis was induced in primary cultured Luteal Cells, when they were pretreated with TNF-alpha and IFN-gamma and then incubated with TNF-alpha, IFN-gamma, and mouse recombinant FasL (rFasL). However, no apoptosis was detected in the Cells, when they were treated with rFasL alone, TNF-alpha alone, IFN-gamma alone, TNF-alpha and rFasL, IFN-gamma and rFasL, or TNF-alpha and IFN-gamma. Fas mRNA expression in cultured Luteal Cells was up-regulated by the treatment of TNF-alpha, IFN-gamma, or TNF-alpha and IFN-gamma. The expression of FasB mRNA was down-regulated, when the Cells were treated with TNF-alpha and IFN-gamma, but its expression was not changed by the treatment of TNF-alpha alone or IFN-gamma alone. We conclude that FasB inhibits the apoptosis induction in Luteal Cells of normal Luteal bodies, and that decreased FasB production induced by TNF-alpha and IFN-gamma made possible the apoptosis induction in the Luteal Cells of regressing Luteal bodies.
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soluble fas fasb regulates Luteal Cell apoptosis during luteolysis in murine ovaries
Molecular Reproduction and Development, 2003Co-Authors: Kohji Komatsu, Noboru Manabe, Minako Kiso, Munetake Shimabe, Hajime MiyamotoAbstract:During luteolysis, Luteal Cell apoptosis is induced by the Fas ligand (FasL)/Fas system. In murine Luteal bodies, we demonstrated the expression of mRNA of soluble form of Fas (FasB), which binds to FasL and prevents apoptosis induction. By in situ hybridization, strong expression of FasB mRNA was observed in normal Luteal bodies, in which no apoptotic Cells were detected, but negative/trace expression in regressing Luteal bodies, in which many apoptotic Cells were observed. Immunohistochemical staining revealed that Fas and TNF-α were localized in both normal and regressing Luteal bodies, but IFN-γ was localized only in regressing Luteal bodies. Apoptosis was induced in primary cultured Luteal Cells, when they were pretreated with TNF-α and IFN-γ and then incubated with TNF-α, IFN-γ, and mouse recombinant FasL (rFasL). However, no apoptosis was detected in the Cells, when they were treated with rFasL alone, TNF-α alone, IFN-γ alone, TNF-α and rFasL, IFN-γ and rFasL, or TNF-α and IFN-γ. Fas mRNA expression in cultured Luteal Cells was up-regulated by the treatment of TNF-α, IFN-γ, or TNF-α and IFN-γ. The expression of FasB mRNA was down-regulated, when the Cells were treated with TNF-α and IFN-γ, but its expression was not changed by the treatment of TNF-α alone or IFN-γ alone. We conclude that FasB inhibits the apoptosis induction in Luteal Cells of normal Luteal bodies, and that decreased FasB production induced by TNF-α and IFN-γ made possible the apoptosis induction in the Luteal Cells of regressing Luteal bodies. Mol. Reprod. Dev. 65: 345–352, 2003. © 2003 Wiley-Liss, Inc.
