• 한국어업기술학회:학술대회논문집
• /
• 한국어업기술학회 2002년도 춘계 수산관련학회 공둥학술발표회
• /
• pp.427-428
• /
• 2002

• 한국양식학회:학술대회논문집
• /
• 한국양식학회 2002년도 춘계 한국양식학회 학술대회 발표요지
• /
• pp.230.2-231
• /
• 2002

• Animal cells and systems
• /
• 제5권3호
• /
• pp.217-224
• /
• 2001

The present study examines the expression and regulation of gonadotropin-releasing hormone (GnRH) and its receptor (GnRH-R) mRNA levels during mouse ovarian development. A fully processed, mature GnRH mRNA together with intron-containing primary transcripts was expressed in the immature mouse ovary as determined by Northern blot analysis and reverse transcription-polymerase chain reaction (RT-PCR). The size of ovarian GnRH mRNA was similar to that of hypothalamus, but its amount was much lower than that in the hypothalamus. Quantitative RT-PCR procedure also revealed the expression of GnRH-R mRNA in the ovary, but the estimated amount was a thousand-fold lower than that in the pituitary gland. We also examined the regulation of ovarian GnRH and GnRH-R mRNA levels during the follicular development induced by pregnant mare's serum gonadotropin (PMSG) and/or human chorionic gonadotropin (hCG). Ovarian luteinizing hormone receptor (LH-R) mRNA was abruptly increased st 48 h after the PMSG administration and rapidly decreased to the basal level thereafter. Ovarian GnRH mRNA level was slightly decreased at 48 h after the PMSG administration, and then returned to the basal value. GnRH-R mRNA level began to increase at 24 h after the PMSG treatment, decreased below the uninduced basal level at 48 h, and gradually increased thereafter. HCG administration did not alter ovarian GnRH mRNA level, while it blocked the PMSG-induced increase in GnRH mRNA level. Taken together, the present study demonstrates that the expression of GnRH and GnRH-R mRNA are regulated by gonadotropin during follicular development, suggesting possible intragonadal paracrine roles of GnRH and GnRH-R in the mouse ovarian development.

• 한국발생생물학회지:발생과생식
• /
• 제1권2호
• /
• pp.157-164
• /
• 1997

To study the regulation of porcine follicular cell apostosis by gonadotropin, steroid, and nitric oxide, we analyzed DNA fragmentation, the hallmark of apoptosis, and nitrite production of porcine granulosa cells. Dissected indiidual follicles from ovary were separated in size (small, 2-3 mm; medium, 5-6 mm; large, 7-8 mm) and isolated granulosa cells were classified morpholocally as atretic or nonatretic. Nitrite concentration was measured by mixing follicular fluids with an equal volume of Griess reagent. Follicular nitric oxide (NO) concentration of healthy follicles was higher than that of atretic follicles. Apoptotic DNA fragmentation was suppressed in non-apoptotic granulosa cells. Follicular apoptosis was induced by androgen but prevented by gonadotropin in vitro. Apoptosis was confined to the granulosa cells. But it was not clear whether apoptosis of granulosa cells were isolated, incubated with or without gonadotropin, androgen and sodium nitroprusside (SNP), respectively at $37^{\circ}C$ for 24 hrs. Cultured granulosa cells were used to extract genomic DNA and culture media was asssayed for nitrite concentration. Nitrite production of culture media was increased, while apoptotic DNA fragmentation was suppressed in PMSG, hCG, testosterone+SNP and SNP treated groups. Nitrite concentration in culture media was decreased, but apoptotic DNA fragmentation was induced in testosterone treated group. These data suggest that NO production and apoptosis may be involved of granulosa cell apoptosis induced by testosterone.

• 한국발생생물학회지:발생과생식
• /
• 제28권1호
• /
• pp.1-12
• /
• 2024

Gonadotropin-releasing hormone (GnRH), a critical hormone produced in the hypothalamus, is essential for regulating reproductive processes. It has also been demonstrated the presence of GnRH and its receptors (GnRHR) in ovarian and uterine tissues, but little was known about the regulation mechanism of their expression in these organs and ovarian aging. Therefore, the aim of this study was to investigate the expression of GnRHR in the ovary and uterus of mice, particularly after high-dose gonadotropin treatments and in relation to aging. Quantitative real-time-PCR (qRT-PCR) revealed that pituitary gland had the highest GnRHR expression in both young and aged mice. In addition, liver expression was higher in young mice, whereas thymus expression was higher in aged mice. GnRHR mRNA was present in the ovaries of both young and aged mice but nearly undetectable in the uterus of aged mice. We next examined the expression of GnRHR in the ovary and uterus in response to high-dose administration of pregnant mare serum gonadotropin (PMSG). After PMSG administration, GnRH mRNA levels were significantly decreased in the ovary but increased in the uterus. The expression of GnRH mRNA in these organs showed opposite trends to that of GnRHR expression. These results suggest the involvement of GnRH in age-related reproductive decline and the potential effects of high-dose gonadotropin treatments on reproductive organ function.

• 한국발생생물학회지:발생과생식
• /
• 제1권2호
• /
• pp.165-172
• /
• 1997

the pupose of this study was to investigate the effects of gonadotropin and nitric oxide (NO) on the expression of mouse follicular bad and bax genes that are known induce apoptosis. Large and midium size follicles of immature mice were obtained at 0, 24, and 48 hours time intervals after Pregnant Mare's Serum gonadotropins(PMSG, 5 I.U.) injection. Preovulatory follicles collected at 24 hrs after PMSG injection were cultured with or without various chemicals such as gonadotropin, gonadotropin Releasing hormone(GnRH), testosterone, Sodium nitroprusside (SNP) for 24 hrs at $37^{\circ}C$. After 24 hrs culture, the culture media was used for nitrite assay and total RNA was extracted, subjected to RT-PCT for the analyses of bad and bax expression. We found that expression of bad and bax genes in follicles was markedly reduced before and after in vivo priming with hCG. When the preovulatory follicles were cultured for 24 hrs in culture media with PMSG and hCG, the expression of bad and bax genes was decreased. Moreover, SNP (NO generating agent) can significantly suppress the expression of bad and bax genes in follicles when apoptosis was induced by GnRH agonist and testosterone. At the same time, nitrite production of culture media was increased in GnRH agonist + SNP, testosterone + SNP and SNP treated groups than control group. These data demonstrated for the first time that peptide hormones and NO may play important roles in the regulation of mouse follicular differentiation and may prevent apoptosis via supressing the expression of bad and bax genes.

• Animal cells and systems
• /
• 제11권2호
• /
• pp.93-98
• /
• 2007

Gonadotropin-releasing hormone (GnRH), synthesized in the hypothalamus, plays a pivotal role in the regulation of vertebrate reproduction. Since molecular isoforms of GnRH and their receptors (GnRHR) have been isolated in a broad range of vertebrate species, GnRH and GnRHR provide an excellent model for understanding the molecular co-evolution of a peptide ligand-receptor pair. Vertebrate species possess multiple forms of GnRH, which have been created through evolutionary mechanisms such as gene/chromosome duplication, gene deletion and modification. Similar to GnRHs, GnRH receptors (GnRHR) have also been diversified evolutionarily. Comparative ligand-receptor interaction studies for non-mammalian and mammalian GnRHRs combined with mutational mapping studies of GnRHRs have aided the identification of domains or motifs responsible for ligand binding and receptor activation. Here we discuss the molecular basis of GnRH-GnRHR co-evolution, particularly the structure-function relationship regarding ligand selectivity and signal transduction of mammalian and non-mammalian GnRHRs.

• Fisheries and Aquatic Sciences
• /
• 제18권2호
• /
• pp.211-220
• /
• 2015

We investigated the differences in the expression of the neurohormones kisspeptin (Kiss) and gonadotropin-inhibitory hormone (GnIH) and cytochrome P450 aromatase (P450arom), gonadotropin hormones (GTHs), and sex steroids in the goldfish Carassius auratus exposed to light-emitting diodes (LEDs). The expression levels of Kiss1, Kiss2, G-protein-coupled receptor 54 (GPR54), GTHs, GnIH, and P450arom were compared between the control (white light) and LED-treated goldfish. Furthermore, we measured the plasma levels of follicle-stimulating hormone (FSH) and luteinizing hormone (LH). The levels of Kiss1 mRNA and protein; Kiss2, GPR54, and $GTH{\alpha}$ protein; GTH mRNA; and plasma FSH and LH in the hypothalamus and cultured hypothalamus cells were significantly higher in the green and purple LED treatment groups than in the other groups. These results suggested that red LEDs inhibit the sex maturation hormones, Kiss, GPR54, GTHs, and P450arom, and that GnIH plays a role in the negative regulation of reproductive function in goldfish.

• Animal cells and systems
• /
• 제13권4호
• /
• pp.429-437
• /
• 2009

The control mechanism of gonadotropin-releasing hormone (GnRH) on gonadotropin (GTH) release was studied using cultured pituitary cell or cultured whole pituitary obtained from Testosterone (T) treated and control immature rainbow trout. The release of FSH was not changed by salmon type GnRH (sGnRH), chiken-II type (cGnRH-II), GnRH analogue ([des-$Gly^{10}D-Ala^6$] GnRH ethylamide) and GnRH antagonist ([Ac-3, 4-dehydro-$Pro^1$, D-p-F-$Phe^2$, D-$Trp^{3,6}$] GnRH) in cultured pituitary cells of T-treated and control fish. Indeed, FSH release was not also altered by sGnRH in cultured whole pituitary. All tested drugs had no effect on the release of LH in both culture systems of control fish. The levels of LH, in contrast, such as the pituitary content, basal release and responsiveness to GnRH were increased by T administration in both culture systems. In addition, the release of LH in response to sGnRH or cGnRH-II induced in a dose-dependent manner from cultured pituitary cells of T-treated fish, but which is not significantly different between in both GnRH at the concentration examined. Indeed, LH release was also increased by sGnRH in cultured whole pituitary of T-treated fish. GnRH antagonist suppressed the release of LH by sGnRH ($10^{-8}\;M$) and GnRH analogue ($10^{-8}\;M$) stimulation in a dose-dependent manner from cultured pituitary cells of T-treated fish, and which were totally inhibited by $10^{-7}\;M$ GnRH antagonist. These results indicate that the sensitivity of pituitary cells to GnRH is elevated probably through the T treatment, and that GnRH is involved in the regulation of LH release. GnRH-stimulated LH release is inhibited by GnRH antagonist in a dose-dependent manner. The effects of gonadal steroids on FSH levels are less clear.

• Clinical and Experimental Reproductive Medicine
• /
• 제38권1호
• /
• pp.18-23
• /
• 2011

Objective: Peroxiredoxins (Prxs) play an important role in regulating cellular differentiation and proliferation in several types of mammalian cells. This report examined the expression of Prx isotype I in the rat ovary after hormone treatment. Methods: Immature rats were injected with 10 IU of pregnant mare's serum gonadotropin (PMSG) to induce the growth of multiple preovulatory follicles and 10 IU of human chorionic gonadotropin (hCG) to induce ovulation. Immature rats were also treated with diethylstilbestrol (DES), an estrogen analogue, to induce the growth of multiple immature follicles. Northern blot analysis was performed to detect gene expression. Cell-type specific localization of Prx I mRNA were detected by in situ hybridization analysis. Results: During follicle development, ovarian Prx I gene expression was detected in 3-day-old rats and had increased in 21-day-old rats. The levels of Prx I mRNA slightly declined one to two days following treatment with DES. A gradual increase in Prx I gene expression was observed in ovaries obtained from PMSG-treated immature rats. Furthermore, hCG treatment of PMSG-primed rats resulted in a gradual stimulation of Prx I mRNA levels by 24 hours (2.1-fold increase) following treatment, which remained high until 72 hours following treatment. In situ hybridization analysis revealed the expression of the Prx I gene in the granulosa cells of PMSG-primed ovaries and in the corpora lutea of ovaries stimulated with hCG for 72 hours. Conclusion: These results demonstrate the gonadotropin and granulosa cell-specific stimulation of Prx I gene expression, suggesting its role as a local regulator of follicle development.