scholarly journals Localization of gonadotrophin-releasing hormone I, bradykinin and their receptors in the ovaries of non-mammalian vertebrates

Reproduction ◽  
2007 ◽  
Vol 133 (5) ◽  
pp. 969-981 ◽  
Author(s):  
Padmasana Singh ◽  
Amitabh Krishna ◽  
Rajagopala Sridaran
Keyword(s):  
Granulosa Cells ◽  
Follicular Development ◽  
Cell Types ◽  
Physiological Significance ◽  
Rt Pcr ◽  
Releasing Hormone ◽  
Theca Cells ◽  
Gonadotrophin Releasing Hormone

GnRH I and its receptors have been demonstrated in the ovaries of various vertebrates, but their physiological significance in reproductive cascade is fragmentary. Bradykinin is a potent GnRH stimulator in the hypothalamus. In the present study, the presence of GnRH I and its receptor, and bradykinin and its receptor in the ovaries of non-mammalian vertebrates were investigated to understand their physiological significance. GnRH I immunoreactivity in the ovaries of fish, frog, reptile and bird were mainly found in the oocyte of early growing follicles and granulosa cells and theca cells of previtellogenic follicles. Vitellogenic follicles showed mild GnRH immunoreactivity. GnRH I-receptor and bradykinin were localized in the same cell types of the ovaries of these vertebrates. The presence of GnRH I, GnRH I-receptor and bradykinin in the ovaries of these vertebrates was confirmed by immunoblotting. The presence of GnRH I mRNA was demonstrated in the ovary of vertebrates using RT-PCR. The ovaries of reptiles and birds showed significantly higher intensity of immunoreactivity for GnRH I-receptor as compared with the fish and amphibian. This may have a correlation with the higher yolk content in the ovary of reptile and bird. These results suggest the possibility of GnRH I and bradykinin as important regulators of follicular development and vitellogenesis in the vertebrate ovary.

scholarly journals Expression and effect of NAMPT (visfatin) on progesterone secretion in hen granulosa cells

Reproduction ◽  
2015 ◽  
Vol 150 (1) ◽  
pp. 53-63 ◽  
Author(s):  
Mélodie Diot ◽  
Maxime Reverchon ◽  
Christelle Ramé ◽  
Yannick Baumard ◽  
Joëlle Dupont
Keyword(s):  
Granulosa Cells ◽  
Specific Inhibitor ◽  
Follicular Development ◽  
Rt Pcr ◽  
Nicotinamide Phosphoribosyltransferase ◽  
Theca Cells ◽  
Protein Levels ◽  
Progesterone Secretion ◽  
Ovulatory Follicles

In mammals, nicotinamide phosphoribosyltransferase (NAMPT) is an adipokine produced by adipose tissue that is found in intracellular and extracellular compartments. The intracellular form of NAMPT is a nicotinamide phosphoribosyltransferase, whereas the extracellular form is considered an adipokine. In humans, NAMPT regulates energy metabolism and reproductive functions, such as ovarian steroidogenesis. To date, no study has investigated the role of NAMPT in hen ovaries. We investigated whether NAMPT is present in hen ovarian follicles and its role in granulosa cells. Using RT-PCR, western blotting and immunocytochemistry, we detected mRNA transcripts and proteins related to NAMPT in theca and granulosa cells from pre-ovulatory follicles. Using RT-PCR, we demonstrated that mRNA NAMPT levels were higher in granulosa cells than they were in theca cells and that during follicle development, theca cell levels decreased, whereas levels remained unchanged in granulosa cells. NAMPT protein quantities were significantly higher in theca cells than they were in granulosa cells, but they were unchanged during follicular development. Plasma NAMPT levels, as determined by ELISA and immunoblotting, were significantly lower in adult hens than they were in juveniles. In vitro, treatment with human recombinant NAMPT (100 ng/ml, 48 h) halved basal and IGF1-induced progesterone secretion, and this was associated with a reduction in STAR and HSD3B protein levels and MAPK3/1 phosphorylation levels in granulosa cells. These effects were abolished by the addition of FK866, a specific inhibitor of NAMPT enzymatic activity. Moreover, NAMPT had no effect on granulosa cell proliferation. In conclusion, NAMPT is present in hen ovarian cells and inhibits progesterone production in granulosa cells.

scholarly journals The hedgehog-patched signaling pathway and function in the mammalian ovary: a novel role for hedgehog proteins in stimulating proliferation and steroidogenesis of theca cells

Reproduction ◽  
2009 ◽  
Vol 138 (2) ◽  
pp. 329-339 ◽  
Author(s):  
Leon J Spicer ◽  
Satoko Sudo ◽  
Pauline Y Aad ◽  
Lora Shuo Wang ◽  
Sang-Young Chun ◽  
...  
Keyword(s):  
Granulosa Cells ◽  
Follicular Development ◽  
Mrna Abundance ◽  
Rt Pcr ◽  
Theca Cells ◽  
Qrt Pcr ◽  
Hedgehog Proteins ◽  
Patched 1 ◽  
And Function ◽  
First Time

The expression of hedgehog (Hh) genes, their receptor, and the co-receptor in mice, rat, and bovine ovaries were investigated. RT-PCR of ovarian transcripts in mice showed amplification of transcripts for Indian (Ihh) and desert (Dhh) Hh, patched 1 (Ptch1), and smoothened (Smo) genes. Semi-quantitative RT-PCR and northern blot analyses showed that whole ovarianIhhandDhhtranscripts decreased 4–24 h after hCG versus 0–48 h after pregnant mares serum gonadotrophin treatment in mice, whereas mousePtch1andSmotranscripts were expressed throughout the gonadotropin treatments. Quantitative real-time RT-PCR (qRT-PCR) revealed that the expression of the Hh-patched signaling system withIhhmRNA abundance in granulosa cells was greater, whereasSmoandPtch1mRNA abundance was less in theca cells of small versus large follicles of cattle. In cultured rat and bovine theca-interstitial cells, qRT-PCR analyses revealed that the abundance ofGli1andPtch1mRNAs were increased (P<0.05) with sonic hedgehog (SHH) treatment. Additional studies using cultured bovine theca cells indicated that SHH induces proliferation and androstenedione production. IGF1 decreasedIhhmRNA abundance in bovine granulosa cells. The expression and regulation ofIhhtranscripts in granulosa cells andPtch1mRNA in theca cells suggest a potential paracrine role of this system in bovine follicular development. This study illustrates for the first time Hh activation of Gli1 transcriptional factor in theca cells and its stimulation of theca cell proliferation and androgen biosynthesis.

The antagonistic effect of exogenous LH pulses on FSH-stimulated preovulatory follicle growth in ewes chronically treated with a gonadotrophin-releasing hormone agonist

1990 ◽  
Vol 127 (2) ◽  
pp. 273-283 ◽  
Author(s):  
H. M. Picton ◽  
C. G. Tsonis ◽  
A. S. McNeilly
Keyword(s):  
Luteal Phase ◽  
Follicular Development ◽  
High Amplitude ◽  
Follicle Growth ◽  
High Concentration ◽  
Continuous Administration ◽  
Releasing Hormone ◽  
Low Concentrations ◽  
Gonadotrophin Releasing Hormone ◽  
The Mean

ABSTRACT The hypogonadotrophism model induced by the chronic administration of gonadotrophin-releasing hormone (GnRH) agonist was used to investigate the effects of different concentrations of FSH with or without LH pulses on the stimulation of follicular development in the ewe. Continuous administration of an agonist (buserelin) by osmotic minipump to thirty-six Welsh Mountain ewes from the early luteal phase for 5 weeks resulted in a sustained suppression of the plasma concentration of FSH and inhibited the pulsatile release of LH. The inhibition of gonadotrophin secretion was due to the desensitization and/or down-regulation of pituitary gonadotroph function, since the agonist-treated animals showed no response to a challenge of 1 μg GnRH. During week 6 of agonist treatment, ewes were infused with either 4-hourly pulses of ovine LH (9 μg/pulse), low concentrations of ovine FSH (3 μg/h) or high concentrations of FSH (9 μg/h) alone or with 4-hourly pulses of LH. After 5 days of gonadotrophin infusion, there was no difference between the mean number of follicles per ewe from the animals treated with LH alone, low concentrations of FSH with or without LH pulses or the high concentration of FSH alone compared with the mean number of follicles from control ewes on day 8 of the luteal phase. Infusion of the high concentration of FSH alone stimulated the development of an increased number of large oestrogenic follicles (follicles > 2·5 mm in diameter and secreting > 3·7 nmol oestradiol/h in vitro) compared with control ewes. The addition of high-amplitude LH pulses to the infusion of the high concentration of FSH prevented follicles developing beyond 2·5 mm in diameter, but doubled the number of small follicles (≤2·5 mm) present in the ovaries. These results show that normal follicular development can be induced by physiological concentrations of FSH alone in the absence of pulsatile LH release. The addition of high-amplitude LH pulses antagonized this stimulatory effect of FSH on follicle growth in the ewe. Journal of Endocrinology (1990) 127, 273–283

Effect of basal and pulsatile LH release on FSH-stimulated follicle growth in ewes chronically treated with gonadotrophin-releasing hormone agonist

1991 ◽  
Vol 128 (3) ◽  
pp. 449-456 ◽  
Author(s):  
H. M. Picton ◽  
A. S. McNeilly
Keyword(s):  
Gnrh Agonist ◽  
Follicular Development ◽  
Follicle Growth ◽  
Releasing Hormone ◽  
Normal Number ◽  
Stage Of Development ◽  
Normal Diameter ◽  
Lh Release ◽  
Gonadotrophin Releasing Hormone ◽  
Follicular Response

ABSTRACT Ewes chronically treated with gonadotrophin-releasing hormone (GnRH) agonist were used to investigate the importance of the peripheral concentration of LH in FSH-stimulated follicular development. Twenty-four Welsh Mountain ewes were treated with two agonist implants containing 3·3 mg buserelin. During week 6 of treatment all the ewes were given a 72-h continuous infusion of ovine FSH alone (3 μg/h) or FSH with large (7·5 μg)- or small (2·5 μg) amplitude pulses of ovine LH delivered at 4-hourly intervals. The importance of baseline LH throughout the FSH infusion was evaluated in six animals which were treated with a specific antiserum against bovine LH (LH-AS) 15–20 h before the start of FSH treatment. In the absence of LH-AS, infusion of FSH alone or with large or small pulses of LH stimulated the development of a normal number of small follicles (≤ 2·5 mm in diameter) and large follicles (> 2·5 mm in diameter). These follicles had normal diameter and steroid secretion compared with control ewes on day 8 of the luteal phase. In contrast, the animals pretreated with LH-AS developed no follicles > 2·0 mm in diameter but the number of small follicles per ewe was significantly (P < 0·05) increased. These results support the hypothesis that FSH in the absence of pulsatile LH release stimulates preovulatory follicular development in ewes treated with GnRH agonist. The follicular response to LH pulses of different amplitude is dependent on both the stage of development of the follicle and the peripheral concentration of FSH. The endogenous basal level of LH present throughout the FSH infusion is essential for FSH to induce follicle growth beyond > 2·5 mm in diameter. Journal of Endocrinology (1991) 128, 449–456

scholarly journals Corticotrophin-releasing hormone inhibits insulin-like growth factor-I release from primary cultures of rat granulosa cells

2002 ◽  
Vol 174 (3) ◽  
pp. 493-498 ◽  
Author(s):  
AE Calogero ◽  
A Barreca ◽  
N Burrello ◽  
I Palermo ◽  
G Giordano ◽  
...  
Keyword(s):  
Growth Factor ◽  
Granulosa Cells ◽  
Primary Cultures ◽  
Cell Types ◽  
Suppressive Effect ◽  
Insulin Like Growth Factor ◽  
Sprague Dawley ◽  
Releasing Hormone ◽  
Igf I ◽  
Igfbp 3

Corticotrophin-releasing hormone (CRH), a neuropeptide which modulates gonadal function during stress, is expressed by several cell types of the rat ovary and is able to suppress oestrogen release from rat granulosa cells. The mechanism of this effect is, however, not known. Since insulin-like growth factor (IGF)-I is produced by rat granulosa cells and exerts a synergistic role with FSH on granulosa cell steroidogenesis, we hypothesised that CRH may suppress oestrogen release from granulosa cells by inhibiting IGF-I release and/or stimulating the release of its binding protein (IGFBP-3). To test this hypothesis, granulosa cells were obtained from immature female Sprague-Dawley rats primed with diethylstilboestrol, and hormone concentrations were measured in the conditioned medium by radioimmunoassay. CRH suppressed oestrogen and IGF-I release stimulated by FSH used at a concentration of 1 IU/l, whereas it did not have any statistically significant effect on oestrogen and IGF-I release in basal conditions or in response to 5 IU/l FSH. The suppressive effects of CRH on oestrogen and IGF-I release were antagonised by a selective CRH receptor antagonist. CRH had no effects on IGFBP-3 release. CRH did not have any effect on oestrogen release stimulated by increasing concentrations of IGF-I and its suppressive effect on FSH-stimulated oestrogen release was overcome by the addition of low doses of exogenous IGF-I. In conclusion, CRH suppressed the release of oestrogen and IGF-I, but not of IGFBP-3. Thus, the inhibitory effects of CRH on oestrogen release could be mediated, partly, by a suppression of the autocrine/paracrine action of IGF-I.

scholarly journals miR-375 mediates CRH signaling pathway in inhibiting E2 synthesis in porcine ovary

Reproduction ◽  
2017 ◽  
Vol 153 (1) ◽  
pp. 63-73 ◽  
Author(s):  
Chulin Yu ◽  
Meiling Li ◽  
Yue Wang ◽  
Ying Liu ◽  
Chengzhi Yan ◽  
...  
Keyword(s):  
Signaling Pathway ◽  
Granulosa Cells ◽  
Reproductive System ◽  
Follicular Development ◽  
Cell Types ◽  
Signaling System ◽  
Key Factor ◽  
The Relationship

The corticotropin-releasing hormone (CRH) signaling system is involved in numbers of stress-related physiological and pathological responses, including its inhibiting effects on estradiol (E2) synthesis and follicular development in the ovary. In addition, there are reports that microRNAs (miRNAs) can control the function of animal reproductive system. The aim of present study was to investigate the functions of miR-375 and the relationship between miR-375 and CRH signaling molecules in the porcine ovary. First, our common PCR results show that miR-375 and the CRH receptor 1 (CRHR1) are expressed in porcine ovary, whereas CRH receptor 2 (CRHR2) is not detected. We further have located the cell types of miR-375 and CRHR1 by in situ hybridization (ISH), and the results show that miR-375 is located only in the granulosa cells, whereas CRHR1 is positive in all of granulosa cells and oocytes, inferring that miR-375 and CRHR1 are co-localized in granulosa cells. Second, we show that overexpression of miR-375 in cultured granulosa cells suppresses the E2 production, whereas miR-375 knockdown demonstrates the opposite result. Besides, our in vitro results demonstrate that miR-375 mediates the signaling pathway of CRH inhibiting E2 synthesis. Finally, our data show that the action of miR-375 is accomplished by directly binding to the 3′UTR of specificity protein1 (SP1) mRNA to decrease the SP1 protein level. Thus, we conclude that miR-375 is a key factor in regulating E2 synthesis by mediating the CRH signaling pathway.

scholarly journals Effects of a long-acting gonadotrophin-releasing hormone agonist (Leuprolide) on ovarian follicular development in prepubertal heifer calves

1994 ◽  
Vol 74 (4) ◽  
pp. 649-656 ◽  
Author(s):  
A. C. O. Evans ◽  
N. C. Rawlings
Keyword(s):  
Gnrh Agonist ◽  
Follicular Development ◽  
Ovarian Follicles ◽  
Follicular Growth ◽  
Long Term Effects ◽  
Releasing Hormone ◽  
Gonadotrophin Secretion ◽  
Gonadotrophin Releasing Hormone ◽  
Ovarian Follicular Development ◽  
Ovarian Follicular Growth

We studied the effects of reducing gonadotrophin secretion on ovarian follicular development in young prepubertal heifer calves. Calves received a GnRH agonist (n = 5, 15 mg of Leuprolide acetate, i.m.) or carrier (n = 5) at 8 and 12 w of age. Starting at 8 and 34 w of age, ovarian follicles were monitored daily for 17 d, and at 10, 15, 25 and 35 w of age, blood samples were collected every 15 min for 12 h for measurement of serum concentration of LH and FSH. GnRH agonist treatment did not affect the age and body weight at puberty (P > 0.05). Agonist treatment suppressed follicle numbers and in two heifers follicle emergence (growth above 4–5 mm) was blocked immediately. In three agonist-treated heifers, follicle emergence was blocked after one extended wave of follicular growth. At 34 w of age the pattern of ovarian follicular growth did not differ between groups but oestradiol secretion was lower in agonist-treated heifers. During agonist treatment basal and mean concentrations of FSH, and LH and FSH pulse amplitude were decreased but basal LH concentrations increased (P < 0.05). At 25 and 35 w of age some rebound in gonadotrophin secretion was seen.We concluded that disrupting gonadotrophin secretion in young prepubertal heifer calves by GnRH agonist treatment, suppressed ovarian follicular growth but that a rebound in gonadotrophin secretion prevented long term-effects on sexual development. Key words: Follicle stimulating hormone, gonadotrophin-releasing hormone, heifer calves, luteinising hormone ovarian follicles

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