scholarly journals Androgen and Follicle-Stimulating Hormone Interactions in Primate Ovarian Follicle Development

1999 ◽  
Vol 84 (8) ◽  
pp. 2951-2956 ◽  
Author(s):  
Stacie Weil ◽  
Keith Vendola ◽  
Jian Zhou ◽  
Carolyn A. Bondy
Keyword(s):  
Ovarian Follicle ◽  
Follicle Stimulating Hormone ◽  
Follicle Development ◽  
Ovarian Follicle Development ◽  
Hormone Interactions ◽  
Stimulating Hormone

scholarly journals The Increased Expression of Connexin and VEGF in Mouse Ovarian Tissue Vitrification by Follicle Stimulating Hormone

2015 ◽  
Vol 2015 ◽  
pp. 1-13 ◽  
Author(s):  
Yanzhou Yang ◽  
Jie Chen ◽  
Hao Wu ◽  
Xiuying Pei ◽  
Qing Chang ◽  
...  
Keyword(s):  
Real Time ◽  
Real Time Pcr ◽  
Caspase 3 ◽  
Ischemia Reperfusion ◽  
Ovarian Tissue ◽  
Ovarian Follicle ◽  
Follicle Stimulating Hormone ◽  
Vegf Receptor ◽  
Follicle Development ◽  
Ovarian Follicle Development

Ovarian follicular damages were caused by cryoinjury during the process of ovarian vitrification and ischemia/reperfusion during the process of ovarian transplantation. And appropriate FSH plays an important role in antiapoptosis during ovarian follicle development. Therefore, in this study, 0.3 IU/mL FSH was administered into medium during mouse ovarian cryopreservation by vitrification to ascertain the function of FSH on ovarian vitrification and avascular transplantation. The results suggested that the expressions of Cx37, Cx43, apoptotic molecular caspase-3, and angiogenesis molecular VEGF were confirmed using immunohistochemistry, western blotting, and real-time PCR, and the results suggested that the treatment with FSH remarkably increased the number of morphologically normal follicles in vitrified/warmed ovaries by upregulating the expression of Cx37, Cx43, VEGF, and VEGF receptor 2, but downregulating the expression of caspase-3. In addition, the vitrified/warmed ovaries were transplanted, and the related fertility was analyzed, and the results suggested that the fertility, neoangiogenesis, and follicle reserve were remarkably increased in the FSH administrated group. Taken together, administration of 0.3 IU/mL FSH during ovarian cryopreservation by vitrification can maintain ovarian survival during ovarian vitrification and increases the blood supply with avascular transplantation via upregulation of Cx43, Cx37, and VEGF/VEGFR2, as well as through its antiapoptotic effects.

183 ULTRASONOGRAPHIC MONITORING OF CANINE OVARIES CLAMPED AT SUBCUTANEOUS SITE AFTER FOLLICLE-STIMULATING HORMONE TREATMENT

2015 ◽  
Vol 27 (1) ◽  
pp. 183
Author(s):  
T. Terazono ◽  
V. V. Luu ◽  
L. T. K. Do ◽  
M. Taniguchi ◽  
M. Takagi ◽  
...  
Keyword(s):  
Ovarian Follicle ◽  
Follicle Stimulating Hormone ◽  
Follicular Development ◽  
Hormone Treatment ◽  
Follicular Growth ◽  
Ovarian Follicle Development ◽  
Suspensory Ligament ◽  
Abdominal Approach ◽  
Vaginal Cytology ◽  
Stimulating Hormone

Follicle-stimulating hormone (FSH) alone can induce oestrus in bitches, but few reports describe oestrous induction by FSH because pregnant mare serum gonadotrophin (PMSG) has been more successful than FSH for oestrus induction. Real-time ultrasonography can show canine ovarian follicle development, but no method can determine or predict ovulation accurately. Moreover, the ovary location and size complicate imaging. Using ultrasonography, we investigated FSH treatment stimulation of canine ovary follicles, with clamping of the ovaries at a subcutaneous site. Bilateral malacotomy of four 5-year-old Beagle bitches (mean weight 10.3 ± 2.0 kg) with normal oestrous cycles was done using a ventral flank abdominal approach with routine techniques and materials. Each ovary that maintained blood circulation from the suspensory ligament was clamped at a subcutaneous site through muscles of the abdomen. After about six months of bilateral malacotomy, four bitches at the anestrous (two bitches) and diestrous (two bitches) stages of the oestrous cycle were given 0.5 Armour units of FSH twice daily for 5 days. Examinations with ovarian ultrasonography with 7.5 MHz sector transducer, vaginal cytology, and serum concentrations of progesterone and oestradiol were performed daily from the day before the start of FSH treatment through 7 days after FSH treatment. After 15 days of ovarian examination, each bitch received the same FSH treatment twice continually at 15-day intervals. No serosanguineous vaginal discharge was observed during the ovarian examination. The concentrations of progesterone (<0.045–9.6 ng mL–1) and oestradiol (<9.7–81.4 pg mL–1) varied through all treatments. Comparison of the concentrations of progesterone (<0.045–7.6 ng mL–1) and oestradiol (<9.7–30.3 pg mL–1) at the start of FSH administration in each trial revealed that elevated concentrations of both progesterone and oestradiol were observed in the first treatment in 3 bitches. Regarding the second and third treatments, no elevation of concentration was found for progesterone or oestradiol. A new follicular growth was observed in 1 animal after the third FSH treatment, but no follicular growth was found for the other animals. No correlation was found between follicular development and the profile of either progesterone or oestradiol. Ultrasonography proved that FSH stimulation alone cannot induce follicular growth by a single treatment, but it might increase the levels of progesterone and oestradiol, which are not correlated with follicular development and oestrous cycles at the start of FSH treatment.

Morphogenesis of the silkworm egg

Development ◽  
1976 ◽  
Vol 36 (1) ◽  
pp. 13-18
Author(s):  
J. M. Legay
Keyword(s):  
Ovarian Follicle ◽  
Temporal Organization ◽  
Width Ratio ◽  
Follicle Development ◽  
Ovarian Follicle Development ◽  
Length Width ◽  
Form Stability

Ovarian follicle development, which accompanies morphogenesis of the silkworm egg has three distinct phases: spheric, ellipsoidal and flattened-ellipsoid. Transitions between phases are rapid and form-stability (characterized by length/width ratio) is preserved from the beginning of the ellipsoidal phase. The geometric stability of the follicle-oocyte-ovariole system, the polarity of the egg and the determinism in form changes reveal strikingly coordinated spatial and temporal organization.

scholarly journals An epigenetic switch repressingTet1in gonadotropes activates the reproductive axis

2017 ◽  
Vol 114 (38) ◽  
pp. 10131-10136 ◽  
Author(s):  
Yahav Yosefzon ◽  
Cfir David ◽  
Anna Tsukerman ◽  
Lilach Pnueli ◽  
Sen Qiao ◽  
...  
Keyword(s):  
Ovarian Function ◽  
Ovarian Follicle ◽  
Gene Promoter ◽  
Follicle Development ◽  
Mrna Levels ◽  
Epigenetic Switch ◽  
Ovarian Follicle Development ◽  
Reproductive Axis ◽  
Poorly Differentiated ◽  
Tet Enzymes

The TET enzymes catalyze conversion of 5-methyl cytosine (5mC) to 5-hydroxymethyl cytosine (5hmC) and play important roles during development. TET1 has been particularly well-studied in pluripotent stem cells, butTet1-KO mice are viable, and the most marked defect is abnormal ovarian follicle development, resulting in impaired fertility. We hypothesized that TET1 might play a role in the central control of reproduction by regulating expression of the gonadotropin hormones, which are responsible for follicle development and maturation and ovarian function. We find that all three TET enzymes are expressed in gonadotrope-precursor cells, butTet1mRNA levels decrease markedly with completion of cell differentiation, corresponding with an increase in expression of the luteinizing hormone gene,Lhb. We demonstrate that poorly differentiated gonadotropes express a TET1 isoform lacking the N-terminal CXXC-domain, which repressesLhbgene expression directly and does not catalyze 5hmC at the gene promoter. We show that this isoform is also expressed in other differentiated tissues, and that it is regulated by an alternative promoter whose activity is repressed by the liganded estrogen and androgen receptors, and by the hypothalamic gonadotropin-releasing hormone through activation of PKA. Its expression is also regulated by DNA methylation, including at an upstream enhancer that is protected by TET2, to allowTet1expression. The down-regulation of TET1 relieves its repression of the methylatedLhbgene promoter, which is then hydroxymethylated and activated by TET2 for full reproductive competence.

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