FSHR and LHR Expression and Signaling as Well as Maturation and Apoptosis of Cumulus-Oocyte Complexes Following Treatment with FSH Receptor Binding Inhibitor in Sheep

Wei, Shaozhong; Shen, Xıaoyun; Gong, Zhuandı; Deng, Yingying; Lai, Liangxue; Liang, Huaping

doi:10.1159/000480650

Cited by 19 publications

(12 citation statements)

References 25 publications

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“…On the other hand, the maturation rate was greatly decreased in FSH + LH treatment group. These observed results are different from those established in a previous report on IVM of oocytes in the presence of FSH + LH hormones (Manabe et al, 2004 (Song et al, 2014;Wei et al, 2017). Thus, autophagy is preferred over apoptosis during the oocyte maturation in the presence of rapamycin.…”

Section: Discussioncontrasting

confidence: 99%

Influence of Autophagy Induction after Hormone Treatment on Oocytes Maturation of Porcine

Kim

Yoon

2018

J Anim Reprod Biotechnol

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Here, we evaluated the mode of programmed cell death during porcine oocyte maturation by comparing the two major pathways associated with programmed cell death, apoptosis (type I), and autophagy (type II). We investigated the expression and localization of major genes involved in autophagy and apoptosis at mRNA and protein levels. Furthermore, the effect of hormonal stimulation on autophagy and apoptosis was analyzed. We found that the activity of autophagy-associated genes was increased in the cumulus-oocyte complexes (COCs) following follicle-stimulating hormone (FSH) treatment, while the addition of luteinizing hormone (LH) reversed this effect. The expression of proteins associated with autophagy was the highest in FSH-treated COCs. On the other hand, caspase-3 protein level was maximum in COCs cultured with LH. The treatment with rapamycin resulted in the effect similar to that observed with FSH treatment and increased autophagy activity. Thus, hormonal stimulation of pig oocytes resulted in distinct patterns of maturation. The high-quality oocytes majorly relied on the type II pathway (autophagy), while the type I pathway (apoptosis) was more prominent among poor-quality oocytes. Further investigation of this distinction may allow the development of techniques to produce high-quality oocytes in porcine in vitro fertilization.

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Section: Discussioncontrasting

confidence: 99%

Influence of Autophagy Induction after Hormone Treatment on Oocytes Maturation of Porcine

Kim

Yoon

2018

J Anim Reprod Biotechnol

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“…Our initial study revealed that the addition of 10 to 40 μg/mL FRBI into in vitro maturation (IVM) medium reduced the maturation rate, enhanced the apoptosis rate, and decreased the proliferation capacity of sheep cumulus-oocyte complex. Additionally, FRBI decreased FHS concentrations and increased estradiol (E 2 ) concentrations in the IVM medium (15). Currently, there is scarce information about effects of FRBI on the gene levels associated with ovarian cancers in humans and animals (16).…”

Section: Introductionmentioning

confidence: 99%

FSH receptor binding inhibitor up-regulates ARID1A and PTEN genes associated with ovarian cancers in mice

Gong

Shen

Yang

et al. 2019

Braz J Med Biol Res

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Experiments were conducted to determine if the follicle-stimulating hormone (FSH) receptor binding inhibitor (FRBI) impacts the expression levels of AT-rich interactive domain-containing protein 1A (ARID1A) and phosphatase and tensin homolog (PTEN) in ovaries and blood, as well as expressions of follicle-stimulating hormone cognate receptor (FSHR) gene and proteins. Mice in FRBI-10, FRBI-20, FRBI-30, and FRBI-40 groups were intramuscularly injected with 10, 20, 30, and 40 mg FRBI/kg, respectively, for five consecutive days. Western blotting and qRT-PCR were utilized to determine expression levels of ARID1A and PTEN proteins and mRNAs. Serum ARID1A and PTEN concentrations of the FRBI-40 group were higher than the control group (CG) and FSH group (P<0.05). FSHR mRNA levels of FRBI-20, FRBI-30, and FRBI-40 groups were lower than that of CG and FSH groups on day 15 (P<0.05 or P<0.01). Expression levels of FSHR proteins of FRBI-30 and FRBI-40 groups were lower than those of CG and FSH groups (P<0.05). Levels of ARID1A and PTEN proteins of the FRBI-30 group were greater than CG on days 20 and 30 (P<0.05). FRBI doses had significant positive correlations to levels of ARID1A and PTEN proteins. Additionally, ARID1A and PTEN had negative correlations to FSHR mRNAs and proteins. A high dose of FRBI could promote the expression levels of ARID1A and PTEN proteins in ovarian tissues. FRBI increased serum concentrations of ARID1A and PTEN. However, FRBI depressed expression levels of FSHR mRNAs and proteins in mouse ovaries.

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“…No nuclear atypia was found. Our results revealed supplement of FRBI into the IVM media could reduce the maturation rate, enhance the apoptosis rate, and decreased proliferation capacity of sheep COCs [ 11 ]. FRBI could suppress the mRNA and protein expression levels of FSHR and LHR in sheep cumulus-oocyte complex (COCs), additionally decreased FHS production and increased estradiol (E2) production of sheep COCs [ 11 , 12 ].…”

Section: Introductionmentioning

confidence: 99%

“…Our results revealed supplement of FRBI into the IVM media could reduce the maturation rate, enhance the apoptosis rate, and decreased proliferation capacity of sheep COCs [ 11 ]. FRBI could suppress the mRNA and protein expression levels of FSHR and LHR in sheep cumulus-oocyte complex (COCs), additionally decreased FHS production and increased estradiol (E2) production of sheep COCs [ 11 , 12 ]. Up to date, no reports have as yet documented about FRBI effects on the ovarian oncogenesis and genes related to ovarian cancerin humans and animals [ 9 , 13 , 14 ].…”

Section: Introductionmentioning

confidence: 99%

FSH receptor binding inhibitor impacts K-Ras and c-Myc of ovarian cancer and signal pathway

et al. 2018

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The present study aimed to investigate FSHreceptor binding inhibitor (FRBI) effects on relative factors (K-Ras, c-Myc and Vascular endothelial growth factor (VEGF)) to ovarian cancer, and expression levels of FSH receptor (FSHR) mRNAs and proteins in the cumulus-oocyte complex (COCs), to determine changes of protein kinase A (PKA) in sheep granulosa cells, further to elucidate signaling pathway of FRBI action. COCs were cultured in vitro for 24h under supplementation of varying concentrations of FRBI (0, 10, 20, 30 and 40μg/mL) or FSH (10IU/mL). Concentrations of K-Ras, c-Myc, VEGF, cAMP and FSH were detected in IVM media fluids, respectively. The results showed that the concentrations of c-Myc, K-Ras and FSH of FRBI groups were gradually reduced with the increase of FRBI doses. VEGF level of the FRBI-4 group was significantly greater than control group (CG). Expression levels FSHR mRNA and protein and PKA of FRBI-3 and FRBI-4 groups were less than that of CG or FSH group (P<0.05 or P<0.01). Inositol trisphosphate (IP3) concentrations of FRBI-3 and FRBI-4 groups were less than FSH group (P<0.05). FRBI administration doses had significant negative correlations to levels or concentrations of K-Ras, c-Myc, VEGF, FSHR mRNA and protein and PKA protein. K-Ras had significant positive correlations with FSHR mRNA and protein and PKA protein. In conclusion, FRBI could promote the production of VEGF of sheep COCs. Higher doses of FRBI (30 and 40μg/mL) suppressed the production of c-Myc and K-Ras, and declined FSH concentrations in the IVM medium fluid, and decreased the expressions of FSHR at the gene and protein levels, additionally attenuated expression of PKA protein in the granulosa cells.

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FSHR and LHR Expression and Signaling as Well as Maturation and Apoptosis of Cumulus-Oocyte Complexes Following Treatment with FSH Receptor Binding Inhibitor in Sheep

Cited by 19 publications

References 25 publications

Influence of Autophagy Induction after Hormone Treatment on Oocytes Maturation of Porcine

Influence of Autophagy Induction after Hormone Treatment on Oocytes Maturation of Porcine

FSH receptor binding inhibitor up-regulates ARID1A and PTEN genes associated with ovarian cancers in mice

FSH receptor binding inhibitor impacts K-Ras and c-Myc of ovarian cancer and signal pathway

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