Expression of GnIH and its effects on follicle development and steroidogenesis in quail ovaries under different photoperiods

Zhou, Xiaoli; Jiang, Danli; Zhang, Zhuoshen; Shen, Xu; Pan, Jianqiu; Xu, Danning; Tian, Yunbo; Huang, Yunmao

doi:10.1016/j.psj.2022.102227

Cited by 2 publications

(3 citation statements)

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“…GnIH, a t12-amino acid residue neuropeptide hormone, is concerned with numerous behavioral and physiological functions in animal reproduction [ 10 ], including the suppression of steroidogenesis and follicular growth in female ovarian tissues [ 26 , 30 , 31 ]. The reproductive performance of mammals is primarily affected by the number of mature follicles that can develop to ovulation.…”

Section: Discussionmentioning

confidence: 99%

“…Thus, we speculated that RFRP-3 inhibited follicular growth by increasing the GnIH concentration in vivo and blocked the crucial pathway of steroidogenesis mostly via reducing the mRNA abundances of LHR , 3β-HSD , and StAR . Similarly, granulosa cells of quail and duck showed a considerable dose-dependent reduction of the expression levels of the core factors in the steroidogenic pathway [ 30 , 47 ]. Consistent with our findings, treatment with GnIH dose-dependently decreased the mRNA abundances of StAR and 3β-HSD and repressed the synthesis of the steroid hormone in mice [ 26 ].…”

Section: Discussionmentioning

confidence: 99%

“…A recent study on mice indicated that ovarian activity and follicular growth are suppressed after treatment with RFRP-3 [ 26 ]. Immunohistochemistry (IHC) found that RFRP-3 and its receptors are primarily expressed in GCs and membrane cells of bird and pig ovarian follicles [ 25 , 30 ], and GnIH/RFRP-3 plays a crucial regulatory effect in the ovaries via combining with its receptors, such as adjusting apoptosis, proliferation, and steroidogenesis [ 31 ]. However, as the main domestic animal in the Qinghai-Tibet Plateau region and nearby areas, whether the low reproductive efficiency of female yak is related to GnIH/RFRP-3 remains unclear and needs further investigation, as well as to evaluate whether RFRP-3 exerts conserved function across various species.…”

Section: Introductionmentioning

confidence: 99%

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RFRP-3 Influences Apoptosis and Steroidogenesis of Yak Cumulus Cells and Compromises Oocyte Meiotic Maturation and Subsequent Developmental Competence

Xiong

Pan

et al. 2023

IJMS

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RF amide-related peptide 3 (RFRP-3), a mammalian ortholog of gonadotropin-inhibitory hormone (GnIH), is identified to be a novel inhibitory endogenous neurohormonal peptide that regulates mammalian reproduction by binding with specific G protein-coupled receptors (GPRs) in various species. Herein, our objectives were to explore the biological functions of exogenous RFRP-3 on the apoptosis and steroidogenesis of yak cumulus cells (CCs) and the developmental potential of yak oocytes. The spatiotemporal expression pattern and localization of GnIH/RFRP-3 and its receptor GPR147 were determined in follicles and CCs. The effects of RFRP-3 on the proliferation and apoptosis of yak CCs were initially estimated by EdU assay and TUNEL staining. We confirmed that high-dose (10−6 mol/L) RFRP-3 suppressed viability and increased the apoptotic rates, implying that RFRP-3 could repress proliferation and induce apoptosis. Subsequently, the concentrations of E2 and P4 were significantly lower with 10−6 mol/L RFRP-3 treatment than that of the control counterparts, which indicated that the steroidogenesis of CCs was impaired after RFRP-3 treatment. Compared with the control group, 10−6 mol/L RFRP-3 treatment decreased the maturation of yak oocytes efficiently and subsequent developmental potential. We sought to explore the potential mechanism of RFRP-3-induced apoptosis and steroidogenesis, so we observed the levels of apoptotic regulatory factors and hormone synthesis-related factors in yak CCs after RFRP-3 treatment. Our results indicated that RFRP-3 dose-dependently elevated the expression of apoptosis markers (Caspase and Bax), whereas the expression levels of steroidogenesis-related factors (LHR, StAR, 3β-HSD) were downregulated in a dose-dependent manner. However, all these effects were moderated by cotreatment with inhibitory RF9 of GPR147. These results demonstrated that RFRP-3 adjusted the expression of apoptotic and steroidogenic regulatory factors to induce apoptosis of CCs, probably through binding with its receptor GPR147, as well as compromised oocyte maturation and developmental potential. This research revealed the expression profiles of GnIH/RFRP-3 and GPR147 in yak CCs and supported a conserved inhibitory action on oocyte developmental competence.

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