Expression of Kisspeptin and its receptor in the hypothalamus of cyclic and acyclic buffalo (Bubalus bubalis)

Mishra, G K; Patra, Manas Kumar; Singh, Laishram Kipjen; Sheikh, P. A.; Upmanyu, Vikramaditya; Chakravarti, Soumendu; Karikalan, M.; Sonwane, Arvind; Singh, SK; Das, G.; Kumar, Harendra; Krishnaswamy, Narayanan

doi:10.1016/j.theriogenology.2019.08.009

Cited by 6 publications

(1 citation statement)

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“…The presence of Kp and its receptors in the ovarian follicle of rat (Castellano et al., 2006; Zhou et al., 2014), Siberian hamster (Shahed & Young, 2009), human (Gaytan et al., 2014), sow (Basini et al., 2018; Saadeldin et al., 2012), bitch (Cielesh et al., 2017) and cow (Liu et al., 2017) has prompted investigations of extra‐hypothalmic role of Kp in the regulation of ovarian function. Recently, our laboratory demonstrated the presence of kisspeptinergic system in the hypothalamus, ovarian follicle and CL of buffalo (Mishra et al., 2018; Mishra, Patra, Singh, Sheikh, et al., 2019; Mishra, Patra, Singh, Upmanyu, et al., 2019; Rajin et al., 2022).…”

Section: Introductionmentioning

confidence: 99%

Kisspeptin stimulates oestradiol biosynthesis by upregulating steroidogenic transcripts and proliferation markers in the bubaline granulosa cells in vitro

Sharma,

Patra,

Puttanarsappa

et al. 2024

Reprod Domestic Animals

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Kisspeptin (Kp), an upstream regulator of GnRH release, is essential for the development and function of reproductive axis. Previously, we demonstrated the localization of Kp and its receptor (Kiss1r) in the active follicle in the bubaline ovary. Present study aimed to determine the effect of Kp on granulosa cell (GCs) functions, especially oestradiol (E2) and progesterone (P4) production, and differential expression of genes regulating the proliferation, apoptosis and steroidogenesis in the buffalo. The ovaries with 6–10 mm size follicles obtained from the cyclic buffaloes after slaughtering were used for isolation of GCs for in vitro study. The primary GCs culture was treated with Kp (0, 10, 50 and 100 nM) and incubated for 48 h. Production of E2 and P4 was estimated in the culture supernatant by ELISA. The expression of gonadotropin receptors (FSHR and LHR), steroidogenic genes (STAR, 3β‐HSD, CYP19A1), proliferation marker (PCNA), apoptotic factors (CASP3 and BCL2) and Kp signalling molecule (extracellular signal‐regulated kinase 1/2, ERK1/2 and p‐ERK1/2) was studied in the GCs by qPCR. Significant E2 production was found in the Kp 50 and 100 nM groups (p < .05), whereas P4 production was reduced in Kp 100 nM group (p < .05). There was concomitant upregulation of FSHR, ERK1/2, STAR and CYP19A1 in the Kp 100 nM treated GCs. In addition, Kp at 100 nM stimulated the proliferation of GCs by upregulating the expression of BCL2 (5.0 fold) and PCNA (94.9 fold). Further, high immunoreactivity of p‐ERK1/2 was observed in the Kp‐treated GCs. It was concluded that Kp at 100 nM concentration stimulated E2 production by upregulating the steroidogenic pathway through ERK1/2, STAR and CYP19A1 and modulating PCNA and BCL2 expressions in the GCs. Further experiments are warranted using Kp antagonist in different combinations to establish the signalling pathway in Kp‐mediated steroidogenesis in the GCs for developing strategies to control ovarian functions.

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