ArticleBiochemistry and biophysics reports2020
Roles of intracerebral activin, inhibin, and follistatin in the regulation of Kiss-1 gene expression: Studies using primary cultures of fetal rat neuronal cells.
Article in Biochemistry and biophysics reports, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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5 citing papers in PubMed, 2 citations in OpenAlex.
- Molecular characterization of circannual interval timing in the preoptic area and anteroventral periventricular nucleus in the Djungarian hamster (Phodopus sungorus).Journal of neuroendocrinology · 2026Article
- Differential Expression of Hypothalamic Genes in Laying Hens Housed in Caged and Cage-Free Systems Under Commercial Conditions in the Tropics.Animals : an open access journal from MDPI · 2026Article
- The Role of Cytokines in the Development and Functioning of the Hypothalamic-Pituitary-Gonadal Axis in Mammals in Normal and Pathological Conditions.International journal of molecular sciences · 2025Review
- Potential role of kisspeptin in the estradiol-induced modulation of inhibin subunit gene expression: Insights from in vivo rat models and hypothalamic cell models.Endocrine journal · 2025Article
- Differing coronavirus genres alter shared host signaling pathways upon viral infection.Scientific reports · 2022Article
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Authors and funding
6 authors at 1 institution in 1 country.
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No grant is acknowledged in the PubMed record.
Abstract
Hypothalamic kisspeptin, encoded by the Kiss-1 gene, governs the hypothalamic-pituitary-gonadal axis by directly regulating the release of gonadotropin-releasing hormone. In this study, we examined the roles of activin, inhibin, and follistatin in the regulation of Kiss-1 gene expression using primary cultures of fetal rat neuronal cells, which express the Kiss-1 gene and kisspeptin. Stimulation with activin significantly increased Kiss-1 gene expression in these cultures by 2.02 ± 0.39-fold. In contrast, a significant decrease in Kiss-1 gene expression was observed with inhibin A and follistatin treatment. Inhibin B did not modulate Kiss-1 gene expression. Activin, inhibin, and follistatin were also expressed in fetal rat brain cultures and their expression was controlled by estradiol (E2). The inhibin α, βA, and βB subunits were upregulated by E2. Similarly, follistatin gene expression was significantly increased by E2 in these cells. Our results suggest the possibility that activin, inhibin, and follistatin expressed in the brain participate in the E2-induced feedback control of the hypothalamic-pituitary-gonadal axis.
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