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Effect of relaxin‐3 on Kiss‐1, gonadotropin‐releasing hormone, and gonadotropin subunit gene expression
PURPOSE: Relaxin‐3 is a hypothalamic neuropeptide that belongs to the insulin superfamily. We examined whether relaxin‐3 could affect hypothalamic Kiss‐1, gonadotropin‐releasing hormone (GnRH), and pituitary gonadotropin subunit gene expression. METHODS: Mouse hypothalamic cell models, mHypoA‐50 (or...
Autores principales: | , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
John Wiley and Sons Inc.
2019
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6780024/ https://www.ncbi.nlm.nih.gov/pubmed/31607801 http://dx.doi.org/10.1002/rmb2.12298 |
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author | Kanasaki, Haruhiko Tumurbaatar, Tuvshintugs Tumurgan, Zolzaya Oride, Aki Okada, Hiroe Kyo, Satoru |
author_facet | Kanasaki, Haruhiko Tumurbaatar, Tuvshintugs Tumurgan, Zolzaya Oride, Aki Okada, Hiroe Kyo, Satoru |
author_sort | Kanasaki, Haruhiko |
collection | PubMed |
description | PURPOSE: Relaxin‐3 is a hypothalamic neuropeptide that belongs to the insulin superfamily. We examined whether relaxin‐3 could affect hypothalamic Kiss‐1, gonadotropin‐releasing hormone (GnRH), and pituitary gonadotropin subunit gene expression. METHODS: Mouse hypothalamic cell models, mHypoA‐50 (originated from the hypothalamic anteroventral periventricular region), mHypoA‐55 (originated from arcuate nucleus), and GT1‐7, and the mouse pituitary gonadotroph LβT2 were used. Expression of Kiss‐1, GnRH, and luteinizing hormone (LH)/follicle‐stimulating hormone (FSH) β‐subunits was determined after stimulation with relaxin‐3. RESULTS: RXFP3, a principle relaxin‐3 receptor, was expressed in these cell models. In mHypoA‐50 cells, relaxin‐3 did not exert a significant effect on Kiss‐1 expression. In contrast, the Kiss‐1 gene in mHypoA‐55 was significantly increased by 1 nmol/L relaxin‐3. These cells also express GnRH mRNA, and its expression was significantly stimulated by relaxin‐3. In GT1‐7 cells, relaxin‐3 significantly upregulated Kiss‐1 expression; however, GnRH mRNA expression in GT1‐7 cells was not altered. In primary cultures of fetal rat neuronal cells, 100 nmol/L relaxin‐3 significantly increased GnRH expression. In pituitary gonadotroph LβT2, both LHβ‐ and FSHβ‐subunit were significantly increased by 1 nmol/L relaxin‐3. CONCLUSIONS: Our findings suggest that relaxin‐3 exerts its effect by modulating the expression of Kiss‐1, GnRH, and gonadotropin subunits, all of which are part of the hypothalamic‐pituitary‐gonadal axis. |
format | Online Article Text |
id | pubmed-6780024 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2019 |
publisher | John Wiley and Sons Inc. |
record_format | MEDLINE/PubMed |
spelling | pubmed-67800242019-10-11 Effect of relaxin‐3 on Kiss‐1, gonadotropin‐releasing hormone, and gonadotropin subunit gene expression Kanasaki, Haruhiko Tumurbaatar, Tuvshintugs Tumurgan, Zolzaya Oride, Aki Okada, Hiroe Kyo, Satoru Reprod Med Biol Original Articles PURPOSE: Relaxin‐3 is a hypothalamic neuropeptide that belongs to the insulin superfamily. We examined whether relaxin‐3 could affect hypothalamic Kiss‐1, gonadotropin‐releasing hormone (GnRH), and pituitary gonadotropin subunit gene expression. METHODS: Mouse hypothalamic cell models, mHypoA‐50 (originated from the hypothalamic anteroventral periventricular region), mHypoA‐55 (originated from arcuate nucleus), and GT1‐7, and the mouse pituitary gonadotroph LβT2 were used. Expression of Kiss‐1, GnRH, and luteinizing hormone (LH)/follicle‐stimulating hormone (FSH) β‐subunits was determined after stimulation with relaxin‐3. RESULTS: RXFP3, a principle relaxin‐3 receptor, was expressed in these cell models. In mHypoA‐50 cells, relaxin‐3 did not exert a significant effect on Kiss‐1 expression. In contrast, the Kiss‐1 gene in mHypoA‐55 was significantly increased by 1 nmol/L relaxin‐3. These cells also express GnRH mRNA, and its expression was significantly stimulated by relaxin‐3. In GT1‐7 cells, relaxin‐3 significantly upregulated Kiss‐1 expression; however, GnRH mRNA expression in GT1‐7 cells was not altered. In primary cultures of fetal rat neuronal cells, 100 nmol/L relaxin‐3 significantly increased GnRH expression. In pituitary gonadotroph LβT2, both LHβ‐ and FSHβ‐subunit were significantly increased by 1 nmol/L relaxin‐3. CONCLUSIONS: Our findings suggest that relaxin‐3 exerts its effect by modulating the expression of Kiss‐1, GnRH, and gonadotropin subunits, all of which are part of the hypothalamic‐pituitary‐gonadal axis. John Wiley and Sons Inc. 2019-09-05 /pmc/articles/PMC6780024/ /pubmed/31607801 http://dx.doi.org/10.1002/rmb2.12298 Text en © 2019 The Authors. Reproductive Medicine and Biology published by John Wiley & Sons Australia, Ltd on behalf of Japan Society for Reproductive Medicine. This is an open access article under the terms of the http://creativecommons.org/licenses/by/4.0/ License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited. |
spellingShingle | Original Articles Kanasaki, Haruhiko Tumurbaatar, Tuvshintugs Tumurgan, Zolzaya Oride, Aki Okada, Hiroe Kyo, Satoru Effect of relaxin‐3 on Kiss‐1, gonadotropin‐releasing hormone, and gonadotropin subunit gene expression |
title | Effect of relaxin‐3 on Kiss‐1, gonadotropin‐releasing hormone, and gonadotropin subunit gene expression |
title_full | Effect of relaxin‐3 on Kiss‐1, gonadotropin‐releasing hormone, and gonadotropin subunit gene expression |
title_fullStr | Effect of relaxin‐3 on Kiss‐1, gonadotropin‐releasing hormone, and gonadotropin subunit gene expression |
title_full_unstemmed | Effect of relaxin‐3 on Kiss‐1, gonadotropin‐releasing hormone, and gonadotropin subunit gene expression |
title_short | Effect of relaxin‐3 on Kiss‐1, gonadotropin‐releasing hormone, and gonadotropin subunit gene expression |
title_sort | effect of relaxin‐3 on kiss‐1, gonadotropin‐releasing hormone, and gonadotropin subunit gene expression |
topic | Original Articles |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6780024/ https://www.ncbi.nlm.nih.gov/pubmed/31607801 http://dx.doi.org/10.1002/rmb2.12298 |
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