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FSH promotes immature porcine Sertoli cell proliferation by activating the CCR7/Ras-ERK signaling axis
IN BRIEF: The appropriate growth and functions of Sertoli cells are crucial to testis development and spermatogenesis in mammals. This study reveals a novel mechanism of follicle-stimulating hormone in immature porcine Sertoli cell proliferation. ABSTRACT: Follicle-stimulating hormone (FSH) is a maj...
Autores principales: | , , , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Bioscientifica Ltd
2023
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10235919/ https://www.ncbi.nlm.nih.gov/pubmed/37000598 http://dx.doi.org/10.1530/REP-22-0441 |
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author | Yin, Yanfei Ma, Jiajia Lu, Xiaofang Yan, Saina Jiang, Qianqian Wu, Dazhi Chen, Bin Weng, Bo Ran, MaoLiang |
author_facet | Yin, Yanfei Ma, Jiajia Lu, Xiaofang Yan, Saina Jiang, Qianqian Wu, Dazhi Chen, Bin Weng, Bo Ran, MaoLiang |
author_sort | Yin, Yanfei |
collection | PubMed |
description | IN BRIEF: The appropriate growth and functions of Sertoli cells are crucial to testis development and spermatogenesis in mammals. This study reveals a novel mechanism of follicle-stimulating hormone in immature porcine Sertoli cell proliferation. ABSTRACT: Follicle-stimulating hormone (FSH) is a major Sertoli cell mitogen that binds to the FSH receptor. Sertoli cells are indispensable for testis development and spermatogenesis. However, the regulatory mechanisms of FSH in immature Sertoli cell proliferation have not been determined, particularly in domestic animals. In the present study, we identified the regulatory mechanisms of FSH during immature porcine Sertoli cell proliferation. Transcriptome analysis revealed 114 differentially expressed genes that were induced by FSH treatment, which contains 68 upregulated and 46 downregulated genes. These differentially expressed genes were enriched in multiple pathways, including the Ras signaling pathway. Knockdown of the CC-chemokine receptor 7 (CCR7) gene, which was upregulated by FSH, inhibited cell cycle progression by arresting cells in the G1 phase and reduced the cell proliferation and ERK1/2 phosphorylation. In addition, Kobe0065 inhibited Ras signaling in a similar manner as CCR7 knockdown. Furthermore, FSH abolished the effects of Ras signaling pathway inhibition and CCR7 knockdown. Collectively, FSH promotes immature porcine Sertoli cell proliferation by activating the CCR7/Ras-ERK signaling axis. Our results provide novel insights into the regulatory mechanism of FSH in porcine testis development and spermatogenesis by deciding the fate of immature porcine Sertoli cells. |
format | Online Article Text |
id | pubmed-10235919 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2023 |
publisher | Bioscientifica Ltd |
record_format | MEDLINE/PubMed |
spelling | pubmed-102359192023-06-03 FSH promotes immature porcine Sertoli cell proliferation by activating the CCR7/Ras-ERK signaling axis Yin, Yanfei Ma, Jiajia Lu, Xiaofang Yan, Saina Jiang, Qianqian Wu, Dazhi Chen, Bin Weng, Bo Ran, MaoLiang Reproduction Research IN BRIEF: The appropriate growth and functions of Sertoli cells are crucial to testis development and spermatogenesis in mammals. This study reveals a novel mechanism of follicle-stimulating hormone in immature porcine Sertoli cell proliferation. ABSTRACT: Follicle-stimulating hormone (FSH) is a major Sertoli cell mitogen that binds to the FSH receptor. Sertoli cells are indispensable for testis development and spermatogenesis. However, the regulatory mechanisms of FSH in immature Sertoli cell proliferation have not been determined, particularly in domestic animals. In the present study, we identified the regulatory mechanisms of FSH during immature porcine Sertoli cell proliferation. Transcriptome analysis revealed 114 differentially expressed genes that were induced by FSH treatment, which contains 68 upregulated and 46 downregulated genes. These differentially expressed genes were enriched in multiple pathways, including the Ras signaling pathway. Knockdown of the CC-chemokine receptor 7 (CCR7) gene, which was upregulated by FSH, inhibited cell cycle progression by arresting cells in the G1 phase and reduced the cell proliferation and ERK1/2 phosphorylation. In addition, Kobe0065 inhibited Ras signaling in a similar manner as CCR7 knockdown. Furthermore, FSH abolished the effects of Ras signaling pathway inhibition and CCR7 knockdown. Collectively, FSH promotes immature porcine Sertoli cell proliferation by activating the CCR7/Ras-ERK signaling axis. Our results provide novel insights into the regulatory mechanism of FSH in porcine testis development and spermatogenesis by deciding the fate of immature porcine Sertoli cells. Bioscientifica Ltd 2023-03-31 /pmc/articles/PMC10235919/ /pubmed/37000598 http://dx.doi.org/10.1530/REP-22-0441 Text en © The Authors https://creativecommons.org/licenses/by/4.0/This work is licensed under a Creative Commons Attribution 4.0 International License. (https://creativecommons.org/licenses/by/4.0/) |
spellingShingle | Research Yin, Yanfei Ma, Jiajia Lu, Xiaofang Yan, Saina Jiang, Qianqian Wu, Dazhi Chen, Bin Weng, Bo Ran, MaoLiang FSH promotes immature porcine Sertoli cell proliferation by activating the CCR7/Ras-ERK signaling axis |
title | FSH promotes immature porcine Sertoli cell proliferation by activating the CCR7/Ras-ERK signaling axis |
title_full | FSH promotes immature porcine Sertoli cell proliferation by activating the CCR7/Ras-ERK signaling axis |
title_fullStr | FSH promotes immature porcine Sertoli cell proliferation by activating the CCR7/Ras-ERK signaling axis |
title_full_unstemmed | FSH promotes immature porcine Sertoli cell proliferation by activating the CCR7/Ras-ERK signaling axis |
title_short | FSH promotes immature porcine Sertoli cell proliferation by activating the CCR7/Ras-ERK signaling axis |
title_sort | fsh promotes immature porcine sertoli cell proliferation by activating the ccr7/ras-erk signaling axis |
topic | Research |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10235919/ https://www.ncbi.nlm.nih.gov/pubmed/37000598 http://dx.doi.org/10.1530/REP-22-0441 |
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