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<p>Abnormal levels of Inhibin B (INH-B), a major regulator of ovarian activity, are closely linked to the development and prognosis of several ovarian disorders. Understanding the molecular mechanisms governing its regulation in granulosa cells is essential for both diagnosis and therapy. Our earlier work demonstrated the precise localization of lncPrep + 96&#xa0;kb in granulosa cells and its central influence on the estrogen biosynthetic pathway. In this study, the impact of lncPrep + 96&#xa0;kb on INH-B expression was investigated further. We created knockout mice lacking the long non-coding RNA lncPrep + 96&#xa0;kb, which is specifically expressed in granulosa cells of the ovary. RNA sequencing revealed that the inhibin subunit βB (INHBB) was significantly elevated in knockout mice. ELISA was utilized to quantify INH-B levels in serum and granulosa cell supernatants, revealing a significant increase in knockout mice compared to wild-type controls. Overexpression of lncPrep + 96&#xa0;kb fragments (2.2&#xa0;kb and 2.8&#xa0;kb) reduced INH-B expression. Endothelial differentiation-related factor 1 (EDF1), a key intracellular transcription factor, was found to be upregulated by lncPrep + 96&#xa0;kb, resulting in decreased INH-B expression. In summary, lncPrep + 96&#xa0;kb regulates INH-B secretion in granulosa cells by modulating of EDF1, providing new insights into the mechanism of INH-B expression and offering new research directions for diagnostic and therapeutic studies of abnormal ovarian functions.</p>

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LncPrep + 96 kb Inhibits the Secretion of Inhibin B in Ovarian Granulosa Cells Through Regulating Endothelial Differentiation-Associated Factor 1

  • 期刊论文

  • 发表日期：

    2025年11月5日

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  • Hongdan Zhang,
  • Jianwei Liu,
  • Canglang Mou,
  • Yingqi Tang,
  • Yangfan Lv

摘要

Abnormal levels of Inhibin B (INH-B), a major regulator of ovarian activity, are closely linked to the development and prognosis of several ovarian disorders. Understanding the molecular mechanisms governing its regulation in granulosa cells is essential for both diagnosis and therapy. Our earlier work demonstrated the precise localization of lncPrep + 96 kb in granulosa cells and its central influence on the estrogen biosynthetic pathway. In this study, the impact of lncPrep + 96 kb on INH-B expression was investigated further. We created knockout mice lacking the long non-coding RNA lncPrep + 96 kb, which is specifically expressed in granulosa cells of the ovary. RNA sequencing revealed that the inhibin subunit βB (INHBB) was significantly elevated in knockout mice. ELISA was utilized to quantify INH-B levels in serum and granulosa cell supernatants, revealing a significant increase in knockout mice compared to wild-type controls. Overexpression of lncPrep + 96 kb fragments (2.2 kb and 2.8 kb) reduced INH-B expression. Endothelial differentiation-related factor 1 (EDF1), a key intracellular transcription factor, was found to be upregulated by lncPrep + 96 kb, resulting in decreased INH-B expression. In summary, lncPrep + 96 kb regulates INH-B secretion in granulosa cells by modulating of EDF1, providing new insights into the mechanism of INH-B expression and offering new research directions for diagnostic and therapeutic studies of abnormal ovarian functions.