Scholarlink

<p>Polycystic ovary syndrome (PCOS) is one of the most common endocrine disorders associated with female infertility. Increasing evidence suggests that impaired endometrial receptivity, in addition to ovulatory dysfunction, may contribute to infertility in women with PCOS. However, the molecular mechanisms underlying defective decidualization in PCOS remain poorly understood. We observed impaired decidualization in both a prenatally androgenized mouse model and primary endometrial stromal cells from patients with PCOS. Testis-specific Y-encoded-like protein 2 (TSPYL2) displayed aberrant expression dynamics in PCOS, with elevated expression in the proliferative phase but insufficient induction during decidualization. Silencing TSPYL2 impaired decidualization and reduced implantation capacity in vitro and in vivo. Transcriptomic analysis further showed that TSPYL2 knockdown was associated with increased cell-cycle-associated signatures and reduced expression of hormone-responsive, decidualization- and endometrial receptivity-associated genes. Serum miR-301a-3p was upregulated during the secretory phase in PCOS and directly targeted the 3′ untranslated region of TSPYL2, suppressing its expression. Our findings suggest that elevated miR-301a-3p may impair decidualization by targeting TSPYL2, thereby contributing to defective endometrial function in PCOS.</p>

错误：搜索内容不能为空，请输入英文关键词
错误：关键词超出字数限制，请精简
高级检索

TSPYL2 regulated by miR-301a-3p contributes to impaired decidualization in polycystic ovary syndrome

  • 期刊论文

  • 出版模式：

    开放获取

  • 发表日期：

    2026年8月5日

查看全文
  • Jiali Ruan,
  • Ayako Muraoka,
  • Akira Yokoi,
  • Bayasula,
  • Kosuke Yoshida,
  • Takehiko Takeda,
  • Tomomi Seki,
  • Natsuki Miyake,
  • Reina Sonehara,
  • Tomoko Nakamura,
  • Satoko Osuka,
  • Hiroaki Kajiyama

摘要

Polycystic ovary syndrome (PCOS) is one of the most common endocrine disorders associated with female infertility. Increasing evidence suggests that impaired endometrial receptivity, in addition to ovulatory dysfunction, may contribute to infertility in women with PCOS. However, the molecular mechanisms underlying defective decidualization in PCOS remain poorly understood. We observed impaired decidualization in both a prenatally androgenized mouse model and primary endometrial stromal cells from patients with PCOS. Testis-specific Y-encoded-like protein 2 (TSPYL2) displayed aberrant expression dynamics in PCOS, with elevated expression in the proliferative phase but insufficient induction during decidualization. Silencing TSPYL2 impaired decidualization and reduced implantation capacity in vitro and in vivo. Transcriptomic analysis further showed that TSPYL2 knockdown was associated with increased cell-cycle-associated signatures and reduced expression of hormone-responsive, decidualization- and endometrial receptivity-associated genes. Serum miR-301a-3p was upregulated during the secretory phase in PCOS and directly targeted the 3′ untranslated region of TSPYL2, suppressing its expression. Our findings suggest that elevated miR-301a-3p may impair decidualization by targeting TSPYL2, thereby contributing to defective endometrial function in PCOS.