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Introduction <p>Postmenopausal osteoporosis is a critical task in the clinical management of older individuals. Numerous studies have proposed various pathophysiological mechanisms for postmenopausal osteoporosis. Tmem119 is a crucial factor for osteoblastic bone formation, and we previously clarified its contribution to the bone anabolic effects of various osteotropic factors. However, the roles of Tmem119 in postmenopausal osteoporosis and the effects of estrogen on bone remain unknown. Therefore, we herein investigated the roles of Tmem119 in bilateral ovariectomized mice with or without Tmem119 deficiency and/or the administration of estrogen.</p> Materials and methods <p>Wild-type and Tmem119-deficient mice underwent bilateral ovariectomy (OVX) and subcutaneous injections of 17β-estradiol for 6&#xa0;weeks. We measured bone parameters in the femurs of mice using micro-computed tomography.</p> Results <p>OVX reduced the uterine weight and trabecular bone parameters, which were increased by estrogen administration. Tmem119 deficiency significantly blunted estrogen-induced increases in uterine weight, trabecular bone volume, and trabecular thickness in OVX mice. Tmem119 deficiency also significantly blunted estrogen-induced increases in alkaline phosphatase activity in mouse osteoblasts.</p> Conclusion <p>Our data indicated that Tmem119 is partly involved in the effects of estrogen on trabecular osteopenia induced by estrogen deficiency presumably by affecting osteoblasts in female mice.</p>

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The role of Tmem119 in the estrogen action on bone in mice

  • 期刊论文

  • 发表日期：

    2025年10月4日

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  • Akihito Nishikawa,
  • Naoyuki Kawao,
  • Yuya Mizukami,
  • Koji Goto,
  • Hiroshi Kaji

摘要

Introduction

Postmenopausal osteoporosis is a critical task in the clinical management of older individuals. Numerous studies have proposed various pathophysiological mechanisms for postmenopausal osteoporosis. Tmem119 is a crucial factor for osteoblastic bone formation, and we previously clarified its contribution to the bone anabolic effects of various osteotropic factors. However, the roles of Tmem119 in postmenopausal osteoporosis and the effects of estrogen on bone remain unknown. Therefore, we herein investigated the roles of Tmem119 in bilateral ovariectomized mice with or without Tmem119 deficiency and/or the administration of estrogen.

Materials and methods

Wild-type and Tmem119-deficient mice underwent bilateral ovariectomy (OVX) and subcutaneous injections of 17β-estradiol for 6 weeks. We measured bone parameters in the femurs of mice using micro-computed tomography.

Results

OVX reduced the uterine weight and trabecular bone parameters, which were increased by estrogen administration. Tmem119 deficiency significantly blunted estrogen-induced increases in uterine weight, trabecular bone volume, and trabecular thickness in OVX mice. Tmem119 deficiency also significantly blunted estrogen-induced increases in alkaline phosphatase activity in mouse osteoblasts.

Conclusion

Our data indicated that Tmem119 is partly involved in the effects of estrogen on trabecular osteopenia induced by estrogen deficiency presumably by affecting osteoblasts in female mice.