<p>To date, Despite the widespread and mature clinical application of fracture treatment techniques, a large number of patients still suffer from nonunion due to impaired bone regeneration function. In the past few years, growing evidence has shown that microRNAs (miRNAs) play important roles in many physiological processes and are involved in the regulation of bone metabolic diseases. In this study, we evaluated the role of miR-34c-5p in in vitro osteogenesis using methods including Alizarin Red S staining, ALP staining, quantitative PCR, and western blotting. Additionally, we established a mouse fracture model, utilized micro-CT to visualize callus formation at the fracture site, and observed the formation of trabecular bone at the fracture end in mice through histopathological staining, aiming to clarify the role of miR-34c-5p as a promoter of fracture healing in vivo. Findings demonstrated that miR-34c-5p was capable of effectively boosting osteogenic differentiation in vitro and remarkably facilitating fracture regeneration in vivo. <i>Notch2</i> was identified as a downstream target through which miR-34c-5p effectively promotes osteogenesis. In summary, miR-34c-5p positively regulates osteoblast differentiation by targeting <i>Notch2</i>, providing a new direction for the treatment of various bone metabolic diseases such as poor fracture healing.</p>

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miR-34c-5p targets Notch2 to promote fracture healing

  • Kechi Li,
  • Guoxiang Liu,
  • Feiyu Chen,
  • Xiaolong Sun,
  • Bin Liu

摘要

To date, Despite the widespread and mature clinical application of fracture treatment techniques, a large number of patients still suffer from nonunion due to impaired bone regeneration function. In the past few years, growing evidence has shown that microRNAs (miRNAs) play important roles in many physiological processes and are involved in the regulation of bone metabolic diseases. In this study, we evaluated the role of miR-34c-5p in in vitro osteogenesis using methods including Alizarin Red S staining, ALP staining, quantitative PCR, and western blotting. Additionally, we established a mouse fracture model, utilized micro-CT to visualize callus formation at the fracture site, and observed the formation of trabecular bone at the fracture end in mice through histopathological staining, aiming to clarify the role of miR-34c-5p as a promoter of fracture healing in vivo. Findings demonstrated that miR-34c-5p was capable of effectively boosting osteogenic differentiation in vitro and remarkably facilitating fracture regeneration in vivo. Notch2 was identified as a downstream target through which miR-34c-5p effectively promotes osteogenesis. In summary, miR-34c-5p positively regulates osteoblast differentiation by targeting Notch2, providing a new direction for the treatment of various bone metabolic diseases such as poor fracture healing.