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MiR-138-5p Targets MACF1 to Aggravate Aging-related Bone Loss

Zhihao Chen1,2, Ying Huai1, Gaoyang Chen3

  • 1Lab for Bone Metabolism, Xi'an Key Laboratory of Special Medicine and Health Engineering; Key Lab for Space Biosciences and Biotechnology, Research Center for Special Medicine and Health Systems Engineering, NPU-UAB Joint Laboratory for Bone Metabolism, School of Life Sciences, Northwestern Polytechnical University, Xi'an, Shaanxi, 710072, China.

International Journal of Biological Sciences
|August 19, 2022
PubMed

Insights

High levels of microRNA-138-5p worsen bone loss in aging individuals by impairing osteoblast function. Inhibiting this microRNA (miRNA) shows promise for treating senile osteoporosis.

Area of Science:

  • Biomedical Science
  • Molecular Biology
  • Gerontology

Background:

  • Senile osteoporosis is a significant health concern in aging populations.
  • Osteoblast dysfunction contributes to age-related bone loss.
  • MicroRNAs (miRNAs) are increasingly recognized for their role in regulating osteoblast function.

Purpose of the Study:

  • To investigate the role of microRNA-138-5p (miR-138-5p) in senile osteoporosis.
  • To elucidate the molecular mechanism by which miR-138-5p affects osteoblast differentiation and bone formation.
  • To evaluate the therapeutic potential of inhibiting miR-138-5p for senile osteoporosis.

Main Methods:

  • Bioinformatic analysis and experimental verification of miR-138-5p levels in osteoporotic bone specimens.
  • In vitro studies on aged osteoblast differentiation with varying miR-138-5p levels.
  • In vivo studies using aged miR-138-5p transgenic mice.
  • Identification and validation of microtubule actin cross-linking factor 1 (MACF1) as a target of miR-138-5p.
  • Therapeutic inhibition of miR-138-5p in aged mice.

Main Results:

  • miR-138-5p levels negatively correlated with bone mineral density (BMD) and osteogenic markers in senile osteoporotic patients.
  • Elevated miR-138-5p aggravated aged osteoblast dysfunction and exacerbated bone loss in vivo.
  • miR-138-5p was confirmed to target MACF1, a protein that attenuates senile osteoporosis.
  • Therapeutic inhibition of miR-138-5p successfully counteracted bone loss and improved bone formation in aged mice.

Conclusions:

  • miR-138-5p plays a critical role in aging-related bone loss through the regulation of osteoblast differentiation via MACF1.
  • Inhibiting miR-138-5p represents a potential therapeutic strategy for ameliorating senile osteoporosis.
Keywords:
MACF1aging-related bone lossmiR-138-5posteoblast differentiationsenile osteoporosis

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