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PiR48444 inhibits MSC osteogenic differentiation and bone regeneration via targeting METTL7A/eIF4E-mediated BMP2 m6A

Zhichao Zheng1,2, Xingyang Li1, Wenguang Qin1

  • 1School and Hospital of Stomatology, Guangdong Engineering Research Center of Oral Restoration and Reconstruction & Guangzhou Key Laboratory of Basic and Applied Research of Oral Regenerative Medicine, Guangzhou Medical University, Guangzhou, China.

Communications Biology
|January 29, 2026
PubMed

Insights

Piwi-interacting RNA 48444 (piR48444) negatively regulates mesenchymal stem cell (MSC) osteogenesis by targeting METTL7A and BMP2 mRNA methylation. Its inhibition enhances bone regeneration, suggesting piR48444 as a therapeutic target for bone repair.

Area of Science:

  • Stem cell biology
  • RNA biology
  • Regenerative medicine

Background:

  • Non-coding RNAs, including piwi-interacting RNAs (piRNAs), regulate osteogenic differentiation in mesenchymal stem cells (MSCs).
  • The specific role of piRNAs in MSCs from various sources and their involvement in bone regeneration remain largely unexplored.
  • Understanding piRNA regulation is crucial for advancing MSC-based therapies.

Purpose of the Study:

  • To investigate the role of piR48444 in osteogenic differentiation of MSCs from diverse origins.
  • To elucidate the underlying molecular mechanisms of piR48444 in regulating osteogenesis.
  • To evaluate the therapeutic potential of targeting piR48444 for bone regeneration.

Main Methods:

  • Identification and characterization of piR48444 expression in different MSCs.
  • Functional assays to assess the impact of piR48444 manipulation on osteogenic differentiation.
  • In vivo studies using mouse models for bone defect repair and osteolysis.
  • Mechanistic studies involving RNA-protein interactions and mRNA methylation analysis.

Main Results:

  • piR48444 was found to be downregulated during osteogenic differentiation of stem cells from exfoliated deciduous teeth (SHED) and upregulated in inflamed/aged bone marrow-derived mesenchymal stem cells (BMSCs).
  • Overexpression of piR48444 inhibited osteogenesis, while its knockdown enhanced differentiation and bone defect repair capacity in MSCs.
  • piR48444 antagomir administration promoted bone regeneration in vivo.
  • Mechanistically, piR48444 targets METTL7A, suppressing BMP2 mRNA N6-methyladenosine (m6A) methylation, thereby inhibiting osteogenesis.

Conclusions:

  • piR48444 acts as a negative regulator of MSC osteogenesis via the METTL7A-mediated BMP2 mRNA m6A methylation pathway.
  • Targeting piR48444 offers a promising therapeutic strategy to enhance MSC-based bone regeneration.
  • Further research into piRNA regulation could unlock novel approaches for treating bone disorders.

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