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Setd2 is associated with strontium-induced bone regeneration.

Xiaoshi Jia1, Qiaoyun Long2, Richard J Miron3

  • 1The State Key Laboratory Breeding Base of Basic Science of Stomatology (Hubei-MOST) & Key Laboratory of Oral Biomedicine Ministry of Education, Wuhan University, Wuhan, China.

Acta Biomaterialia
|February 22, 2017
PubMed
Summary

Strontium (Sr) in scaffolds promotes bone regeneration by increasing the expression of Set2, a histone methylase. This epigenetic factor enhances osteoblast differentiation via the MAPK pathway, offering new therapeutic targets for osteoporosis.

Keywords:
Bone regenerationH3K36me3OsteoporosisRNA-seqSetd2Sr-MBG

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Area of Science:

  • Biomaterials Science
  • Regenerative Medicine
  • Epigenetics

Background:

  • Strontium ranelate is used for osteoporosis, and strontium-mesoporous bioactive glass (Sr-MBG) scaffolds enhance bone formation.
  • The epigenetic mechanisms of strontium's bone-promoting effects remain unclear.

Purpose of the Study:

  • To investigate the bone-inducing properties of strontium (Sr) using RNA-sequencing.
  • To elucidate the role of Set2 in strontium-mediated new bone formation and osteoblast differentiation.

Main Methods:

  • RNA-sequencing (RNA-seq) on in vivo tissue samples.
  • Immunofluorescent staining for Set2, H3K36me3, and Runx2.
  • In vitro studies with MG63 cells, including Set2 knockdown and overexpression with/without SrCl2 stimulation.
  • Analysis of MAPK pathway activation.

Main Results:

  • Sr-MBG scaffolds significantly increased Set2 and H3K36me3 expression compared to MBG alone.
  • Set2 and H3K36me3 were localized in Runx2-positive cells in Sr-MBG treated defects.
  • Strontium chloride (SrCl2) stimulated MAPK pathway activation, specifically ERK.
  • Set2 overexpression enhanced SrCl2-induced osteoblast differentiation, while knockdown reduced it.
  • Set2 regulates ERK activation, creating a positive feedback loop in osteoblast differentiation.

Conclusions:

  • Set2 plays a crucial role in strontium-enhanced osteoblast differentiation.
  • Set2 acts as a key epigenetic regulator in the bone formation process.
  • Set2 represents a potential epigenetic target for novel osteoporosis treatments and bone regeneration scaffolds.