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Pharmacological rescue of diabetic skeletal stem cell niches

Ruth Tevlin1,2, Eun Young Seo1,2, Owen Marecic1,2

  • 1Hagey Laboratory for Pediatric Regenerative Medicine and Department of Surgery, Stanford University, Palo Alto, CA 94305, USA.

Science Translational Medicine
|January 13, 2017
PubMed

Insights

Diabetes impairs bone healing by reducing Indian hedgehog (Ihh) signaling in skeletal stem cells. Restoring Ihh levels with hydrogel delivery effectively rescued bone repair in diabetic mice.

Area of Science:

  • Biomedical Engineering
  • Stem Cell Biology
  • Metabolic Diseases

Background:

  • Diabetes mellitus (DM) is linked to poor bone healing, but the underlying molecular mechanisms are unclear.
  • Skeletal stem cell (SSC) dysfunction is implicated in diabetic skeletal complications.
  • Identifying specific molecular defects in diabetic SSCs is crucial for therapeutic development.

Purpose of the Study:

  • To investigate molecular abnormalities in mouse skeletal stem cells (mSSCs) from diabetic mice.
  • To determine the role of Indian hedgehog (Ihh) signaling in impaired bone healing in diabetes.
  • To develop a targeted therapy to restore bone healing in diabetic conditions.

Main Methods:

  • Advanced stem cell characterization techniques were used to analyze mSSC function in diabetic mice.
  • The impact of tumor necrosis factor-alpha (TNF-α) on Ihh expression in mSSCs was assessed.
  • Fracture repair was studied with and without Ihh inhibition and with Ihh delivery via hydrogel.

Main Results:

  • High serum TNF-α in diabetic mice repressed Ihh expression in mSSCs and progenitors.
  • Inhibition of hedgehog signaling during fracture repair suppressed mSSC expansion and impaired healing.
  • Delivery of exogenous Ihh via a slow-release hydrogel restored mSSC function and rescued bone healing.

Conclusions:

  • TNF-α-mediated repression of Ihh signaling is a key mechanism for impaired bone healing in diabetes.
  • Targeted delivery of Ihh can restore mSSC function and correct skeletal defects in diabetic mice.
  • This study offers a therapeutic strategy for treating skeletal complications associated with systemic diseases.

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