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  4. 17b-Estradiol Protects Human Eyelid-Derived Adipose Stem Cells against Cytotoxicity and Increases Transplanted Cell Survival in Spinal Cord injury

17b-Estradiol Protects Human Eyelid-Derived Adipose Stem Cells against Cytotoxicity and Increases Transplanted Cell Survival in Spinal Cord injury

J. Cell. Mol. Med., 2014 · DOI: 10.1111/jcmm.12191 · Published: February 1, 2014

Spinal Cord InjuryRegenerative MedicineNeurology

Simple Explanation

Stem cell transplantation is a promising strategy for spinal cord injury (SCI) repair, but the low survival rate of transplanted cells hinders its success. 17b-estradiol (E2) has shown protective effects on cells. This study examined E2's effects on human eyelid adipose-derived stem cells (hEASCs) in a hydrogen peroxide-induced cell model in vitro and a rat SCI model in vivo. E2 protected hEASCs against cell death in vitro and enhanced grafted hEASCs survival in vivo by reducing apoptosis. E2 also enhanced growth factor secretion by hEASCs, improving the local microenvironment for tissue regeneration. E2 administration enhanced hEASCs transplantation's therapeutic efficacy and facilitated motor function recovery after SCI, suggesting it may enhance transplanted hEASCs survival after SCI.

Study Duration
6 weeks
Participants
48 adult male Sprague–Dawley rats
Evidence Level
Not specified

Key Findings

  • 1
    E2 protects hEASCs against H2O2-induced cell death in vitro.
  • 2
    E2 enhances the survival of grafted hEASCs in vivo by reducing apoptosis.
  • 3
    E2 enhances the secretion of growth factors by hEASCs, thereby making the local microenvironment more conducive for tissue regeneration.

Research Summary

The study investigates the cytoprotective effects of 17b-estradiol (E2) on human eyelid adipose-derived stem cells (hEASCs) against oxidative stress induced by hydrogen peroxide (H2O2) in vitro and in a rat spinal cord injury (SCI) model in vivo. Results show that E2 protects hEASCs from H2O2-induced cell death in vitro and enhances the survival of transplanted hEASCs in vivo by reducing apoptosis and promoting growth factor secretion, leading to improved motor function recovery in SCI rats. The findings suggest that E2 administration, in combination with hEASCs transplantation, presents a promising chemo-cell cocktail strategy for SCI treatment by creating a more favorable microenvironment for tissue regeneration.

Practical Implications

Therapeutic Strategy for SCI

The combination of E2 and hEASCs could be a new therapeutic approach for SCI treatment.

Improved Cell Survival

E2 administration can improve the survival rate of transplanted hEASCs, a major obstacle in stem cell therapy.

Enhanced Tissue Regeneration

E2 promotes a microenvironment conducive to tissue regeneration by reducing apoptosis and enhancing growth factor secretion.

Study Limitations

  • 1
    Differentiation ratio of hEASCs into neural lineages in vivo is very low.
  • 2
    Transplantation of hEASCs alone may not be sufficient for efficient repair of SCI.
  • 3
    Electrophysiology studies were unable to achieve depolarization and repolarization

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