CD34+ Orbital Fibroblasts Contribute to the Pathogenesis of Thyroid Eye Disease via miR-182-5p
Authors' conclusion
The IL-6/STAT3/miR-182-5p pathway led to activation of CD34+ OFs. MiR-182-5p promoted the proliferation, migration, fibrosis, and anti-apoptosis of CD34+ OFs via targeting Smad7. Our findings suggest that miR-182-5p may potentially serve as a therapeutic target for TED.
Study context
- Population
- Orbital connective tissues (OCTs) and orbital fibroblasts (OFs) from thyroid eye disease (TED) patients and healthy donors
- Participants
- 25 vs 24
- Comparison
- TED patients vs healthy donors
- TEDn = 25
- Healthy donorsn = 24reference
- Outcome
- Regulatory effects of miR-182-5p on CD34+ OFs
Main finding
As reported in the abstract
- MiR-182-5p highly expressed in TED OCTs and their derived CD34+ OFs
- TED OCTs: increased expression of IL-6, IL-17A, CD34 and phosphorylated STAT3 at Ser727 and Tyr705
- Activation of IL-6/STAT3 signaling promoted miR-182-5p expression in CD34+ OFs
- MiR-182-5p enhanced wound repair, proliferation and RANTES expression and inhibited apoptosis in CD34+ OFs
- CD34+ OFs transfected with miR-182-5p susceptible to TGF-β-initiated myofibroblast differentiation
- Smad7 identified as downstream target of miR-182-5p (luciferase reporter and pull-down assays), modulating proliferation, migration, fibrosis and apoptosis of CD34+ OFs
Observational data: associations, not effects.
Original publication
CD34+ Orbital Fibroblasts Contribute to the Pathogenesis of Thyroid Eye Disease via miR-182-5p. J Clin Endocrinol Metab. Published 18 December 2024. doi:10.
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