Protein ID'd With Possible Therapeutic Properties for Thyroid Eye Disease

Prevent formation of TGF-β-dependent myofibroblasts, dependent on AHR expression
Prevent formation of TGF-β-dependent myofibroblasts, dependent on AHR expression

HealthDay News — Aryl hydrocarbon receptor (AHR) and AHR ligands prevent formation of transforming growth factor (TGF)-β-dependent myofibroblast formation in thyroid eye disease (TED), according to research published online November 11 in The American Journal of Pathology.

Noting that the signaling pathway for TGF-β, which induces myofibroblast formation, is influenced by AHR signaling pathways, Collynn F. Woeller, PhD, from the Flaum Eye Institute in Rochester, New York, and colleagues examined whether AHR agonists could prevent myofibroblast formation in fibroblasts from patients with TED. Patients with TED had orbital fibroblasts explanted and were treated with TGF-β to induce myoblast formation, contraction, and proliferation. 

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The researchers found that AHR ligands averted formation of TGF-β-dependent myofibroblasts, and this was dependent on AHR expression. The AHR and AHR ligands blocked profibrotic Wnt signaling by inhibition of GSK3β phosphorylation in order to prevent formation of myofibroblasts.

"These results provide new insight into the molecular pathways underlying orbital scarring in TED," the authors write. "These novel studies highlight the potential of the AHR and AHR ligands as future therapeutic options for eye diseases and possibly also for other scarring conditions."

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