![]() ![]() In addition, pretreatment of OFs with thiophenecarboxamide (TPCA-1) inhibits retinoid-induced MCP-1 induction, suggesting an NF-κB (nuclear factor kappa-light-chain-enhancer of activated B cells)–dependent mechanism. We performed retinoic acid treatment on both normal and TED patient–derived orbital fibroblasts (OFs) followed by mRNA and protein isolation, quantitative real-time polymerase chain reaction (qRT-PCR), enzyme-linked immunosorbent assay, RNA sequencing, and Western blot analyses.īoth normal and TED patient–derived OFs display robust induction of monocyte chemoattractant protein 1 (MCP-1) upon retinoid treatment TED OFs secrete significantly more MCP-1 than normal OFs. Whereas the pathology of both TED and GD is driven by autoantibodies, it is unclear why symptoms manifest specifically in the orbit. ![]() The most prevalent of these conditions, thyroid eye disease (TED), occurs in up to 50% of patients with Graves’ disease (GD). The orbit displays unique vulnerability to inflammatory conditions.
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