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The Graves’ disease is an autoimmune disease highly associated with thyroid cancer. The Graves’ ophthalmopathy (GO) is a special Graves’ disease with inflammatory ophthalmopathy being a typical extrathymic complication. GO is caused by the formation of orbital fat and extraocular muscle fibrosis due to the inflammation of orbital connective tissues. Thus, controlling extraocular muscle fibrosis is critical for the prognosis of GO. The objective of this study is to identify and experimentally validate key genes associated with GO and explore their potential function mechanisms especially on extraocular muscle fibrosis. Specifically, we first created a GO mouse model, and performed RNA sequencing on the extraocular muscles of fibrotic GO mice and controls.  SRC  was identified as the most significant unstudied differentially expressed gene between GO mice and controls. Thus, we conducted a few  in vitro  analyses to explore the roles and functions of  SRC  in GO, for which we selected primary cultured orbital fibroblast (OF) as the  in vitro  cell line model. It is known that myofibroblast (MFB), which expresses α-SMA, is an important target cell in the process of fibrosis. Our experiment suggests that TGF-β can induce the transformation from OF to MFB, however, the transformation was inhibited by silencing the  SRC  gene in OF. In addition, we also inhibited TGF-β/Smad, NF-κB, and PI3K/Akt signaling pathways to analyze the interaction between these pathways and  SRC . In conclusion, the silence of  SRC  in OF can inhibit the transformation from OF to MFB, which might be associated with the interaction between  SRC  and a few pathways such as TGF-β/Smad, NF-κB, and PI3K/Akt.

Exploring the Role of SRC in Extraocular Muscle Fibrosis of the Graves’ Ophthalmopathy