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This galley proof is being listed electronically before publishing the final manuscript (It's not final version).

Ganglioside GT1b increases hyaluronic acid synthase 2 via PI3K activation with TLR2 dependence in orbital fibroblasts from thyroid eye disease patients
Hyun Kyu Yoo1,# (clinical fellow), Hyunju Park2,# (Research professor), Hye Suk Hwang1 (Research worker), Hee Ja Kim2 (Research worker), Koung Hoon Kook 1,* (Professor)
1Department of Ophthalmology, Ajou University School of Medicine, Suwon, Korea,
2Department of Physiology, Inflammation-Cancer Microenvironment Research Center, Ewha Womans University School of Medicine, Seoul, Korea
Thyroid eye disease (TED) is a complex autoimmune disease with a spectrum of signs. we previously reported that trisialoganglioside (GT)1b is significantly overexpressed in the orbital tissue of TED patients, and that exogenous GT1b strongly induced HA synthesis in orbital fibroblasts. However, the signaling pathway in GT1b-induced hyaluronic acid synthase (HAS) expression in orbital fibroblasts from TED patients have rarely been investigated. Here, we demonstrated that GT1b induced phosphorylation of Akt/mTOR in a dose-dependent manner in orbital fibroblasts from TED patients. Both co-treatment with a specific inhibitor for PI3K and siRNA knockdown of TLR2 attenuated GT1b-induced Akt phosphorylation. GT1b significantly induced HAS2 expression at both the transcriptional and translational level, which was suppressed by specific inhibitors of PI3K or Akt/mTOR, and by siRNA knockdown of TLR2. In conclusion, GT1b induced HAS2 in orbital fibroblasts from TED patients via activation of the PI3K-related signaling pathway, dependent on TLR2.
Abstract, Accepted Manuscript(in press) [Submitted on August 26, 2020, Accepted on December 17, 2020]
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