Ganglioside GT1b increases hyaluronic acid synthase 2 via PI3K activation with TLR2 dependence in orbital fibroblasts from thyroid eye disease patients

Hyun Kyu Yoo, Hyunju Park, Hye Suk Hwang, Hee Ja Kim, Youn Hee Choi, Koung Hoon Kook

Research output: Contribution to journalArticlepeer-review

4 Scopus citations

Abstract

Thyroid eye disease (TED) is a complex autoimmune disease with a spectrum of signs. we previously reported that trisialoganglio-side (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.

Original languageEnglish
Pages (from-to)136-141
Number of pages6
JournalBMB Reports
Volume54
Issue number2
DOIs
StatePublished - 2021

Bibliographical note

Funding Information:
This study was supported by Basic Science Research Program through the National Research Foundation of Korea (NRF) funded by the Ministry of Science, ICT & Future Planning (NRF-2016R 1A2B1014704) (K.H.K) and by RP-Grant 2018 of Ewha Womans University (H.P.).

Publisher Copyright:
© 2021. by the The Korean Society for Biochemistry and Molecular Biology.

Keywords

  • Orbital fibroblast
  • Phosphoinositide 3-kinase
  • Thyroid eye disease
  • Toll-like receptor 2
  • Trisialoganglioside 1b

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