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Ganglioside GT1b increases hyaluronic acid synthase 2 via PI3K activation with TLR2 dependence in orbital fibroblasts from thyroid eye disease patients
- Title
- Ganglioside GT1b increases hyaluronic acid synthase 2 via PI3K activation with TLR2 dependence in orbital fibroblasts from thyroid eye disease patients
- Authors
- Yoo, Hyun Kyu; Park, Hyunju; Hwang, Hye Suk; Kim, Hee Ja; Choi, Youn-Hee; Kook, Koung Hoon
- Ewha Authors
- 최윤희; 박현주
- SCOPUS Author ID
- 최윤희; 박현주
- Issue Date
- 2021
- Journal Title
- BMB REPORTS
- ISSN
- 1976-6696
1976-670X
- Citation
- BMB REPORTS vol. 54, no. 2, pp. 136 - 141
- Keywords
- Orbital fibroblast; Phosphoinositide 3-kinase; Thyroid eye disease; Toll-like receptor 2; Trisialoganglioside 1b
- Publisher
- KOREAN SOCIETY BIOCHEMISTRY &
MOLECULAR BIOLOGY
- Indexed
- SCIE; SCOPUS; KCI
- Document Type
- Article
- Abstract
- 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.
- DOI
- 10.5483/BMBRep.2021.54.2.178
- Appears in Collections:
- 의과대학 > 의학과 > Journal papers
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