All-trans retinoic acid increases NF-κB activity in PMA-stimulated THP-1 cells upon unmethylated CpG challenge by enhancing cell surface TLR9 expression
- Authors
- Trinh, T.-A.; Hoang, T.X.; Kim, J.Y.
- Issue Date
- Oct-2020
- Publisher
- Springer
- Keywords
- All-trans retinoic acid; ODN2006; Phorbol-12-myristate-13-acetate; THP-1; Toll-like receptor 9; Unmethylated CpG
- Citation
- Molecular and Cellular Biochemistry, v.173, no.1, pp.167 - 177
- Journal Title
- Molecular and Cellular Biochemistry
- Volume
- 173
- Number
- 1
- Start Page
- 167
- End Page
- 177
- URI
- https://scholarworks.bwise.kr/gachon/handle/2020.sw.gachon/78230
- DOI
- 10.1007/s11010-020-03817-4
- ISSN
- 0300-8177
- Abstract
- An active metabolite of vitamin A, all-trans retinoic acid (ATRA), is known to exert immunomodulatory functions. This study investigates the possible immune potentiating effect of ATRA on NF-κB activity in human monocytic THP-1 cells after exposure to unmethylated CpG DNA ODN2006. We observed that challenge with ODN2006 significantly enhanced the NF-κB activity of PMA-differentiated THP-1 cells. ATRA synergistically enhanced NF-κB activity of cells, in a concentration- and time-dependent manner. The enhanced NF-κB activity of PMA-differentiated THP-1 cells after ODN2006 challenge was dependent on the RAR/RXR pathway. To determine the mechanism involved in increasing in the NF-κB activity of stimulated THP-1 cells, we examined the effects of PMA and ATRA on the expression of TLR9 (a receptor of ODN2006) in THP-1 cells. PMA treatment significantly enhanced both the intracellular and cell surface expression of TLR9, while ATRA alone showed no effect. However, ATRA synergistically enhanced the cell surface TLR9 expression of PMA-differentiated cells. To determine whether the ATRA-enhanced NF-κB activity is due to the enhanced cell surface TLR9 expression, we examined NF-κB activity after treatment with anti-TLR9 blocking antibody. Results revealed that the anti-TLR9 antibody treatment almost completely reverses the ATRA-enhanced NF-κB activity, suggesting that ATRA enhances NF-κB activity through upregulation of the cell surface TLR9 expression in PMA-differentiated and unmethylated CpG challenged THP-1 cells. © 2020, Springer Science+Business Media, LLC, part of Springer Nature.
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