Chitosan Oligosaccharide Promotes Junction Barrier through Modulation of PI3K/AKT and ERK Signaling Intricate Interplay in T84 Cells
Issued Date
2023-04-01
Resource Type
eISSN
20734360
Scopus ID
2-s2.0-85152859007
Journal Title
Polymers
Volume
15
Issue
7
Rights Holder(s)
SCOPUS
Bibliographic Citation
Polymers Vol.15 No.7 (2023)
Suggested Citation
Mehmood T., Pichyangkura R., Muanprasat C. Chitosan Oligosaccharide Promotes Junction Barrier through Modulation of PI3K/AKT and ERK Signaling Intricate Interplay in T84 Cells. Polymers Vol.15 No.7 (2023). doi:10.3390/polym15071681 Retrieved from: https://repository.li.mahidol.ac.th/handle/20.500.14594/81989
Title
Chitosan Oligosaccharide Promotes Junction Barrier through Modulation of PI3K/AKT and ERK Signaling Intricate Interplay in T84 Cells
Author(s)
Author's Affiliation
Other Contributor(s)
Abstract
Chitosan oligosaccharide (COS) is a breakdown product of chitin, a polymer of N-acetyl-D-glucosamine. COS promotes barrier function in intestinal epithelial cells. However, the exact mechanism of COS-induced barrier function remains unknown. This study was aimed to explore the intricate signaling cascades in the junction barrier induced by COS (100 μg/mL) in human intestinal epithelial cells (T84 cells). COS (100 μg/mL) promoted tight junction assembly and increased transepithelial electrical resistance (TEER). COS inhibited FITC-dextran flux in T84 cell monolayers at 2 h, 4 h, 6 h and 24 h post treatment. In addition, the effect of COS on TEER and FITC-dextran flux was abrogated by pre-incubation of wortmannin (2 μM), an AKT (protein kinase B) inhibitor, at 2 h and 4 h post treatment, indicating that COS-induced tight junction integrity was mediated at least in part by AKT activation. COS-induced TEER was amplified at 24 h and 48 h post treatment by pre-incubation with SC79 (2.5 μM), an AKT activator. Moreover, COS induced inhibition of extracellular signal-regulated kinase (ERK) in T84 cells. Wortmannin and SC79 pre-incubation promoted ERK activation and ERK inhibition, respectively, suggesting that COS-induced ERK inhibition was mediated by AKT. Collectively, this study reveals that COS promotes junction barrier integrity via regulating PI3K/AKT and ERK signaling intricate interplay in T84 cell monolayers. COS may be beneficial in promoting junction barrier in intestinal disorders.