Phosphorylation of tyrosine-14 on Caveolin-1 enhances lipopolysaccharide-induced inflammation in human intestinal Caco-2 cellsopen access
- Authors
- Bae, Gong Deuk; Kim, Kyong; Jang, Se-Eun; Baek, Dong-Jae; Park, Eun-Young; Oh, Yoon Sin
- Issue Date
- Dec-2023
- Publisher
- 한국응용생명화학회
- Keywords
- Caveolin-1 · High fat diet · Intestine · Permeability · Tight junction protein
- Citation
- Journal of Applied Biological Chemistry, v.66, pp.311 - 319
- Journal Title
- Journal of Applied Biological Chemistry
- Volume
- 66
- Start Page
- 311
- End Page
- 319
- URI
- https://scholarworks.bwise.kr/gachon/handle/2020.sw.gachon/88705
- DOI
- 10.3839/jabc.2023.043
- ISSN
- 1976-0442
- Abstract
- Caveolin-1 (Cav-1) is the main structural component of the caveolae on the plasma membrane, which regulates various cellular processes, including cell growth, differentiation, and endocytosis. Although a recent study demonstrated that Cav-1 might be involved in diabetes-associated inflammation, its exact role in the intestine was unclear. In this study, we examined the intestinal expression of Cav-1 in diabetic conditions. We also investigated its effect on lipopolysaccharide (LPS)-induced inflammation by expressing this protein in human intestinal Caco- 2 cells lacking Cav-1. We observed that increased Cav-1 levels and decreased expression of tight junction proteins affected intestinal permeability in high-fat diet-induced diabetic mice.
When Caco-2 cells were treated with LPS, Cav-1 enhanced the NF-κB signaling. Moreover, LPS reduced the expression of tight junction proteins while it increased cell-cell permeability and reactive oxygen species generation in Caco-2 cells and this effect was amplified by cav-1 overexpression. LPS treatment promoted phosphorylation of tyrosine-14 (Y14) on Cav-1, and the LPSinduced NF-κB signaling was suppressed in cells expressing nonphosphorylatable Cav-1 (tyrosine-14 to phenylalanine mutant), which reduced intestinal barrier permeability. These results suggest that Cav-1 expression promotes LPS-induced inflammation in Caco-2 cells, and phosphorylation of Y14 on Cav-1 might contribute to the anti-inflammatory response in LPS-induced NF- κB signaling and cell permeability.
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