1. Hypoxia regulates human mast cell adhesion to fibronectin via the PI3K/AKT signaling pathway.
- Author
-
Pastwińska J, Walczak-Drzewiecka A, Łukasiak M, Ratajewski M, and Dastych J
- Subjects
- Cell Adhesion drug effects, Cell Hypoxia drug effects, Cell Line, Humans, Integrin alpha5beta1 metabolism, Mast Cells drug effects, Oligopeptides pharmacology, Phosphatidylinositol 3-Kinases pharmacology, Phosphoinositide-3 Kinase Inhibitors pharmacology, Protein Kinase Inhibitors pharmacology, Receptors, Cell Surface metabolism, Stem Cell Factor pharmacology, Wortmannin pharmacology, Fibronectins pharmacology, Mast Cells cytology, Mast Cells enzymology, Phosphatidylinositol 3-Kinases metabolism, Proto-Oncogene Proteins c-akt metabolism, Signal Transduction drug effects
- Abstract
A decrease in oxygen concentration is a hallmark of inflammatory reactions resulting from infection or homeostasis disorders. Mast cells interact with extracellular matrix and other cells by adhesion receptors. We investigated the effect of hypoxia on integrin-mediated mast cell adhesion to fibronectin. We found that it was mediated by the α5/β1 receptor and that hypoxia significantly upregulated this process. Hypoxia-mediated increases in mast cell adhesion occurred without increased surface expression of integrins, suggesting regulation by inside-out integrin signaling. Hypoxia also mediated an increase in phosphorylation of Akt, and PI3'kinase inhibitors abolished hypoxia-mediated mast cell adhesion. Hypoxia upregulates the function of integrin receptors by PI3' kinase-dependent signaling. This process might be important for the location of mast cells at inflammatory sites.
- Published
- 2020
- Full Text
- View/download PDF