Interleukin-17 Reduces βENaC via MAPK Signaling in Vascular Smooth Muscle Cells.

ABSTRACT: Degenerin proteins, such as the beta epithelial Na+ channel (βENaC), are essential in the intracellular signaling of pressure-induced constriction, an important vascular smooth muscle cell (VSMC) function. While certain cytokines reduce ENaC protein in epithelial tissue, it is unknown if interleukin-17 (IL-17), a potent pro-inflammatory cytokine, directly mediates changes in membrane-associated βENaC in VSMCs. Therefore, we tested the hypothesis that exposure to IL-17 reduces βENaC in VSMCs through canonical mitogen-activated protein kinase (MAPK) signaling pathways. We treated cultured rat VSMCs (A10 cell line) with IL-17 (1-100 ng/mL) for 15 min to 16 h and measured expression of βENaC, p38MAPK, c-jun kinase (JNK), and nuclear factor kappa-light-chain-enhancer of activated B cells (NFκB)

SUBMITTER: Duncan JW 

PROVIDER: S-EPMC7215799 | biostudies-literature | 2020 Apr

REPOSITORIES: biostudies-literature