Abstract
Collagen type I production decreases with aging, leading to wrinkles and impaired skin function. Prostaglandin E2 (PGE2), a lipid-derived signaling molecule produced from arachidonic acid by cyclo-oxygenase, inhibits collagen production, and induces matrix metallopeptidase 1 (MMP1) expression by fibroblasts in vitro. PGE2-induced collagen expression inhibition and MMP1 promotion are aging mechanisms. This study investigated the role of E-prostanoid 1 (EP1) in PGE2 signaling in normal human dermal fibroblasts (NHDFs). When EP1 expression was inhibited by EP1 small interfering RNA (siRNA), there were no significant changes in messenger RNA (mRNA) levels of collagen, type I, alpha 1 (COL1A1)/MMP1 between siRNA-transfected NHDFs and siRNA-transfected NHDFs with PGE2. This result showed that EP1 is a PGE2 receptor. Extracellular signal-regulated kinase 1/2 (ERK1/2) phosphorylation after PGE2 treatment significantly increased by ~2.5 times. In addition, PGE2 treatment increased the intracellular Ca2+ concentration in NHDFs. These results indicated that PGE2 is directly associated with EP1 pathway-regulated ERK1/2 and inositol trisphosphate (IP3) signaling in NHDFs.
Highlights
The elderly have typically thin and fragile skin, with increased susceptibility to bruising and impaired wound healing [1]
This study investigated the role of E-prostanoid 1 (EP1) in Prostaglandin E2 (PGE2) signaling in normal human dermal fibroblasts (NHDFs)
PGE2-induced NHDF apoptosis gradually increased with the PGE2 concentration
Summary
The elderly have typically thin and fragile skin, with increased susceptibility to bruising and impaired wound healing [1] These aging-related alterations largely reflect collagen fragmentation and reduction. Fibroblasts attach to the surrounding ECM to form adhesion complexes, which, in turn, act through the cytoskeleton to exert contractile forces. Resistance to these contractile forces produces mechanical forces in the fibroblasts, which primarily determine morphology, cytoskeletal tissue organization, gene expression, and signaling transduction [5,6,7]. Fibroblasts in aging skin display an increase in PGE2 levels [10,11,12]. This study investigated the role of EP1 in PGE2 signaling in normal human dermal fibroblasts (NHDFs)
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