Preprint Article Version 1 This version is not peer-reviewed

Prostaglandin E2 induces Skin Aging via E-prostanoid 1 in Normal Human Dermal Fibroblasts

Version 1 : Received: 25 October 2019 / Approved: 27 October 2019 / Online: 27 October 2019 (11:04:31 CET)

A peer-reviewed article of this Preprint also exists.

Shim, J.H. Prostaglandin E2 Induces Skin Aging via E-Prostanoid 1 in Normal Human Dermal Fibroblasts. Int. J. Mol. Sci. 2019, 20, 5555. Shim, J.H. Prostaglandin E2 Induces Skin Aging via E-Prostanoid 1 in Normal Human Dermal Fibroblasts. Int. J. Mol. Sci. 2019, 20, 5555.

Journal reference: Int. J. Mol. Sci. 2019, 20, 5555
DOI: 10.3390/ijms20225555

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.

Subject Areas

PGE2; EP1; skin-aging; ERK1/2; intracellular calcium

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