Prostaglandin F2α in vitro can affect basic inflammatory parameters of mesenchymal stem cells and slight modulating some of their immunomodulatory properties

Prostaglandins Leukot Essent Fatty Acids. 2020 Dec:163:102210. doi: 10.1016/j.plefa.2020.102210. Epub 2020 Nov 12.

Abstract

In the last decade, mesenchymal stem cells (MSCs) have been gaining attention due their ability to influence the function of other cells as well as modulate the inflammatory response. This occurs via their immunomodulatory functions, acting through direct cell-cell interaction or by releasing a broad spectrum of bioactive factors such as cytokines and growth factors. In addition, prostaglandins are arachidonic acid metabolites that play a key role in the generation and modulation of the inflammatory response. Among the bioactive prostaglandins, PGF is able to stimulate cell proliferation as well as act to inhibit progenitor cell differentiation, but no information about this prostaglandin's action on the immunoregulatory function of MSCs has been reported. In this study we evaluate important aspects of the influence of PGF analog (17-phenyl-trinor PGF), which is a potent prostaglandin FP receptor agonist, on some mechanisms that control the main functions of MSCs. C3H10T1/2, a mesenchymal stem cell linage, was stimulated with PGF under inflammatory conditions trigged by LPS in order to investigate PGF inflammatory parameters as well as its ability to immunoregulate macrophages and lymphocytes. PGF has the ability to increase proliferation tax without altering the cell viability of LPS-stimulated MSCs, while also diminishing the phosphorylation of NFκB transcription factor leading to attenuation of IL-1β and GM-CSF production. Additionally, MSC-s conditioned media from cells stimulated with PGF was able to increase the lymphocytes' IL-10 production. Overall, this study implied that PGF are able to modify some properties of MSCs.

Keywords: Macrophages and lymphocytes; Mesenchymal stem cells; Prostaglandin f2α; cytokines; immunomodulation.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Cell Line
  • Dinoprost / pharmacology*
  • Granulocyte-Macrophage Colony-Stimulating Factor / immunology*
  • Immunomodulation / drug effects*
  • Inflammation / chemically induced
  • Inflammation / immunology
  • Inflammation / pathology
  • Interleukin-1beta / immunology*
  • Lipopolysaccharides / toxicity
  • Mesenchymal Stem Cells / immunology*
  • Mesenchymal Stem Cells / pathology
  • Mice

Substances

  • IL1B protein, mouse
  • Interleukin-1beta
  • Lipopolysaccharides
  • Granulocyte-Macrophage Colony-Stimulating Factor
  • Dinoprost