Inhibition of Microglial TGFβ Signaling Increases Expression of Mrc1

Microglia are constantly surveying their microenvironment and rapidly react to impairments by changing their morphology, migrating toward stimuli and adopting gene expression profiles characterizing their activated state. The increased expression of the M2-like marker ( ), which is also referred to...

Ausführliche Beschreibung

Gespeichert in:
Bibliographische Detailangaben
Veröffentlicht in:Frontiers in cellular neuroscience 2020-03, Vol.14, p.66-66
Hauptverfasser: von Ehr, Alexander, Attaai, Abdelraheim, Neidert, Nicolas, Potru, Phani Sankar, Ruß, Tamara, Zöller, Tanja, Spittau, Björn
Format: Artikel
Sprache:eng
Schlagworte:
Online-Zugang:Volltext
Tags: Tag hinzufügen
Keine Tags, Fügen Sie den ersten Tag hinzu!
Beschreibung
Zusammenfassung:Microglia are constantly surveying their microenvironment and rapidly react to impairments by changing their morphology, migrating toward stimuli and adopting gene expression profiles characterizing their activated state. The increased expression of the M2-like marker ( ), which is also referred to as CD206, in microglia has been reported after M2-like activation and . is a 175-kDa transmembrane pattern recognition receptor which binds a variety of carbohydrates and is involved in the pinocytosis and the phagocytosis of immune cells, including microglia, and thought to contribute to a neuroprotective microglial phenotype. Here we analyzed the effects of TGFβ signaling on expression in microglia and . Using C57BL/6 wild type and mice-derived microglia, we show that the silencing of TGFβ signaling results in the upregulation of , whereas recombinant TGFβ1 induced the delayed downregulation of . Furthermore, chromatin immunoprecipitation experiments provided evidence that is not a direct Smad2/Smad4 target gene in microglia. Altogether our data indicate that the changes in expression after the activation or the silencing of microglial TGFβ signaling are likely to be mediated by modifications of the secondary intracellular signaling events influenced by TGFβ signaling.
ISSN:1662-5102
1662-5102
DOI:10.3389/fncel.2020.00066