| First Author | von Ehr A | Year | 2020 |
| Journal | Front Cell Neurosci | Volume | 14 |
| Pages | 66 | PubMed ID | 32296307 |
| Mgi Jnum | J:311414 | Mgi Id | MGI:6752329 |
| Doi | 10.3389/fncel.2020.00066 | Citation | von Ehr A, et al. (2020) Inhibition of Microglial TGFbeta Signaling Increases Expression of Mrc1. Front Cell Neurosci 14:66 |
| abstractText | 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 Mannose receptor 1 (Mrc1), which is also referred to as CD206, in microglia has been reported after M2-like activation in vitro and in vivo. Mrc1 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 TGFbeta signaling on Mrc1 expression in microglia in vivo and in vitro. Using C57BL/6 wild type and Cx3cr1 (CreERT2) :R26-YFP:Tgfbr2 (fl/fl) mice-derived microglia, we show that the silencing of TGFbeta signaling results in the upregulation of Mrc1, whereas recombinant TGFbeta1 induced the delayed downregulation of Mrc1. Furthermore, chromatin immunoprecipitation experiments provided evidence that Mrc1 is not a direct Smad2/Smad4 target gene in microglia. Altogether our data indicate that the changes in Mrc1 expression after the activation or the silencing of microglial TGFbeta signaling are likely to be mediated by modifications of the secondary intracellular signaling events influenced by TGFbeta signaling. |
