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• W2929384972 endingPage "48" @default.
• W2929384972 startingPage "37" @default.
• W2929384972 abstract "Fundamentally, microglia have two activation states, a pro-inflammatory neurotoxic (M1) and an anti-inflammatory neuroprotective (M2) phenotype, and their conversion from M1-like to M2-like microglia may provide therapeutic benefits to prevent neuronal loss in neurodegenerative diseases such as Parkinson's disease (PD). Previously, we showed that Salmeterol, a long-acting β2-adrenergic receptor (β2-AR) agonist, has neuroprotective effects in PD models in vitro and in vivo through the β-arrestin2-dependent inhibition of pro-inflammatory M1-type mediator production. In the present study, we explored whether Salmeterol can mediate phenotypic conversion in LPS-activated murine microglial BV2 cells from the neurotoxic M1-like to a neuroprotective M2-like phenotype. Salmeterol inhibited the production of LPS-induced mediators of the pro-inflammatory M1 phenotype such as tumor necrosis factor-α (TNF-α), IL-(interleukin) 18, IL-6, chemokines (CCL2, CCL3, CCL4) and reactive oxygen species from BV2 cells. Conversely, treatment with Salmeterol and other β2-AR agonists robustly enhances the production of the M2 cytokine IL-10 from LPS-activated microglia. In addition, Salmeterol upregulates the expression of arginase-1 and CXCL14. Furthermore, using siRNA approach we found that silencing of the transcription factor Creb abrogates the Salmeterol-mediated production of IL-10 in LPS-activated BV2 cells, but silencing of β-arrestin2 with Arrb2 siRNA did not. In addition, our data shows conversion from an M1- to M2-like phenotype in LPS-activated microglia by β2-AR agonists involves activation of the classical cAMP/PKA/CREB as well as the PI3K and p38 MAPK signaling pathways, and provides a novel therapeutic approach targeting microglial cell activation and inducing their phenotypic conversion in the treatment of neuroinflammatory diseases such as PD." @default.
• W2929384972 created "2019-04-11" @default.
• W2929384972 creator A5044962291 @default.
• W2929384972 creator A5067094023 @default.
• W2929384972 creator A5085575361 @default.
• W2929384972 date "2019-07-01" @default.
• W2929384972 modified "2023-09-24" @default.
• W2929384972 title "Mechanism underlying β2-AR agonist-mediated phenotypic conversion of LPS-activated microglial cells" @default.
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• W2929384972 doi "https://doi.org/10.1016/j.jneuroim.2019.03.017" @default.
• W2929384972 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/30933849" @default.
• W2929384972 hasPublicationYear "2019" @default.
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