Connections of annexin A1 and translocator protein-18â¯kDa on toll like receptor stimulated BV-2 cells.
Exp Cell Res
; 367(2): 282-290, 2018 06 15.
Article
en En
| MEDLINE
| ID: mdl-29649428
ABSTRACT
BACKGROUND:
Annexin A1 (ANXA1) and Translocator Protein-18KDa (TSPO) down-regulate neuroinflammation. We investigated the role of recombinant ANXA1 (rANXA) on TSPO functions on Toll Like Receptor (TLR) activated microglia.METHODS:
BV-2 cells (murine microglia), were stimulated by E. coli Lipopolysaccharide (LPS) and treated with rANXA1 in order to measure TSPO expression and inflammatory parameters. Anti-sense ANXA1 and TLR4 and TSPO shRNA, as well as pharmacological treatments, were employed to assess the mechanisms involved.RESULTS:
LPS-stimulated BV-2 cells caused overexpression of TSPO, which was inhibited by pharmacological blockade of TLR4 or TLR4 mRNA silencing; inhibition of myeloid differentiation primary response gene 88 (MyD88) dimerization; or blocking of nuclear factor κB (NF-κB) activation. rANXA1 treatment impaired LPS-induced TSPO upregulation by down-modulating MyD88 and NF-κB signaling; the effect was abolished by WRW4, an antagonist of formyl peptide receptor 2 (FPR2). rANXA1 treatment also downregulated interleukin 1ß (IL-1ß) and tumor necrosis factor-α (TNFα) secretion in LPS-stimulated BV-2 cells. TSPO knockdown in BV-2 cells augmented LPS-induced TNFα secretion and abolished the inhibitory effect of rANXA1 on TNFα secretion evoked by LPS.CONCLUSIONS:
exogenous ANXA1 down-modulates LPS-induced TSPO via MyD-88/NF-κB pathways, and constitutive TSPO is pivotal for the control of ANXA1 on TNFα secretion. TSPO actions may be involved with the mechanisms of ANXA1 on inflammatory brain diseases.Palabras clave
Texto completo:
1
Banco de datos:
MEDLINE
Asunto principal:
Anexina A1
/
Receptores de GABA
Límite:
Animals
/
Humans
Idioma:
En
Revista:
Exp Cell Res
Año:
2018
Tipo del documento:
Article
País de afiliación:
Brasil