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(Reference retrieved automatically from Web of Science through information on FAPESP grant and its corresponding number as mentioned in the publication by the authors.)

Connections of annexin A1 and translocator protein-18 kDa on toll like receptor stimulated BV-2 cells

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Author(s):
Pantaleao, Lorena [1] ; Oliveira Rocha, Gustavo Henrique [1] ; Reutelingsperger, Chris [2] ; Tiago, Manoela [1] ; Maria-Engler, Silvya Stucchi [1] ; Solito, Egle [3] ; Farsky, Sandra P. [1]
Total Authors: 7
Affiliation:
[1] Univ Sao Paulo, Sch Pharmaceut Sci, Dept Clin & Toxicol Anal, Av Prof Lineu Prestes 580 Bl 13B, BR-05508900 Sao Paulo - Brazil
[2] Maastricht Univ, Cardiovasc Res Inst Maastricht, Dept Biochem, 616 6200 MD, NL-6211 CH Maastricht - Netherlands
[3] Queen Mary Univ, William Harvey Res Inst, Sch Med & Dent, Charterhouse Sq, London EC1M 6BQ - England
Total Affiliations: 3
Document type: Journal article
Source: Experimental Cell Research; v. 367, n. 2, p. 282-290, JUN 15 2018.
Web of Science Citations: 3
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 kappa B (NF-kappa B) activation. rANXA1 treatment impaired LPS-induced TSPO upregulation by down-modulating MyD88 and NF-kappa B signaling; the effect was abolished by WRW4, an antagonist of formyl peptide receptor 2 (FPR2). rANXA1 treatment also downregulated interleukin 1 beta (IL-1 beta) and tumor necrosis factor-alpha (TNF alpha) secretion in LPS-stimulated BV-2 cells. TSPO knockdown in BV-2 cells augmented LPS-induced TNFa secretion and abolished the inhibitory effect of rANXA1 on TNF alpha secretion evoked by LPS. Conclusions: exogenous ANXA1 down-modulates LPS-induced TSPO via MyD-88/NF-kappa B pathways, and constitutive TSPO is pivotal for the control of ANXA1 on TNF alpha secretion. TSPO actions may be involved with the mechanisms of ANXA1 on inflammatory brain diseases. (AU)

FAPESP's process: 14/07328-4 - Identification of endogenous pathways for the control of inflammation
Grantee:Sandra Helena Poliselli Farsky
Support Opportunities: Research Projects - Thematic Grants
FAPESP's process: 13/25903-3 - Annexin A1 modulation mechanism on the expression of the translocator protein (TSPO)
Grantee:Lorena Do Nascimento Pantaleão
Support Opportunities: Scholarships in Brazil - Doctorate