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STUDY OF ANNEXIN A1 EXPRESSION IN A MURINE MODEL OF IMIQUIMODE-INDUCED PSORIASIS

Grant number: 23/13277-2
Support Opportunities:Scholarships in Brazil - Scientific Initiation
Start date: January 01, 2024
End date: December 31, 2025
Field of knowledge:Biological Sciences - Morphology - Histology
Principal Investigator:Cristiane Damas Gil
Grantee:Nathália Rodrigues da Silva
Host Institution: Escola Paulista de Medicina (EPM). Universidade Federal de São Paulo (UNIFESP). Campus São Paulo. São Paulo , SP, Brazil

Abstract

Psoriasis (Pso) is a chronic skin desease that has a genetic predisposition and depends also on environmental factors, with a prevalence of up to 1,3% in the Brazilian population. Its characteristics is the constant peeling of especific areas such as hands, feet, elbows and the back of the neck. Its pathogenesis occurthrough different triggers that will stimulate keratinocytes to secret proteins, such as S100A11, activating dendritic cells that secret IL-23, the mainstimulator of Th17 lymphocytes, in addition to also stimulating IL-17, mast cells,neutrophils and other cytokines (Th1, Th22, IL-19, IL-20, IL-22, IL-36, IFN-gama). By activating different inflammatory cytokines, we highlight annexin A1 (ANXA1), a protein with potent anti-inflammatory actions, such as controlling leukocyte migration and reducing the release of pro-inflammatory cytokines, which can beactivated by its interaction with formylated peptide receptors (FPRs). However, the role of ANXA1 in normal and Pso-affected skin has been poorly explored. Thus, we will analyze in the experimental model of Pso induced by imiquimod,the skin of C57BL/6 mice in following experimental conditions (n = 6 animals/group): Control (Naïve) and Pso (imiquimod). Under those conditions,we will analyze: i) skin histopathology and leukocytes count; ii) localization ofANXA1 and S100A11 protein expressions by immunohistochemistry; and iii) in publicly available transcriptomes of Gene Expression Omnibus (GEO) repository, avaluate transcription levels of ANXA11 and S100A11 in mice skin with induced Pso by imiquimod and controls, and possible therapeutic targets for inflammatory skin processes.

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