Formyl peptide receptor 1 signaling in acute inflammation and neural differentiation induced by traumatic brain injury

Maurizio Evangelista, Roberta Fusco, Enrico Gugliandolo, Rosalba Siracusa, Maria Scuto, Marika Cordaro, Ramona D’Amico, Angelo Peli, Alessio Filippo Peritore, Daniela Impellizzeri, Rosalia Crupi, Salvatore Cuzzocrea, Rosanna Di Paola

Risultato della ricerca: Contributo in rivistaArticolo in rivistapeer review

3 Citazioni (Scopus)

Abstract

Traumatic brain injury (TBI) is a shocking disease frequently followed by behavioral disabilities, including risk of cerebral atrophy and dementia. N-formylpeptide receptor 1 (FPR1) is expressed in cells and neurons in the central nervous system. It is involved in inflammatory processes and during the differentiation process in the neural stem cells. We investigate the effect of the absence of Fpr1 gene expression in mice subjected to TBI from the early stage of acute inflammation to neurogenesis and systematic behavioral testing four weeks after injury. C57BL/6 animals and Fpr1 KO mice were subjected to TBI and sacrificed 24 h or four weeks after injury. Twenty-four hours after injury, TBI Fpr1 KO mice showed reduced histological impairment, tissue damage and acute inflammation (MAPK activation, NF-κB signaling induction, NRLP3 inflammasome pathway activation and oxidative stress increase). Conversely, four weeks after TBI, the Fpr1 KO mice showed reduced survival of the proliferated cells in the Dentate Gyrus compared to the WT group. Behavioral analysis confirmed this trend. Moreover, TBI Fpr1 KO animals displayed reduced neural differentiation (evaluated by beta-III tubulin expression) and upregulation of astrocyte differentiation (evaluated by GFAP expression). Collectively, our study reports that, immediately after TBI, Fpr1 increased acute inflammation, while after four weeks, Fpr1 promoted neurogenesis.
Lingua originaleEnglish
pagine (da-a)1-30
Numero di pagine30
RivistaBiology
Volume9
DOI
Stato di pubblicazionePubblicato - 2020

Keywords

  • Animal model
  • Inflammation
  • Neurogenesis
  • Traumatic brain injury

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