TY - JOUR
T1 - Formyl peptide receptor 1 signaling in acute inflammation and neural differentiation induced by traumatic brain injury
AU - Fusco, R.
AU - Gugliandolo, E.
AU - Siracusa, R.
AU - Scuto, M.
AU - Cordaro, M.
AU - D'amico, R.
AU - Evangelista, M.
AU - Peli, A.
AU - Peritore, A. F.
AU - Impellizzeri, D.
AU - Crupi, R.
AU - Cuzzocrea, S.
AU - Di, Paola R.
PY - 2020
Y1 - 2020
N2 - 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.
AB - 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.
KW - Animal model
KW - Inflammation
KW - Neurogenesis
KW - Traumatic brain injury
KW - Animal model
KW - Inflammation
KW - Neurogenesis
KW - Traumatic brain injury
UR - https://publicatt.unicatt.it/handle/10807/161844
UR - https://www.scopus.com/inward/citedby.uri?partnerID=HzOxMe3b&scp=85092002856&origin=inward
UR - https://www.scopus.com/inward/record.uri?partnerID=HzOxMe3b&scp=85092002856&origin=inward
U2 - 10.3390/biology9090238
DO - 10.3390/biology9090238
M3 - Article
SN - 2079-7737
VL - 9
SP - 1
EP - 30
JO - Biology
JF - Biology
IS - 9
ER -