PMID- 31914916
OWN - NLM
STAT- MEDLINE
DCOM- 20210706
LR  - 20210706
IS  - 1996-3181 (Electronic)
IS  - 1871-5273 (Linking)
VI  - 19
IP  - 1
DP  - 2020
TI  - The Role of Annexin A1 and Formyl Peptide Receptor 2/3 Signaling in Chronic 
      Corticosterone-Induced Depression-Like behaviors and Impairment in 
      Hippocampal-Dependent Memory.
PG  - 27-43
LID - 10.2174/1871527319666200107094732 [doi]
AB  - BACKGROUND: The activity of the Hypothalamic-Pituitary-Adrenal (HPA) axis is 
      commonly dysregulated in stress-related psychiatric disorders. Annexin A1 
      (ANXA1), an endogenous ligand of Formyl Peptide Receptor (FPR) 2/3, is a member 
      of the family of phospholipid- and calcium-binding proteins with a well-defined 
      role in the delayed early inhibitory feedback of Glucocorticoids (GC) in the 
      pituitary gland and implicated in the occurrence of behavioural disorders such as 
      anxiety. OBJECTIVE: The present study aimed to evaluate the potential role of 
      ANXA1 and its main receptor, as a cellular mediator of behavioural disorders, in 
      a model of Corticosterone (CORT)-induced depression and subsequently, the 
      possible correlation between the depressive state and impairment of hippocampal 
      memory. METHODS: To induce the depression model, Wild-Type (WT), ANXA1 Knockout 
      (KO), and FPR2/3 KO mice were exposed to oral administration of CORT for 28 days 
      dissolved in drinking water. Following this, histological, biochemical and 
      behavioural analyses were performed. RESULTS: FPR2/3 KO and ANXA1 KO mice showed 
      improvement in anxiety and depression-like behaviour compared with WT mice after 
      CORT administration. In addition, FPR2/3 KO and ANXA1 KO mice showed a reduction 
      in histological alterations and neuronal death in hippocampal sections. Moreover, 
      CORT+ FPR2/3 KO and ANXA1 KO, exhibited a higher expression of Brain-Derived 
      Neurotrophic Factor (BDNF), phospho-ERK, cAMP response element-binding protein 
      (pCREB) and a decrease in Serotonin Transporter Expression (SERT) compared to 
      WT(CORT+) mice. CONCLUSION: In conclusion, the absence of the ANXA1 protein, even 
      more than the absence of its main receptor (FPR 2/3), was fundamental to the 
      inhibitory action of GC on the HPA axis; it also maintained the hippocampal 
      homeostasis by preventing neuronal damage associated with depression.
CI  - Copyright(c) Bentham Science Publishers; For any queries, please email at 
      epub@benthamscience.net.
FAU - Peritore, Alessio Filippo
AU  - Peritore AF
AD  - Department of Chemical, Biological, Pharmaceutical and Environmental Science, 
      University of Messina, Messina, Italy.
FAU - Crupi, Rosalia
AU  - Crupi R
AD  - Department of Chemical, Biological, Pharmaceutical and Environmental Science, 
      University of Messina, Messina, Italy.
FAU - Scuto, Maria
AU  - Scuto M
AD  - Department of Biomedical and Biotechnological Sciences, University of Catania, 
      Catania, Italy.
FAU - Gugliandolo, Enrico
AU  - Gugliandolo E
AD  - Department of Chemical, Biological, Pharmaceutical and Environmental Science, 
      University of Messina, Messina, Italy.
FAU - Siracusa, Rosalba
AU  - Siracusa R
AD  - Department of Chemical, Biological, Pharmaceutical and Environmental Science, 
      University of Messina, Messina, Italy.
FAU - Impellizzeri, Daniela
AU  - Impellizzeri D
AD  - Department of Chemical, Biological, Pharmaceutical and Environmental Science, 
      University of Messina, Messina, Italy.
FAU - Cordaro, Marika
AU  - Cordaro M
AD  - Department of Chemical, Biological, Pharmaceutical and Environmental Science, 
      University of Messina, Messina, Italy.
FAU - D'amico, Ramona
AU  - D'amico R
AD  - Department of Chemical, Biological, Pharmaceutical and Environmental Science, 
      University of Messina, Messina, Italy.
FAU - Fusco, Roberta
AU  - Fusco R
AD  - Department of Chemical, Biological, Pharmaceutical and Environmental Science, 
      University of Messina, Messina, Italy.
FAU - Di Paola, Rosanna
AU  - Di Paola R
AD  - Department of Chemical, Biological, Pharmaceutical and Environmental Science, 
      University of Messina, Messina, Italy.
FAU - Cuzzocrea, Salvatore
AU  - Cuzzocrea S
AD  - Department of Chemical, Biological, Pharmaceutical and Environmental Science, 
      University of Messina, Messina, Italy.
AD  - Department of Pharmacological and Physiological Science, Saint Louis University 
      School of Medicine, Saint Louis, United Stated.
LA  - eng
PT  - Journal Article
PL  - United Arab Emirates
TA  - CNS Neurol Disord Drug Targets
JT  - CNS & neurological disorders drug targets
JID - 101269155
RN  - 0 (Annexin A1)
RN  - 0 (Brain-Derived Neurotrophic Factor)
RN  - 0 (Glucocorticoids)
RN  - 0 (Receptors, Formyl Peptide)
RN  - 7171WSG8A2 (BDNF protein, human)
RN  - W980KJ009P (Corticosterone)
SB  - IM
MH  - Animals
MH  - Annexin A1/*metabolism
MH  - Brain-Derived Neurotrophic Factor
MH  - Corticosterone/*metabolism
MH  - Depression/*metabolism
MH  - Glucocorticoids/metabolism
MH  - Hippocampus/*metabolism
MH  - Hypothalamo-Hypophyseal System/metabolism
MH  - Memory
MH  - Mice
MH  - Mice, Knockout
MH  - Pituitary-Adrenal System/metabolism
MH  - Receptors, Formyl Peptide/metabolism
MH  - Signal Transduction
OTO - NOTNLM
OT  - Depression
OT  - annexin A1
OT  - corticosterone
OT  - formyl peptide receptor 2/3
OT  - glucorticoid
OT  - hippocampus.
EDAT- 2020/01/10 06:00
MHDA- 2021/07/07 06:00
CRDT- 2020/01/10 06:00
PHST- 2019/09/06 00:00 [received]
PHST- 2019/12/09 00:00 [revised]
PHST- 2019/12/24 00:00 [accepted]
PHST- 2020/01/10 06:00 [pubmed]
PHST- 2021/07/07 06:00 [medline]
PHST- 2020/01/10 06:00 [entrez]
AID - CNSNDDT-EPUB-103517 [pii]
AID - 10.2174/1871527319666200107094732 [doi]
PST - ppublish
SO  - CNS Neurol Disord Drug Targets. 2020;19(1):27-43. doi: 
      10.2174/1871527319666200107094732.