PMID- 30477246
OWN - NLM
STAT- MEDLINE
DCOM- 20190308
LR  - 20200225
IS  - 1422-0067 (Electronic)
IS  - 1422-0067 (Linking)
VI  - 19
IP  - 12
DP  - 2018 Nov 24
TI  - Wnt/beta-Catenin Signaling Pathway Governs a Full Program for Dopaminergic Neuron 
      Survival, Neurorescue and Regeneration in the MPTP Mouse Model of Parkinson's 
      Disease.
LID - 10.3390/ijms19123743 [doi]
LID - 3743
AB  - Wingless-type mouse mammary tumor virus (MMTV) integration site (Wnt) signaling 
      is one of the most critical pathways in developing and adult tissues. In the 
      brain, Wnt signaling contributes to different neurodevelopmental aspects ranging 
      from differentiation to axonal extension, synapse formation, neurogenesis, and 
      neuroprotection. Canonical Wnt signaling is mediated mainly by the 
      multifunctional beta-catenin protein which is a potent co-activator of transcription 
      factors such as lymphoid enhancer factor (LEF) and T-cell factor (TCF). 
      Accumulating evidence points to dysregulation of Wnt/beta-catenin signaling in major 
      neurodegenerative disorders. This review highlights a Wnt/beta-catenin/glial 
      connection in Parkinson's disease (PD), the most common movement disorder 
      characterized by the selective death of midbrain dopaminergic (mDAergic) neuronal 
      cell bodies in the subtantia nigra pars compacta (SNpc) and gliosis. Major 
      findings of the last decade document that Wnt/beta-catenin signaling in partnership 
      with glial cells is critically involved in each step and at every level in the 
      regulation of nigrostriatal DAergic neuronal health, protection, and regeneration 
      in the 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) mouse model of PD, 
      focusing on Wnt/beta-catenin signaling to boost a full neurorestorative program in 
      PD.
FAU - Marchetti, Bianca
AU  - Marchetti B
AUID- ORCID: 0000-0002-9287-8448
AD  - Department of Biomedical and Biotechnological Sciences (BIOMETEC), Pharmacology 
      Section, Medical School, University of Catania, Via Santa Sofia 97, 95123 
      Catania, Italy. biancamarchetti@libero.it.
AD  - OASI Research Institute-IRCCS, Section of Neuropharmacology, Via Conte Ruggero 
      73, 94018 Troina (EN), Italy. biancamarchetti@libero.it.
LA  - eng
PT  - Journal Article
PT  - Review
DEP - 20181124
PL  - Switzerland
TA  - Int J Mol Sci
JT  - International journal of molecular sciences
JID - 101092791
RN  - 0 (CTNNB1 protein, mouse)
RN  - 0 (Hepatocyte Nuclear Factor 1-alpha)
RN  - 0 (Hnf1a protein, mouse)
RN  - 0 (Lef1 protein, mouse)
RN  - 0 (Lymphoid Enhancer-Binding Factor 1)
RN  - 0 (Wnt Proteins)
RN  - 0 (beta Catenin)
SB  - IM
MH  - Animals
MH  - Cell Survival
MH  - Cell- and Tissue-Based Therapy/methods
MH  - Disease Models, Animal
MH  - Dopaminergic Neurons/*metabolism/pathology
MH  - Gene Expression Regulation
MH  - Hepatocyte Nuclear Factor 1-alpha/genetics/metabolism
MH  - Humans
MH  - Lymphoid Enhancer-Binding Factor 1/genetics/metabolism
MH  - Mice
MH  - Neural Stem Cells/metabolism/pathology
MH  - Neurogenesis/*genetics
MH  - Neuroglia/metabolism/pathology
MH  - Parkinsonian Disorders/*genetics/metabolism/pathology/therapy
MH  - Pars Compacta/metabolism/pathology
MH  - Regeneration/*genetics
MH  - Signal Transduction/*genetics
MH  - Wnt Proteins/*genetics/metabolism
MH  - beta Catenin/*genetics/metabolism
PMC - PMC6321180
OTO - NOTNLM
OT  - Parkinson's disease
OT  - Wnt/beta-catenin signaling
OT  - cell death
OT  - dopaminergic neurons
OT  - glia-neuron cross-talk
OT  - neurodegeneration
OT  - neuroprotection
OT  - neurorepair
COIS- The author declares no conflicts of interest.
EDAT- 2018/11/28 06:00
MHDA- 2019/03/09 06:00
PMCR- 2018/12/01
CRDT- 2018/11/28 06:00
PHST- 2018/10/17 00:00 [received]
PHST- 2018/11/12 00:00 [revised]
PHST- 2018/11/17 00:00 [accepted]
PHST- 2018/11/28 06:00 [entrez]
PHST- 2018/11/28 06:00 [pubmed]
PHST- 2019/03/09 06:00 [medline]
PHST- 2018/12/01 00:00 [pmc-release]
AID - ijms19123743 [pii]
AID - ijms-19-03743 [pii]
AID - 10.3390/ijms19123743 [doi]
PST - epublish
SO  - Int J Mol Sci. 2018 Nov 24;19(12):3743. doi: 10.3390/ijms19123743.