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The Involvement of the Decrease of Astrocytic Wnt5a in the Cognitive Decline in Minimal Hepatic Encephalopathy.
Saidan Ding1, Zhu Xu2, Jianjing Yang2
1Zhejiang Provincial Key Laboratory of Aging and Neurological Disease Research, Department of Surgery Laboratory, The First Affiliated Hospital of Wenzhou Medical University, Wenzhou, Zhejiang, 325000, People's Republic of China.
Molecular Neurobiology
|November 24, 2016
Summary
Wnt5a signaling in astrocytes boosts neurotrophin production via the CaMK II-CREB pathway. This pathway is impaired in minimal hepatic encephalopathy (MHE), suggesting a novel mechanism for MHE pathogenesis.
Area of Science:
- Neuroscience
- Molecular Biology
- Pathology
Background:
- Wnt signaling is crucial for neuroprotection and synaptic plasticity.
- Impaired Wnt signaling may affect astrocytic neurotrophin (NTs) production, contributing to minimal hepatic encephalopathy (MHE).
Purpose of the Study:
- To investigate the role of Wnt5a in astrocytic NTs production.
- To explore the underlying molecular mechanisms involving the CaMK II-CREB pathway.
- To elucidate the contribution of impaired Wnt signaling to MHE pathogenesis.
Main Methods:
- Utilized a rat model of MHE.
- Investigated Wnt5a-mediated induction of NTs synthesis in astrocytes.
- Analyzed the CaMK II-CREB pathway activation.
- Assessed spatial learning and memory deficits.
Main Results:
- Wnt5a induces astrocytic NTs synthesis via the CaMK II-CREB pathway.
- Wnt5a administration reversed spatial learning deficits and normalized BDNF/NT-3 levels in MHE rats.
- Wnt5a-induced CaMK II-CREB interaction and CREB phosphorylation were suppressed in MHE.
Conclusions:
- Downregulation of NTs due to impaired Wnt5a-Frizzled-2 interaction in astrocytes contributes to MHE.
- This study reveals a novel pathogenic mechanism in MHE involving Wnt signaling and astrocytic neurotrophins.
