WISP1 (CCN4) Autoregulates its Expression and Nuclear Trafficking of β-Catenin during Oxidant Stress with Limited Effects upon Neuronal Autophagy

Wang, Shaohui; Zhong Chong, Zhao; Chen Shang, Yan; Maiese, Kenneth

doi:10.2174/156720212800410858

Cited by 63Connective Tissue Growth Factor ResearchWnt/β-catenin signaling in development and cancerAutophagy in Disease and Therapy

WISP1 (CCN4) Autoregulates its Expression and Nuclear Trafficking of β-Catenin during Oxidant Stress with Limited Effects upon Neuronal Autophagy

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Wang, Shaohui, Zhong Chong, Zhao, Chen Shang, Yan, Maiese, Kenneth·2012·Current Neurovascular Research

DOI 10.2174/156720212800410858PMC PMC3354035

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Abstract

Wnt1 inducible signaling pathway protein 1 (WISP1/CCN4) is a CCN family member more broadly identified with development and tumorigenesis. However, recent studies have shed new light and enthusiasm on WISP1 as a novel target directed against toxic cell degeneration. Here we show WISP1 prevents apoptotic degeneration in primary neurons during oxidant stress through the activation of protein kinase B (Akt1), the post-translational maintenance of β-catenin integrity that is consistent with inhibition of glycogen synthase kinase-3β (GSK-3β), and the subcellular trafficking of β- catenin to foster its translocation to the nucleus. Interestingly, WISP1 autoregulates its expression through the promotion of β-catenin activity and may employ β-catenin to have a limited control over autophagy, but neuronal injury during oxidant stress as a result of autophagy appears portioned to a small population of neurons without significant impact upon overall cell survival. New strategies that target WISP1, its autoregulation, and the pathways responsible for neuronal cell injury may bring forth new insight for the treatment of neurodegenerative disorders. Keywords: Akt1, apoptosis, autophagy, β-catenin, Beclin 1, CCN4, glycogen synthase kinase-3β, LC3, neurons, oxidative stress, p62, WISP, Wnt1, CCN family, apoptotic degeneration, neurodegenerative, thrombospondin, fracture repair, inhibitory phosphorylation, B-catenin, Calbiochem, Hyperfilm, Cell Signaling Technology

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WISP1 has been shown to be protective against oxidative stress in neurons and to block amyloid toxicity in inflammatory microglia of the brain.
“WISP1 has been shown to be protective against oxidative stress in neurons [10–12] and to block amyloid toxicity in inflammatory microglia of the brain [13].”
From Tuberous Sclerosis Protein 2 (TSC2) Modulates CCN4 Cytoprotection During Apoptotic Amyloid Toxicity in Microglia (2013) · cites this paper as [11]
WISP1 promotes cytoprotection in multiple cell types through pathways that require PI 3-K and Akt and, in microglia, involve mTOR and PRAS40.
“WISP1 promotes cytoprotection in multiple cell types through pathways that not only require phosphatidylinositol-3-kinase (PI 3-K) and protein kinase B (Akt) [7, 8, 10, 11, 20, 21], but also utilize pathways in microglia that involve the mammalian target of rapamycin (mTOR) and the proline rich Akt substrate 40 kDa (PRAS40) [13].”
From Tuberous Sclerosis Protein 2 (TSC2) Modulates CCN4 Cytoprotection During Apoptotic Amyloid Toxicity in Microglia (2013) · cites this paper as [11]

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[15]Nagai Y Watanabe M Ishikawa S Karashima R Kurashige J Iwagami S Clinical significance of Wnt-induced secreted protein-1 [WISP-1/CCN4] in esophageal squamous cell carcinoma Anticancer Res 2011 3 31 3 991 997 21498727

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WISP1
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WISP1
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Authors: Wang, S., Zhong Chong, Z., Chen Shang, Y., & Maiese, K.
Affiliations: Rutgers Cancer Institute (US)
Corresponding author: Maiese, Kenneth
ORCID: Wang, Shaohui
Maiese, Kenneth
Venue: Current Neurovascular Research
Publisher: Bentham Science Publishers Ltd.
Published: 2012-04-01
Volume: 9
Issue: 2
Pages: 91-101
ISSN: 1567-2026 (ISSN-L)
DOI: 10.2174/156720212800410858
PMC: PMC3354035
OpenAlex: W2072343891
Cited by: 63
References: 89
Citations by year: 2026: 3 · 2025: 1 · 2024: 3 · 2023: 4 · 2022: 3 · 2021: 4 · 2020: 3 · 2019: 5 · 2018: 1 · 2017: 5 · 2016: 5 · 2015: 10 · 2014: 6 · 2013: 3 · 2012: 7
FWCI: 3.35
Type: journal article
Language: en
Open access: green
www.ncbi.nlm.nih.gov
Locations: Current Neurovascular Research (publishedVersion)
PubMed (publishedVersion)
Europe PMC (PubMed Central) (acceptedVersion)
PubMed Central (acceptedVersion)
Funders: National Institute of Neurological Disorders and Stroke (R01NS053946)
Topics: Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Connective Tissue Growth Factor Research
Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Wnt/β-catenin signaling in development and cancer
Health Sciences › Medicine › Epidemiology › Autophagy in Disease and Therapy
Keywords: β-catenin, nuclear trafficking, oxidative stress, neuronal apoptosis, neuronal autophagy, AKT1, glycogen synthase kinase-3β, Beclin-1, neurodegeneration, CCN family, neuroprotection
MeSH terms: Animals, Autophagy, Cell Nucleus, Cells, Cultured, Homeostasis, Neurons, Proto-Oncogene Proteins, Subcellular Fractions, Oxidants, Rats, Sprague-Dawley, Oxidative Stress, Protein Transport, Active Transport, Cell Nucleus, beta Catenin, Rats, CCN Intercellular Signaling Proteins

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WISP1 (CCN4) Autoregulates its Expression and Nuclear Trafficking of β-Catenin during Oxidant Stress with Limited Effects upon Neuronal Autophagy

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