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Cited by 64Cell death mechanisms and regulationConnective Tissue Growth Factor ResearchNeurological Disorders and Treatments

Wnt1 Inducible Signaling Pathway Protein 1 (WISP1) Blocks Neurodegeneration through Phosphoinositide 3 Kinase/Akt1 and Apoptotic Mitochondrial Signaling Involving Bad, Bax, Bim, and Bcl-xL

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Wang, Shaohui, Zhong Chong, Zhao, Chen Shang, Yan, Maiese, Kenneth·2012·Current Neurovascular Research
DOI 10.2174/156720212799297137PMC PMC3274638
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Abstract

Wnt1 inducible signaling pathway protein 1 (WISP1) is a member of the CCN family of proteins that determine cell growth, cell differentiation, immune system activation, and cell survival in tissues ranging from the cardiovascular-pulmonary system to the reproductive system. Yet, little is known of the role of WISP1 as a neuroprotective entity in the nervous system. Here we demonstrate that WISP1 is present in primary hippocampal neurons during oxidant stress with oxygen-glucose deprivation (OGD). WISP1 expression is significantly enhanced during OGD exposure by the cysteine-rich glycosylated protein Wnt1. Similar to the neuroprotective capabilities known for Wnt1 and its signaling pathways, WISP1 averts neuronal cell injury and apoptotic degeneration during oxidative stress exposure. WISP1 requires activation of phosphoinositide 3-kinase (PI 3-K) and Akt1 pathways to promote neuronal cell survival, since blockade of these pathways abrogates cellular protection. Furthermore, WISP1 through PI 3-K and Akt1 phosphorylates Bad and GSK-3β, minimizes expression of the Bim/Bax complex while increasing the expression of Bclx(L)/Bax complex, and prevents mitochondrial membrane permeability, cytochrome c release, and caspase 3 activation in the presence of oxidant stress. These studies provide novel considerations for the development of WISP1 as an effective and robust therapeutic target not only for neurodegenerative disorders, but also for disease entities throughout the body.

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Authors
Wang, S., Zhong Chong, Z., Chen Shang, Y., & Maiese, K.
Affiliations
Rutgers New Jersey Medical School (US)
ORCID
Venue
Current Neurovascular Research
Publisher
Bentham Science Publishers Ltd.
Published
2012-02-01
Volume
9
Issue
1
Pages
20-31
ISSN
1567-2026 (ISSN-L)
DOI
10.2174/156720212799297137
PMC
PMC3274638
OpenAlex
W2170396987
Cited by
64
References
2
Citations by year
2026: 3 · 2024: 4 · 2023: 2 · 2022: 4 · 2021: 3 · 2020: 2 · 2019: 6 · 2018: 5 · 2017: 6 · 2016: 4 · 2015: 7 · 2014: 3 · 2013: 4 · 2012: 11
FWCI
3.22
Type
journal article
Language
en
Open access
Licence
public-domain
Locations
  • Current Neurovascular Research (publishedVersion, public-domain)
  • PubMed (publishedVersion)
  • PubMed Central (acceptedVersion)
Funders
  • American Diabetes Association
  • American Heart Association
  • National Institutes of Health
  • National Institute on Aging
  • National Institute of Neurological Disorders and Stroke (R01NS053946)
  • National Institute of Environmental Health Sciences
Topics
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Cell death mechanisms and regulation
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Connective Tissue Growth Factor Research
  • Life Sciences › Neuroscience › Neurology › Neurological Disorders and Treatments
Keywords
WISP1, CCN family proteins, neuroprotection, neurodegeneration, oxidative stress, oxygen-glucose deprivation, hippocampal neurons, Bad phosphorylation, GSK3β, Bax, building information modeling, Bcl-xL, cytochrome c release, caspase-3, Wnt1
MeSH terms
Bcl-2-Like Protein 11, Animals, Cell Survival, Hippocampus, Membrane Proteins, Mitochondria, Nerve Degeneration, Neurons, Proto-Oncogene Proteins, Signal Transduction, Rats, Sprague-Dawley, Apoptosis, Oxidative Stress, Phosphatidylinositol 3-Kinases, In Situ Nick-End Labeling, Immunoprecipitation, Apoptosis Regulatory Proteins, bcl-X Protein, bcl-Associated Death Protein, bcl-2-Associated X Protein, Proto-Oncogene Proteins c-akt, Rats, DNA Fragmentation, CCN Intercellular Signaling Proteins

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