ArticleAmerican journal of physiology. Lung cellular and molecular physiology2009
TNF-induced activation of pulmonary microvessel endothelial cells: a role for GSK3beta.
Article in American journal of physiology. Lung cellular and molecular physiology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 13 citations in OpenAlex.
- Activation of GSK3 Prevents Termination of TNF-Induced Signaling.Journal of inflammation research · 2021Article
- Review
- Wnt/β-catenin signaling plays a key role in the development of spondyloarthritis.Annals of the New York Academy of Sciences · 2016Review
- miR-429 inhibits glioma invasion through BMK1 suppression.Journal of neuro-oncology · 2015Article
- Activation of β-catenin signalling leads to temporomandibular joint defects.European cells & materials · 2014Article
- Conditional activation of β-catenin signaling in mice leads to severe defects in intervertebral disc tissue.Arthritis and rheumatism · 2012Article
- Tumor necrosis factor-α induces increased lung vascular permeability: a role for GSK3α/β.European journal of pharmacology · 2011Article
- Overexpression of alpha-synuclein down-regulates BDNF expression.Cellular and molecular neurobiology · 2010Article
Corrections and comments
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Authors and funding
1 author at 1 institution in 1 country.
Funding
Abstract
The hypothesis tested was PKCalpha mediates the phosphorylation of glycogen synthetase kinase 3beta (GSK3beta) and that the GSK3beta inhibition modulates the response to tumor necrosis factor-alpha (TNF) in rat pulmonary microvessel endothelial cells (PMEC). PMEC were treated with TNF for 4.0 h (100 ng/ml) or vehicle. First, to assess the role of PKCalpha in the phosphorylation of GSK3beta (i.e., an indicator of GSK3beta inhibition), PMEC were pretreated with 1) nonsense-RNA-PKCalpha, 2) siRNA-PKCalpha, and 3) the PKC inhibitor Gö6983. In the nonsense RNA-PKCalpha+TNF and TNF groups, there was increased phosphorylated GSK3beta-Ser9 that did not occur in the Gö6983+TNF group. In the TNF groups, there was a significant correlation between PKCalpha protein and phosphorylated GSK3beta-Ser9 that did not occur in the groups without TNF. Second, to assess the role of GSK3beta in beta-catenin activity, PMEC were pretreated with 1) wild-type (w) GSK3beta plasmid to enhance GSK3beta activity, 2) kinase dead (kd)-GSK3beta plasmid, and 3) the GSK3beta inhibitor SB-216763. In the TNF group, there was increased unphosphorylated beta-catenin-Ser37/33 compared with the control group. In the GSK3beta-inhibited groups (i.e., SB-216763 and kdGSK3beta) +/- TNF, the unphosphorylated beta-catenin-Ser37/33 was similar to the TNF group. In the GSK3beta-enhanced group +/- TNF, the unphosphorylated beta-catenin-Ser37/33 was similar to the control. Finally, PMEC were also treated with TOPflash, a beta-catenin-dependent promoter luciferase reporter, or the mutant construct FOPflash, 2 days before treatment with TNF. In the TNF group, there was an increased TOPflash/FOPflash activity ratio compared with the control group. In the GSK3beta-inhibited groups (i.e., SB-216763 and kdGSK3beta) +/- TNF, the TOPflash/FOPflash activity ratio was similar to the TNF group. In the GSK3beta-enhanced group +/- TNF, the TOPflash/FOPflash activity ratio was similar to the control. The data indicate that TNF induces endothelial activation that is modulated by a PKCalpha-dependent inhibition of GSK3beta.
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Registered trials
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