TNF-induced activation of pulmonary microvessel endothelial cells: a role for GSK3β

Johnson, A.

doi:10.1152/ajplung.90566.2008

Cited by 13 publications

(11 citation statements)

References 31 publications

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“…A previous study proved that GSK3b influences mRNA expression levels of Slug [21]. Phosphorylation at Ser9 of GSK3b can inhibit its activity [22]. Figure 4c shows that Slug expression remarkably increased in the nuclear compartments of SCR/U87 cells with 10 ng/mL HGF stimulation for 1 d (Fig.…”

Section: Bmk1 Promoted Slug Expression Via the Phosphorylation Of Gsk3bmentioning

confidence: 71%

miR-429 inhibits glioma invasion through BMK1 suppression

et al. 2015

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The purpose of this research was to examine the relationship between big mitogen-activated protein kinase 1 (BMK1) and miRNA miR-429 and to determine the effect of miR-429 on glioma invasiveness. Immunohistochemistry was used to evaluate BMK1 expression in glioma tissues. Real-time PCR was used to measure the expression of miR-429 and other RNAs. Western blot was used to detect the expression of BMK1 and other related proteins. Wound healing, Matrigel invasion, and chemotaxis assays were performed to detect the invasion and migration of glioma cell lines. The actual binding site of miR-429 to the 3' untranslated region of BMK1 was confirmed by luciferase assay and RNA immunoprecipitation. BMK1 expression was associated with the World Health Organization grading of glioma and inversely correlated with patient survival. Suppression of BMK1 inhibited the migration and invasion of glioma cells by interfering with mesenchymal transition. Additionally, hepatocyte growth factor-induced GSK3β phosphorylation was suppressed through BMK1 knockdown. Interestingly, our findings validated a novel role for miR-429 in suppressing the migration and invasion of glioma by directly inhibiting BMK1 expression. We also found that miR-429 expression in glioma cells and tissues was lower than that in normal cells and adjacent non-neoplastic tissues, and miR-429 overexpression inhibited invasive activity of glioma cells both in vitro and in vivo. Furthermore, our data validated that miR-429 downregulation was due to the hypermethylation of its promoter region. Our results indicated that BMK1 modulation by miR-429 has an important function in glioma invasion both in vitro and in vivo.

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Section: Bmk1 Promoted Slug Expression Via the Phosphorylation Of Gsk3bmentioning

confidence: 71%

miR-429 inhibits glioma invasion through BMK1 suppression

et al. 2015

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“…The current study is the first to demonstrate that the same signalling mechanism can also induce TMJ cartilage degradation. The potential mechanisms for β-catemn activation in patients with TMJ OA may include activating mutations of the β-catenin gene (Morin et al ., 1997; Simon et al ., 2005; Jamieson et al ., 2004; Derksen et al ., 2004), mechanical loading (Hens et al ., 2005; Robinson et al ., 2006; Sen et al ., 2009) and inflammation (Johnson, 2009; Kaler et al ., 2009). In summary, our studies suggest that β-cateninmay play a role in TMJ cartilage function and may be a mediator in TMJ OA development.…”

Section: Discussionmentioning

confidence: 99%

Activation of β-catenin signalling leads to temporomandibular joint defects

Wang

Xie

et al. 2014

eCM

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Despite extensive research in knee and hip osteoarthritis (OA), the underlying mechanism of temporomandibular joint (TMJ) disorder remains largely unknown. The purpose of this study was to determine whether the constitutive activation of β-catenin in the middle and deep layers of the articular cartilage can compromise the homeostasis of this tissue in the TMJ. Co12CreER T2 transgenic mice were bred with Rosa mT/mG reporter mice to determine Cre recombination efficiency. Co12CreER T2 mice were then crossed with β-catenin flox (ex3)/+ mice to generate β-catenin conditional activation mice, β-catenin(ex3) Co12ER . TMJ samples were harvested when the mice were 1-, 3-or 6-month-old and evaluated using histology, histomorphometry and immunohistochemistry. β-catenin(ex3) Co12ER mice were further crossed with Mmp13 flox/flox and Adamts5 −/− mice to generate β-catenin(ex3)/Mmp13) Co12ER and β-catenin(ex3) Co12ER )/Adamts5 −/− double mutant mice to investigate the role of Mmp13 and Adamts5 in the development of TMJ disorder. High levels of Cre-recombination were seen in Co12CreER T2 ;Rosa mT/mG mice. Progressive TMJ defects developed in 1-, 3-and 6-month-old β-catenin(ex3) Co12ER mice, as revealed by histology and histomorphometry. Results further demonstrated that the defects observed in β-catenin(ex3) Co12ER mice were significantly decelerated after deletion of the Mmp13 or Adamts5 gene in (β-catenin(ex3)/Mmp13) co12ER or β-catenin(ex3) Co12ER / Adamts5 −/− double mutant mice. In summary, we found that β-catenin is a critical gene in the induction of TMJ cartilage degeneration, and over-expressing β-catenin in TMJ cartilage leads to defects assembling an OA-like phenotype. Deletion of Mmp13 and Adamts5 in β-catenin (ex3

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“…Protein identification using PAGE-Western Blot was done with adaptations of previously described techniques from this laboratory (Gertzberg et al, 2004; Johnson, 2009; Neumann et al, 2006). Lung homogenates, 20 μg/lane, were separated on 8% polyacrylamide mini-gels, transferred to PVDF membranes (Immobilon-P, Millipore, Bedford, MA), rinsed in TBS (Tris-HCl: 10 mM-pH 7.5; NaCl: 100 mM) and blocked in Blotto + Phosphatase Inhibitors (BPI) (TTBS: [TBS; Tween-20: 0.05%]; nonfat dry milk: 5.0% w/v; NaF: 50 mM; activated Na 3 VO 4 : 0.1 mM).…”

Section: Methodsmentioning

confidence: 99%

Tumor necrosis factor-α induces increased lung vascular permeability: A role for GSK3α/β

Barton-Pai

Feleder

Johnson

2011

European Journal of Pharmacology

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We tested the hypothesis that glycogen synthase kinase 3α/β (GSK3α/β) modulates tumor necrosis factor-a (TNF) induced increased lung vascular permeability. Rats were treated with TNF (i.v., ~100 ng/ml) or vehicle 0.5 h, 4.0 h and 24.0 h prior to lung isolation. Rats were co-treated with the GSK3α/β inhibitors SB216763 (0.6 mg/kg) or TDZD-8 (1.0 mg/kg). After TNF, the isolated lung was assessed for hemodynamics, wet-dry/dry weight (W-D/D) and extravascular albumin. Extravascular albumin significantly increased at TNF-24 h compared to Control. In the GSK3α/β-inhibited +TNF groups, extravascular albumin was similar to the Control and respective SB216763 and TDZD-8 groups. In separate studies, to assess GSK3α/β-activity, lung lysate was assessed for phospho-GSK3α/β-Ser21/9, total GSK3α/β, un-phospho-β-catenin-Ser33/37and total β-catenin. In the TNF-4.0 h group, there was no change in GSK3α/phospho-GSK3α-Ser21 but there was an increase in GSK3β/GSK3β-Ser9 compared to Control, indicating GSK3β activation at TNF-4.0 h. GSK3β activation was verified because there was a decrease in un-phospho-β-catenin-Ser33/37/β-catenin in the TNF- 4.0 group, a specific outcome for GSK3β activation. In the SB216763+TNF group, un-phospho-β-catenin-Ser33/37 was similar to Control, indicating prevention of TNF-induced GSK3β activation. In the TNF-24 h group, there were increases in the biomarkers of inflammation phospho-eNOS-Ser 1117 and oxidized protein, which did not occur in the SB216763+TNF-24 h and TDZD-8+TNF-24 h groups. In the SB216763+TNF-24 h and TDZD-8+TNF-24 h groups, un-phospho-β-catenin-Ser33/37 was greater than in the Control, indicating continued inhibition of GSK3β. The data indicates that pharmacologic inhibition of GSK3β inhibits TNF induced increased endothelial permeability associated with lung inflammation.

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TNF-induced activation of pulmonary microvessel endothelial cells: a role for GSK3β

Abstract: Johnson A. TNF-induced activation of pulmonary microvessel endothelial cells: a role for GSK3␤.

Cited by 13 publications

References 31 publications

miR-429 inhibits glioma invasion through BMK1 suppression

miR-429 inhibits glioma invasion through BMK1 suppression

Activation of β-catenin signalling leads to temporomandibular joint defects

Tumor necrosis factor-α induces increased lung vascular permeability: A role for GSK3α/β

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