PDGF-α Receptor Subunit Expression Down-regulated by IL-1β in Human Periodontal Ligament Cells

Oates, Thomas W.; Xie, Jianping; Clinton, S.; Hoang, A. M.; Graves, Dana T.; Cochran, David L.

doi:10.1177/00220345980770100601

Cited by 9 publications

(3 citation statements)

References 34 publications

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“…Volume 76 • Number 10 a v, and b 1 integrin subunits. [21][22][23] DNA sequencing of amplicons performed at the University of Texas Health Science Center at San Antonio (UTHSCSA) DNA Core Facility confirmed that the integrin subunits and aldolase corresponded with published gene sequences in GenBank. Following amplification, PCR products were separated on 2% agarose gels, which were stained with ethidium bromide and visualized using ultraviolet illumination.…”

Section: Fibroblast Integrin Expression On Implant Surfacesmentioning

confidence: 79%

Human Gingival Fibroblast Integrin Subunit Expression on Titanium Implant Surfaces

Oates

Maller

West

et al. 2005

Journal of Periodontology

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These results demonstrate the presence of multiple integrin subunits in human gingival fibroblasts grown in contact with titanium implant surfaces and that titanium surface roughness alters cellular morphology but appears to have limited effects on integrin expression. This study provides insight into the complicated cellular and molecular events occurring at the implant surface that may be critical to optimizing the soft tissue interactions with the soft tissue-implant interface.

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Section: Fibroblast Integrin Expression On Implant Surfacesmentioning

confidence: 79%

Human Gingival Fibroblast Integrin Subunit Expression on Titanium Implant Surfaces

Oates

Maller

West

et al. 2005

Journal of Periodontology

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“…In the present only the ligand BMP‐2 was found to induce both Smurf1 and Smad6 mRNA expression in the bone cells, suggesting that surface BMPR‐IB degradation mediated by BMP‐2 up‐regulation of the Smurf1/Smad6 pathway may at least partly explain the apparent anomaly between BMPR‐IB mRNA and surface antigen expression in BMP‐2‐treated bone cells. However, it is also possible that other post‐transcriptional processes could play a part in the regulation of the BMPR‐IB surface antigen, such as rapid breakdown of mRNA transcripts and also shedding of a soluble form of the cell surface antigen, as has previously been reported for a number of other growth factor receptors (Oates et al, 1998; Philip et al, 1999; Yabkowitz et al, 1999; Hanneken, 2001; Hu et al, 2004; Sahin et al, 2004). …”

Section: Discussionmentioning

confidence: 90%

Up‐regulation of bone morphogenetic protein receptor IB by growth factors enhances BMP‐2‐induced human bone cell functions

Singhatanadgit

Salih

Olsen

2006

Journal Cellular Physiology

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Bone morphogenetic proteins (BMP) stimulate osteoblast differentiation by signal transduction via three BMP receptors (BMPR-IA, -IB, and -II). Several growth factors, including transforming growth factor-beta1 (TGF-beta1), fibroblast growth factor-2 (FGF-2) and platelet-derived growth factor-AB (PDGF-AB), have also been shown to play an important part in osteogenesis. The mechanism underlying these activities is unclear, but these growth factors could modulate the BMP/BMPR pathway by up-regulating BMPR expression, thereby enhancing the osteogenic responses of bone cells to the BMP. In this study we have therefore examined the effects of TGF-beta1, FGF-2, and PDGF-AB on BMPR expression and BMP-2-mediated osteoblast functions in primary human bone cells. The results showed that although the ligand BMP-2 and growth factors had little effect on BMPR-IA and -II transcript expression, they significantly up-regulated BMPR-IB mRNA specifically. However, only the growth factors, but not the ligand BMP-2, increased the surface expression of the BMPR-IB antigen, which was found to be due to a differential effect of BMP-2 and the growth factors on the Smurf1/Smad6-induced breakdown process. Pre-incubation of the cells with the growth factors significantly augmented BMP-2-induced Smad1/5/8 phosphorylation, and Dlx5 expression ALP activity, compared with that of cells treated with BMP-2 alone. When cells were transfected with siRNA targeting BMPR-IB, the growth factors neither up-regulated BMPR-IB transcript expression nor enhanced BMP-2-induced Smad1/5/8 phosphorylation, Dlx5 expression and ALP activity. The results indicate that increased BMPR-IB by TGF-beta1, FGF-2, and PDGF-AB significantly enhances BMP-2-induced osteogenic functions in vitro, suggesting that they might positively modulate bone formation by up-regulating BMPR-IB in vivo.

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“…MiR-433 expression was found highly stimulated by IL-1β compared with PBS control-treated hL-MSC (up to 4 fold compared to PBS control, Figure 2A ), suggesting a potential function of miR-433 in response to IL-1β in hL-MSC. To assess the possible target genes that could be suppressed by miR-433 in hL-MSC, we investigated the expression of genes that are known to be inhibited by IL-1β, such as collagen type 2 (COL2A1), endothelial nitric oxide synthase (eNOS), PDGF-alpha receptor subunit (PDGF-αR), glutathione S-transferase GSTA2 and GSTM1, and sodium-taurocholate cotransporting polypeptide (NTCP) [ 28 – 32 ]. Consistent with prior data, these genes were all down-regulated by IL-1β (Figure 2B ).…”

Section: Resultsmentioning

confidence: 99%

IL-1β-stimulated β-catenin up-regulation promotes angiogenesis in human lung-derived mesenchymal stromal cells through a NF-κB-dependent microRNA-433 induction

et al. 2016

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Considerable attentions have been focused on the treatment of lung injury using mesenchymal stem cells that can replenish damaged tissues including the blood vessels. In human lung-derived mesenchymal stem cells (hL-MSC), we investigated the potential role of an IL-1β-stimulated miR-433 pathway in angiogenesis in vitro. The expressions of miR-433 and its target genes were examined in cells treated with IL-1β. The angiogenic activity of hL-MSC was studied by cell migration and tube formation assays in which miR-433 levels were manipulated. The reporter assay and chromatin immunoprecipitation (ChIP) were also performed to analyze the underlying regulations. We found that the expression of miR-433 was enhanced in hL-MSC by IL-1β in a NF-κB dependent manner via a NF-κB binding site at its promoter region. The effects of IL-1β on promoting angiogenic activities in hL-MSC can be mimicked by the overexpression of miR-433 and were blocked by anti-miR-433. Mechanistically, our data suggested that miR-433 directly targets the 3′-UTR of Dickkopf Wnt signaling pathway inhibitor 1 (DKK1) mRNA and decreases its expression. Consistently, the expression of β-catenin, the major mediator of canonical Wnt pathway that is capable of inducing endothelial differentiation and angiogenesis, was upregulated by IL-1β through miR-433. Thus, increasing miR-433 expression by IL-1β in mesenchymal stem cells could stimulate their capacity of vascular remodeling for efficient repair processes, which may be utilized as a therapeutic target in patients suffering from severe lung injury.

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PDGF-α Receptor Subunit Expression Down-regulated by IL-1β in Human Periodontal Ligament Cells

Cited by 9 publications

References 34 publications

Human Gingival Fibroblast Integrin Subunit Expression on Titanium Implant Surfaces

Human Gingival Fibroblast Integrin Subunit Expression on Titanium Implant Surfaces

Up‐regulation of bone morphogenetic protein receptor IB by growth factors enhances BMP‐2‐induced human bone cell functions

IL-1β-stimulated β-catenin up-regulation promotes angiogenesis in human lung-derived mesenchymal stromal cells through a NF-κB-dependent microRNA-433 induction

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