Effect of nifedipine on the expression of keratinocyte growth factor and its receptor in cocultured/monocultured fibroblasts and keratinocytes

Cp, Di; Sun, Yingxun; Zhao, Liang; L, Li; Ding, Chenyue; Xu, Yan; Fan, Yi

doi:10.1111/jre.12064

Cited by 5 publications

(3 citation statements)

References 28 publications

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“…The hematopoietic growth factor GM‐CSF is another growth factor that was found to regulate dermal keratinocyte growth and differentiation [8], playing an important role during the process of wound healing [20]. Fibroblast‐keratinocyte interactions in skin models strongly enhanced the expression of GM‐CSF [9], KGF and its receptor [21], while dermal keratinocyte‐released IL‐1 induced the expression of both KGF and GM‐CSF [10]. The regulatory mechanism of these two factors in skin homeostasis is a feedback loop within the multiple other epithelial‐mesenchymal interactions: skin keratinocytes release IL‐1α and IL‐1β, which stimulate the release of KGF and GM‐CSF by dermal fibroblasts.…”

Section: Discussionmentioning

confidence: 99%

Granulocyte macrophage‐colony stimulating factor and keratinocyte growth factor control of early stages of differentiation of oral epithelium

Das

Vîrlan

Xenaki

et al. 2022

European J Oral Sciences

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Oral epithelial differentiation is known to be directed by underlying fibroblasts, but the responsible factor(s) have not been identified. We aimed here to identify fibroblast‐derived factors responsible for oral epithelial differentiation. Primary normal human oral keratinocytes and fibroblasts were isolated from healthy volunteers after informed consent (n = 5) and 3D‐organotypic (3D‐OT) cultures were constructed. Various growth factors were added at a range of 0.1‐100 ng/ml. 3D‐OTs were harvested after ten days and assessed histologically, by immunohistochemistry and the TUNEL method. Epithelium developed in 3D‐OT without fibroblasts showed an undifferentiated phenotype. Addition of granulocyte macrophage‐colony stimulating factor (GM‐CSF) induced expression of cytokeratin 13 in suprabasal cell layers. Admixture of GM‐CSF and keratinocyte growth factor (KGF) induced, in addition, polarization of epidermal growth factor (EGF) receptor and β1‐integrin to basal cell layer and collagen IV deposition. Terminal differentiation with polarization of TUNEL‐positive cells to superficial layers occurred only in the presence of fibroblasts in collagen gels either in direct contact or at distance from normal oral keratinocytes. Taken together, these results show that major aspects of oral epithelial differentiation are regulated by the synergic combination of GM‐CSF and KGF. However, the terminal stage seems to be controlled by other yet unidentified fibroblast‐derived diffusible factor(s).

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Section: Discussionmentioning

confidence: 99%

Granulocyte macrophage‐colony stimulating factor and keratinocyte growth factor control of early stages of differentiation of oral epithelium

Das

Vîrlan

Xenaki

et al. 2022

European J Oral Sciences

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“…This response may be due to a compensatory interaction between these different cell types. According to Di et al [45], the expression of KGF (keratinocyte growth factor) and KGFR (keratinocyte growth factor receptor) observed in cocultures of keratinocytes and fibroblasts was influenced by the interaction of these different gingival cells. According to these authors, keratinocytes and fibroblasts can interact to dynamically regulate gene expression, what could have had such an effect on gingival cells conditions after treatment.…”

Section: Discussionmentioning

confidence: 99%

Oral microbe-host interactions: influence of β-glucans on gene expression of inflammatory cytokines and metabolome profile

2017

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BackgroundThe aim of this study was to evaluate the effects of β-glucan on the expression of inflammatory mediators and metabolomic profile of oral cells [keratinocytes (OBA-9) and fibroblasts (HGF-1) in a dual-chamber model] infected by Aggregatibacter actinomycetemcomitans. The periodontopathogen was applied and allowed to cross the top layer of cells (OBA-9) to reach the bottom layer of cells (HGF-1) and induce the synthesis of immune factors and cytokines in the host cells. β-glucan (10 μg/mL or 20 μg/mL) were added, and the transcriptional factors and metabolites produced were quantified in the remaining cell layers and supernatant.ResultsThe relative expression of interleukin (IL)-1-α and IL-18 genes in HGF-1 decreased with 10 μg/mL or 20 μg/mL of β-glucan, where as the expression of PTGS-2 decreased only with 10 μg/mL. The expression of IL-1-α increased with 20 μg/mL and that of IL-18 increased with 10 μg/mL in OBA-9; the expression of BCL 2, EP 300, and PTGS-2 decreased with the higher dose of β-glucan. The production of the metabolite 4-aminobutyric acid presented lower concentrations under 20 μg/mL, whereas the concentrations of 2-deoxytetronic acid NIST and oxalic acid decreased at both concentrations used. Acetophenone, benzoic acid, and pinitol presented reduced concentrations only when treated with 10 μg/mL of β-glucan.ConclusionsTreatment with β-glucans positively modulated the immune response and production of metabolites.

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“…Nifedipine is widely used to treat hypertension and/or angina. Nifedipine-induced gingival overgrowth (NGO) is reported to be the most frequent form of DIGO, with an incidence ranging from 6.3% to 83% [4][5][6]. However, the molecular etiology of NGO is not well understood.…”

Section: Introductionmentioning

confidence: 99%

Transcriptional Analysis Reveals Key Genes in the Pathogenesis of Nifedipine-Induced Gingival Overgrowth

Huang

Wang

et al. 2020

Analytical Cellular Pathology

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Background. Nifedipine-induced gingival overgrowth (NGO) is a multifactorial pathogenesis with increased extracellular matrix including collagen and glycans, inflammatory cytokines, and phenotype changes of fibroblasts. However, the molecular etiology of NGO is not well understood. The objective of this study is to investigate the key genes in the pathogenesis of NGO. Methods. In this study, we examined the proliferation and migration abilities of fibroblasts derived from patients with chronic periodontitis, nifedipine nonresponder gingival overgrowth, gingival overgrowth caused by nifedipine, and healthy normal gingiva. We conducted RNA-Seq on these four groups of fibroblasts and analysed the differentially expressed genes (DEGs). Results. Fibroblasts derived from NGO patients had higher proliferation and migration abilities than those of the other groups. Protein-protein interaction network analysis indicated that TGFB2, ITGA8, ITGA11, FGF5, PLA2G4D, PLA2G2F, PTGS1, CSF1, LPAR1, CCL3, and NKX3-1 are involved in the development of NGO. These factors are related to the arachidonic acid metabolism and PI3K/AKT signaling pathways. Conclusion. Transcriptional gene expression analysis identified a number of DEGs that might be functionally related to gingival overgrowth induced by nifedipine. Our study provides important information on the molecular mechanism underlying nifedipine-induced gingival overgrowth.

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Effect of nifedipine on the expression of keratinocyte growth factor and its receptor in cocultured/monocultured fibroblasts and keratinocytes

Cited by 5 publications

References 28 publications

Granulocyte macrophage‐colony stimulating factor and keratinocyte growth factor control of early stages of differentiation of oral epithelium

Granulocyte macrophage‐colony stimulating factor and keratinocyte growth factor control of early stages of differentiation of oral epithelium

Oral microbe-host interactions: influence of β-glucans on gene expression of inflammatory cytokines and metabolome profile

Transcriptional Analysis Reveals Key Genes in the Pathogenesis of Nifedipine-Induced Gingival Overgrowth

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