A Major Human Oral Lysophosphatidic Acid Species, LPA 18:1, Regulates Novel Genes in Human Gingival Fibroblasts

Cerutis, D. Roselyn; Weston, Michael D.; Alnouti, Yazen; Bathena, Sai Praneeth Reddy; Nunn, Martha E.; Ogunleye, Afolabi O.; McVaney, Timothy P.; Headen, Karmel V.; Miyamoto, Takanari

doi:10.1902/jop.2015.140592

Cited by 9 publications

(16 citation statements)

References 58 publications

(100 reference statements)

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“…Therefore, smoother surfaces may promote faster proliferation to the topographical “limit” of the surface. Another factor may be the inflammatory immune response, which is known to be modulated by dental material nanotopography [ 55 ]; indeed, we have shown that healthy HGF can make a large number of inflammation-related gene transcripts [ 56 ]. As HGF are exposed to oral bacterial products in the mouth they elaborate inflammatory cytokines both in health and in periodontal disease [ 57 ].…”

Section: Discussionmentioning

confidence: 99%

Effect of Clinically Relevant CAD/CAM Zirconia Polishing on Gingival Fibroblast Proliferation and Focal Adhesions

et al. 2017

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Mucosal seal formation around dental abutments is critical to the successful integration of dental implants into the human oral cavity. No information exists for how clinically relevant polishing procedures for computer-aided design and computer-aided manufactured (CAD/CAM) zirconia abutments affects cellular responses important to mucosal seal formation. CAD/CAM zirconia was divided into four groups for clinically relevant polishing utilizing commercial polishing heads: control, coarse, coarse plus medium, and coarse plus medium plus fine. Surfaces were analyzed with scanning electron microscopy (SEM), atomic force microscopy (AFM), and optical profilometry (OP). Subsequently, human gingival fibroblasts (HGFs) were seeded onto the zirconia surfaces. Proliferation was measured via a quantitative SEM technique and focal adhesion kinase (FAK) phosphorylation status was measured by an enzyme-linked immunosorbent assay (ELISA). Results showed an increase in proliferation on all polished surfaces as compared to the control. Phosphorylation of FAK at tyrosine 397 (Y397) was up-modulated on the control surfaces. The associated cell adaptation is discussed. In all cases, FAK phosphorylation was greater at 24 h than 48 h. These results suggest that clinicians should be mindful of the effects of abutment polishing methodology, as this may have an impact on early mucosal seal formation.

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Section: Discussionmentioning

confidence: 99%

Effect of Clinically Relevant CAD/CAM Zirconia Polishing on Gingival Fibroblast Proliferation and Focal Adhesions

et al. 2017

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“…Moreover, LPA enhances the survival of human hematopoietic stem/progenitor cells under ischemic conditions[ 17 ]. It is also crucial for periodontal wound healing and gingival inflammation[ 38 ]. LPA enhances the proliferation of human corneal endothelial cells induced by LPA through phosphatidylinositol 3-kinase and Rho-associated protein kinase pathways[ 39 ].…”

Section: Discussionmentioning

confidence: 99%

Effects of lysophosphatidic acid on human periodontal ligament stem cells from teeth extracted from dental patients

Kim

Jun-mei

et al. 2019

J Biomed Res

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Despite their potential applications in future regenerative medicine, periodontal ligament stem cells (PDLSCs) are difficult to obtain in large amounts from patients. Therefore, maintaining stemness while expanding the cell numbers for medical use is the key to transitioning PDLSCs from the bench to the clinic. Lysophosphatidic acid (LPA), which is present in the human body and saliva, is a signaling molecule derived from phospholipids. In this study, we examined the effects of LPA on stemness maintenance in human PDLSCs. Several spindle-shaped and fibroblast-like periodontal ligament stem-like cell lines were established from PDLSC isolation. Among these cell lines, the most morphologically appropriate cell line was characterized. The expression levels of OCT4 , NANOG (a stem cell marker), and CD90 (a mesenchymal stem cell marker) were high. However, CD73 (a negative marker of mesenchymal stem cells) expression was not observed. Notably, immunofluorescence analysis identified the expression of STRO-1 , CD14 6 (a mesenchymal stem cell marker), and sex determining region Y-box 2 at the protein level. In addition, lipid droplets were stained by Oil red O after the induction of adipogenesis for 21 days, and mineralized nodules were stained by Alizarin Red S after the induction of osteogenesis for 14 days. Alkaline phosphate staining also demonstrated the occurrence of osteogenesis. In summary, we established a human PDLSC line, which could be applied as a cell source for tissue regeneration in dental patients. However, further studies are needed to determine the detailed effects of LPA on PDLSCs.

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“…Lysophosphatidic acid is a bioactive phospholipid that can mediate several biological processes that are related to epithelial repair and epithelial barrier function, such as cell proliferation and migration, platelet aggregation, prevention of apoptosis, and cytokine and chemokine secretion . Lysophosphatidic acid is found in human saliva , and is released by fibroblasts and activated platelets present in wound areas. The effects of LPA on HOK are unknown.…”

Section: Discussionmentioning

confidence: 99%

“…Lysophosphatidic acid is produced by a range of cells, including adipocytes, erythrocytes, activated platelets, neural cells, neutrophils, mast cells, mononuclear cells, testis, ovaries, kidneys and intestine, and lung and uterine epithelium . Lysophosphatidic acid is also found in gingival fibroblasts and in human saliva . The levels of LPA in saliva and gingival crevicular fluid (GCF) from patients with periodontitis have been found to be increased by up to 10‐fold .…”

mentioning

confidence: 99%

Lysophosphatidic acid regulates adhesion molecules and enhances migration of human oral keratinocytes

Thorlakson

Schreurs

Schenck

et al. 2016

European J Oral Sciences

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Oral keratinocytes are connected via cell-to-cell adhesions to protect underlying tissues from physical and bacterial damage. Lysophosphatidic acids (LPAs) are a family of phospholipid mediators that have the ability to regulate gene expression, cytoskeletal rearrangement, and cytokine/chemokine secretion, which mediate proliferation, migration, and differentiation. Several forms of LPA are found in saliva and gingival crevicular fluid, but it is unknown how they affect human oral keratinocytes (HOK). The aim of the present study was therefore to examine how different LPA forms affect the expression of adhesion molecules and the migration and proliferation of HOK. Keratinocytes were isolated from gingival biopsies obtained from healthy donors and challenged with different forms of LPA. Quantitative real-time RT-PCR, immunocytochemistry, and flow cytometry were used to analyze the expression of adhesion molecules. Migration and proliferation assays were performed. Lysophosphatidic acids strongly promoted expression of E-cadherin and occludin mRNAs and translocation of E-cadherin protein from the cytoplasm to the membrane. Occludin and claudin-1 proteins were up-regulated by LPA. Migration of HOK in culture was increased, but proliferation was reduced, by the addition of LPA. This indicates that LPA can have a role in the regulation of the oral epithelial barrier by increasing the expression of adhesion molecules of HOK, by promotion of migration and by inhibition of proliferation.

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A Major Human Oral Lysophosphatidic Acid Species, LPA 18:1, Regulates Novel Genes in Human Gingival Fibroblasts

Cited by 9 publications

References 58 publications

Effect of Clinically Relevant CAD/CAM Zirconia Polishing on Gingival Fibroblast Proliferation and Focal Adhesions

Effect of Clinically Relevant CAD/CAM Zirconia Polishing on Gingival Fibroblast Proliferation and Focal Adhesions

Effects of lysophosphatidic acid on human periodontal ligament stem cells from teeth extracted from dental patients

Lysophosphatidic acid regulates adhesion molecules and enhances migration of human oral keratinocytes

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