Browsing by Author "Smith, P. C."

Now showing 1 - 12 of 12
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    Chitosan-triclosan particles modulate inflammatory signaling in gingival fibroblasts
    (2018) Pavez, L.; Tobar, N.; Chacon, C.; Arancibia, R.; Martinez, C.; Tapia, C.; Pastor, A.; Gonzalez, M.; Martinez, J.; Smith, P. C.
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    Effects of cigarette smoke and nicotine on cell viability, migration and myofibroblastic differentiation
    (2012) Silva, D.; Cáceres, M.; Arancibia, R.; Martínez, C.; Martínez, J.; Smith, P. C.
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    Gingival Wound Healing: An Essential Response Disturbed by Aging?
    (2015) Smith, P. C.; Caceres, M.; Martinez, C.; Oyarzun, A.; Martinez, J.
    Gingival wound healing comprises a series of sequential responses that allow the closure of breaches in the masticatory mucosa. This process is of critical importance to prevent the invasion of microbes or other agents into tissues, avoiding the establishment of a chronic infection. Wound healing may also play an important role during cell and tissue reaction to long-term injury, as it may occur during inflammatory responses and cancer. Recent experimental data have shown that gingival wound healing is severely affected by the aging process. These defects may alter distinct phases of the wound-healing process, including epithelial migration, granulation tissue formation, and tissue remodeling. The cellular and molecular defects that may explain these deficiencies include several biological responses such as an increased inflammatory response, altered integrin signaling, reduced growth factor activity, decreased cell proliferation, diminished angiogenesis, reduced collagen synthesis, augmented collagen remodeling, and deterioration of the proliferative and differentiation potential of stem cells. In this review, we explore the cellular and molecular basis of these defects and their possible clinical implications.
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    Involvement of MT1-MMP and TIMP-2 in human periodontal disease
    (WILEY, 2010) Oyarzun, A.; Arancibia, R.; Hidalgo, R.; Penafiel, C.; Caceres, M.; Gonzalez, M J; Martinez, J.; Smith, P. C.
    Objectives:
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    Methylglyoxal and methylglyoxal-modified collagen as inducers of cellular injury in gingival connective tissue cells
    (2016) Retamal, I. N.; Hernández, R.; González-Rivas, C.; Cáceres, M.; Arancibia, R.; Romero, A.; Martínez, Constanza; Tobar, N.; Martínez, J.; Smith, P. C.
    Background and Objectives: Methylglyoxal is a toxic product derived from glucose metabolism that plays a role in inflammation, diabetes and aging. In addition, the periodontal pathogen Tannerella forsythensis may also generate this compound. However, the effects of methylglyoxal on gingival cells are still poorly understood. In the present study, we have explored whether methylglyoxal or methylglyoxal-treated collagen may modulate cell viability, death and proliferation in gingival connective tissue cells. In addition, we have searched for inflammatory mediators secreted by cells upon exposure to these conditions. Material and Methods: Primary cultures of human gingival fibroblasts were stimulated with soluble methylglyoxal or cultured over a collagen matrix glycated by this agent. Cell viability was evaluated through the MTS assay. Cell death was assessed through DAPI nuclear staining, annexin V and propidium iodide assays. Cell proliferation was evaluated through double immunofluorescence for DAPI and Ki67. Protein levels of matrix metalloproteinases and cytokines were assessed through antibody arrays, enzyme-linked immunosorbent assay, real-time reverse transcription polymerase chain reaction and immunofluorescence. Statistical analysis was performed using the Kruskall-Wallis and Mann-Whitney tests. Results: Soluble methylglyoxal, but not culture of gingival fibroblasts over a methylglyoxal-modified collagen matrix, induced a reduction on cell viability. Moreover, soluble methylglyoxal induced apoptotic cell death as indicated by DAPI nuclear staining, annexin V and propidium iodide assays. Neither soluble methylglyoxal, nor methylglyoxal-modified collagen modified cell proliferation. Using an antibody array, enzyme-linked immunosorbent assay and immunofluorescence assays, we determined that both, soluble methylglyoxal and methylglyoxal- modified collagen stimulated an increase in tissue inhibitor of metalloproteinase (TIMP)-1 protein levels. Conclusions: Soluble methylglyoxal is a highly cytotoxic compound that induces cell death through apoptosis in gingival fibroblasts. TIMP-1 is induced in these cells upon direct exposure to methylglyoxal or after culture of gingival fibroblasts over methylglyoxal-treated collagen. As TIMP-1 has been implicated in cell survival and matrix remodeling, we propose that increased TIMP-1 protein levels may be part of a protective response of gingival connective tissue cells upon exposure to methylglyoxal or after the interaction with the collagen matrix that has been modified by this agent.
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    NOX4-dependent ROS production by stromal mammary cells modulates epithelial MCF-7 cell migration
    (2010) Tobar, N.; Guerrero, J.; Smith, P. C.; Martinez, J.
    BACKGROUND: The influence of the stromal microenvironment on the progression of epithelial cancers has been demonstrated. Unravelling the mechanisms by which stromal cells affect epithelial behaviour will contribute in understanding cellular malignancy. It has been proposed that redox environment has a role in the acquisition of malignancy. In this work, we studied the influence of epithelial cells on the stromal redox status and the consequence of this phenomenon on MCF-7 cell motility.
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    Platelet-Poor and Platelet-Rich Plasma Stimulate Bone Lineage Differentiation in Periodontal Ligament Stem Cells
    (2016) Martinez, C. E.; González Bombardiere, Sergio; Palma, V.; Smith, P. C.
    Background: Plasma-derived fractions have been used as an autologous source of growth factors; however, limited knowledge concerning their biologic effects has hampered their clinical application. In this study, the authors analyze the content and specific effect of both platelet-rich plasma (PRP) and platelet-poor plasma (PPP) on osteoblastic differentiation using primary cultures of human periodontal ligament stem cells (HPLSCs). Methods: The authors evaluated the growth factor content of PRP and PPP using a proteome profiler array and enzyme-linked immunosorbent assay. HPLSCs were characterized by flow cytometry and differentiation assays. The effect of PRP and PPP on HPLSC bone differentiation was analyzed by quantifying calcium deposition after 14 and 21 days of treatment. Results: Albeit at different concentrations, the two fractions had similar profiles of growth factors, the most representative being platelet-derived growth factor (PDGF) isoforms (PDGF-AA, -BB, and -AB), insulin-like growth factor binding protein (IGFBP)-2, and IGFBP-6. Both formulations exerted a comparable stimulus on osteoblastic differentiation even at low doses (2.5%), increasing calcium deposits in HPLSCs. Conclusions: PRP and PPP showed a similar protein profile and exerted comparable effects on bone differentiation. Further studies are needed to characterize and compare the effects of PPP and PRP on bone healing in vivo.
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    Simvastatin alters fibroblastic cell responses involved in tissue repair
    (WILEY-BLACKWELL, 2011) Caceres, M.; Romero, A.; Copaja, M.; Diaz Araya, G.; Martinez, J.; Smith, P. C.
    Background and Objective: Statins have been used to control hypercholesterolemia. However, these drugs also exert pleiotropic effects that include the modulation of inflammation and cell signaling. The present study has analyzed the effects of simvastatin on several cell responses involved in tissue repair, including cell adhesion, cell migration and invasion, actin cytoskeleton remodeling and cell viability.
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    Sonic Hedgehog Stimulates Proliferation of Human Periodontal Ligament Stem Cells
    (SAGE PUBLICATIONS INC, 2011) Martinez, C.; Smith, P. C.; Rodriguez, J. P.; Palma, V.
    Regulation of cell renewal in the periodontium is a critical cell function that has not been clarified. Sonic hedgehog (Shh) is a secreted signaling molecule that plays a key role during development and adult tissue homeostasis. In the present study, we have analyzed the role played by Shh in human periodontal ligament stem cell (HPLSC) proliferation. HPLSC were isolated with anti-STRO-1 antibodies. Shh increased the expression of GLI1 and PTC-1 and selectively stimulated cell proliferation in STRO-1(+) derived from adult periodontal ligament. Shh components were localized to primary cilia in STRO-1(+) cells after Shh stimulation. STRO-1(+) also expressed Shh, suggesting an autocrine-regulated phenomenon. Thus, we propose that Shh plays a critical role in the regulation of cell proliferation in STRO-1(+)/HPLSC.
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    The influence of platelet-derived products on angiogenesis and tissue repair: a concise update
    (2015) Martinez, C. E.; Smith, P. C.; Alvarado, V. A. P.
    Platelet degranulation allows the release of a large amount of soluble mediators, is an essential step for wound healing initiation, and stimulates clotting, and angiogenesis. The latter process is one of the most critical biological events observed during tissue repair, increasing the growth of blood vessels in the maturing wound. Angiogenesis requires the action of a variety of growth factors that act in an appropriate physiological ratio to assure functional blood vessel restoration. Platelets release main regulators of angiogenesis: Vascular Endothelial Growth Factors (VEGFs), basic fibroblast growth factor (FGF-2), and Platelet derived growth factors (PDGFs), among others. In order to stimulate tissue repair, platelet derived fractions have been used as an autologous source of growth factors and biomolecules, namely Platelet Rich Plasma (PRP), Platelet Poor Plasma (PPP), and Platelet Rich Fibrin (PRF). The continuous release of these growth factors has been proposed to promote angiogenesis both in vitro and in vivo. Considering the existence of clinical trials currently evaluating the efficacy of autologous PRP, the present review analyses fundamental questions regarding the putative role of platelet derived fractions as regulators of angiogenesis and evaluates the possible clinical implications of these formulations.
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    Triclosan inhibits tumor necrosis factor-alpha-stimulated urokinase production in human gingival fibroblasts
    (WILEY, 2009) Arancibia, R.; Caceres, M.; Martinez, J.; Smith, P. C.
    Background and Objectives: Destruction of the supporting periodontal tissues is mediated by the action of several proteolytic enzymes. Urokinase is a serine protease that plays a key role in connective tissue destruction through conversion of plasminogen into plasmin. The present study was conducted to evaluate the effect of triclosan on the production and activity of urokinase in cultured gingival fibroblasts.
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    Uncoupled inflammatory, proliferative, and cytoskeletal responses in senescent human gingival fibroblasts
    (2020) Páez, J.; Hernández Salinas, Romina; Rojas Cortéz, Leticia Andrea; Espinoza, J.; Martínez, Constanza; Tobar, N.; Martínez, J.; Smith, P. C.