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Myofibroblast Differentiation (myofibroblast + differentiation)

Distribution by Scientific Domains

Medical Sciences	50%

Selected Abstracts

Nicotine inhibits myofibroblast differentiation in human gingival fibroblasts

JOURNAL OF CELLULAR BIOCHEMISTRY, Issue 6 2005
Yiyu Fang
Abstract Cigarette smoking has been suggested as a risk factor for several periodontal diseases. It has also been found that smokers respond less favorably than non-smokers to periodontal therapy. Previous work in our lab has shown that nicotine inhibits human gingival cell migration. Since myofibroblasts play an important role in wound closure, we asked if nicotine affects gingival wound healing process by regulating myofibroblast differentiation. Human gingival fibroblasts (HGFs) from two patients were cultured in 10% fetal bovine serum cell culture medium. Cells were pretreated with different doses of nicotine (0, 0.01, 0.1, and 1 mM) for 2 h, and then incubated with transforming growth factor beta (TGF-,1) (0, 0.25, 0.5, and 1 ng/ml) with or without nicotine for 30 h. The expression level of ,-smooth muscle actin (,-SMA), a specific marker for myofibroblasts, was analyzed by Western blots, immunocytochemistry, and real-time polymerase chain reaction (real-time PCR). Phosphorylated p38 mitogen-activated protein kinase (Phospho-p38 MAPK) activity was analyzed by Western blots. TGF-,1 induced an increase of ,-SMA protein and mRNA expression, while nicotine (1 mM) inhibited the TGF-,1-induced expression of ,-SMA but not ,-actin. Nicotine treatment down-regulated TGF-,1-induced p38 MAPK phosphorylation. Our results demonstrated for the first time that nicotine inhibits myofibroblast differentiation in human gingival fibroblasts in vitro; supporting the hypothesis that delayed wound healing in smokers may be due to decreased wound contraction by myofibroblasts. © 2005 Wiley-Liss, Inc. [source]

Tissue regeneration of the vocal fold using bone marrow mesenchymal stem cells and synthetic extracellular matrix injections in rats,

THE LARYNGOSCOPE, Issue 3 2010
Beatriz Quinchia Johnson DDS
Abstract Objectives/Hypothesis. To determine the effectiveness of bone marrow mesenchymal stem cell (BM-MSC) transplantation in isolation or within a synthetic extracellular matrix (sECM) for tissue regeneration of the scarred vocal fold lamina propria. Methods. In vitro stability and compatibility of mouse BM-MSC embedded in sECM was assessed by flow cytometry detection of BM-MSC marker expression and proliferation. Eighteen rats were subjected to vocal fold injury bilaterally, followed by 1 month post-treatment with unilateral injections of saline or sECM hydrogel (Extracel; Glycosan BioSystems, Inc., Salt Lake City, UT), green fluorescence protein (GFP)-mouse BM-MSC, or BM-MSC suspended in sECM. Outcomes measured 1 month after treatment included procollagen-III, fibronectin, hyaluronan synthase-III (HAS3), hyaluronidase (HYAL3), smooth muscle actin (SMA), and transforming growth factor-beta 1(TGF-,1) mRNA expression. The persistence of GFP BM-MSC, proliferation, apoptosis, and myofibroblast differentiation was assessed by immunofluorescence. Results. BM-MSC grown in vitro within sECM express Sca-1, are positive for hyaluronan receptor CD44, and continue to proliferate. In the in vivo study, groups injected with BM-MSC had detectable GFP-labeled BM-MSC remaining and showed proliferation and low apoptotic or myofibroblast markers compared to the contralateral side. Embedded BM-MSC in the sECM group exhibited increased levels of procollagen III, fibronectin, and TGF-,1. BM-MSC within sECM downregulated the expression of SMA compared to BM-MSC alone and exhibited upregulation of HYAL3 and no change in HAS3 compared to saline. Conclusions. Treatment of vocal fold scarring with BM-MSC injected in a sECM displayed the most favorable outcomes in ECM production, hyaluronan metabolism, myofibroblast differentiation, and production of TGF-,1. Furthermore, the combined treatment had no detectable cytotoxicity and preserved local cell proliferation. Laryngoscope, 2010 [source]

4411: Immunohistochemical methods to evaluate vitreoretinal scaring

ACTA OPHTHALMOLOGICA, Issue 2010
ML BOCHATON-PIALLAT
Purpose Formation of scarlike epiretinal membranes (ERMs) constitutes potentially the end stage of evolution of proliferative vitreoretinopathy (PVR), proliferative diabetic retinopathy (PDR) and idiopathic vitreoretinopathy. Among various cellular populations, ERMs contain cells with contractile features typical of myofibroblasts. Myofibroblasts have been described in granulation tissue during wound healing and in practically all fibrocontractive diseases, in which they participate in the generation of isometric tension and in the synthesis of extracellular matrix components; these phenomena are in turn responsible for granulation tissue remodeling and retraction. The main marker of the myofibroblastic phenotype is the expression of alpha-SMA. The transforming growth factor-beta1 and the ED-A splice variant of cellular fibronectin, an extracellular matrix component, are key players of the complex process of myofibroblast differentiation. Methods Proteins were detected by means of immunohistochemical staining on paraffin sections from formol fixed tissues and double immunofluorescence staining on whole tissues. Samples were observed by using classical light and confocal microscopes. Results The presence of alpha-SM actin-positive myofibroblasts was associated with the expression of TGF-beta1, TGF-beta receptor II, and ED-A FN in all types of ERMs studied. Conclusion The results furnish new data on the mechanism of alpha-SM actin stimulation in fibroblasts in a human pathologic setting. [source]