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Wound Healing Process (wound + healing_process)
Selected AbstractsHypertrophic Scars and Keloids,A Review of Their Pathophysiology, Risk Factors, and Therapeutic ManagementDERMATOLOGIC SURGERY, Issue 2 2009DOLORES WOLFRAM MD BACKGROUND Hypertrophic scars and keloids result from an abnormal fibrous wound healing process in which tissue repair and regeneration-regulating mechanism control is lost. These abnormal fibrous growths present a major therapeutic dilemma and challenge to the plastic surgeon because they are disfiguring and frequently recur. OBJECTIVE To provide updated clinical and experimental information on hypertrophic scars and keloids so that physicians can better understand and properly treat such lesions. METHODS A Medline literature search was performed for relevant publications and for diverse strategies for management of hypertrophic scars and keloids. CONCLUSION The growing understanding of the molecular processes of normal and abnormal wound healing is promising for discovery of novel approaches for the management of hypertrophic scars and keloids. Although optimal treatment of these lesions remains undefined, successful healing can be achieved only with combined multidisciplinary therapeutic regimens. [source] Effects of oestrogen agonists on human dermal fibroblasts in an in vitro wounding assayEXPERIMENTAL DERMATOLOGY, Issue 11 2009Susan Stevenson Abstract:, Oestrogen and dehydroepiandrosterone (DHEA) improve wound healing, but circulating levels decline significantly with age. Recently, the selective oestrogen receptor modulators (SERMs) tamoxifen and raloxifene have been shown to improve age-associated impaired wound healing. Therefore, we have evaluated the effects of 17,-oestradiol, ER, and ER, agonists, tamoxifen, raloxifene and DHEA on human dermal fibroblasts using an in vitro wound assay. An ER, agonist, 17,-oestradiol and DHEA all significantly accelerated cell migration; the DHEA effect was blocked with an aromatase inhibitor. Tamoxifen, raloxifene and DHEA all significantly increased DNA synthesis; the DHEA stimulatory effect was reversed by an aromatase inhibitor. This study demonstrates that 17,-oestradiol, an ER, agonist, tamoxifen, raloxifene and DHEA (following conversion to oestrogen) all have significant effects on human fibroblasts, the key mesenchymal cell involved in the wound healing process. Further understanding of the mechanisms involved may have important implications for the management of age-related impaired wound healing. [source] Serum-free cultured keratinocytes fail to organize fibronectin matrix and possess different distribution of beta-1 integrinsEXPERIMENTAL DERMATOLOGY, Issue 2 2001G. Altankov Abstract: The development of serum free medium formulation for culturing keratinocytes was a breakthrough in achieving a high number of epidermal cells for experimental and therapeutic studies, in particular to support the wound healing process. It is not clear, however, if switching the cells to highly proliferative phenotype may reflect change in other cellular functions important for the wound repair as their adhesive interactions with the extracellular matrix components. Remodelling of the extracellular matrix, particularly of fibronectin plays an essential role for guiding the cells during wound healing. The molecular mechanisms for organization of this provisional fibronectin matrix, however, are still not clear. We found that keratinocytes in serum containing medium, although in fewer numbers than fibroblasts, were able to remove adsorbed fluorescent labelled fibronectin from the substratum and reorganize it in a fibrilar pattern along the cell periphery. After 3 days the secreted fibronectin had also been organized as matrix-like fibers and as clusters deposited on the substratum after migrating cells. In contrast, serum free cultured keratinocytes fail to organize pre-adsorbed fluorescent labelled fibronectin, as well as the secreted fibronectin, although they grow very well under these conditions. Switching the cells to serum containing medium initiates the removal of fluorescent labelled fibronectin from the substratum, however without reorganization in fibrillar pattern. Most likely, these keratinocytes remove fluorescent labelled fibronectin by the expression of proteolytic activity, rather than with the mechanical function of ,1 integrins. The latter were diffusely dispersed in serum containing conditions and tend to organize in focal adhesions in serum free cultured cells. We assumed their transient expression and different affinity state might be important for the keratinocyte migration and matrix assembly mechanism. [source] Physiological changes in tissues denervated by spinal cord injury tissues and possible effects on wound healingINTERNATIONAL WOUND JOURNAL, Issue 3 2008Laurie M Rappl Abstract There are many metabolic and physiological changes that happen to the tissues below the level of a spinal cord injury. These deficits are examined in relation to the series of events that has to take place for wound healing , the "wound healing cascade". The conclusion is that every step of the wound healing process is impaired by the physiological deficits inherent post-spinal cord injury. This may explain, in part, why pressure ulcers on these patients are so difficult to close and to maintain closed. [source] A biodegradable copolymer for the slow release of growth hormone expedites scarring in diabetic ratsJOURNAL OF BIOMEDICAL MATERIALS RESEARCH, Issue 2 2007Francisco García-Esteo Abstract In many diseases wound healing is impaired. This study was designed to establish whether the healing process in diabetes could be improved using a site-specific polymer delivery system containing hGH. The system was first optimized in in vitro experiments performed on cultured fibroblasts taken from healthy and diabetic rats and then tested in an incisional wound model created in the diabetic Wistar rat. In the in vitro experiments using cultured fibroblasts, cell viability, growth, and proliferation were determined, along with polymer degradation, hormone release rates and the expression of TGF,1 in the culture medium. For the in vivo experiments, polymer discs with/without GH were inserted through 3 cm incisions made on the backs of the animals. Wound specimens were obtained 7 and 30 days after surgery to evaluate inflammatory/apoptotic cells, metalloprotease expression and neoangiogenesis using microscopy and immunohistochemical techniques. The local administration of GH using a polymer delivery system did not affect the normal wound healing process. Conversely, when used in diabetic animals, epidermal and dermal repair was expedited. Our findings indicate that GH induces cell proliferation, enhances CD4+ infiltration; increases extracellular matrix protein deposition; stimulates angiogenesis; and diminishes apoptosis at the diabetic wound site. These effects give rise to a comparable wound healing process to that observed in healthy animals. © 2006 Wiley Periodicals, Inc. J Biomed Mater Res Part B: Appl Biomater, 2006 [source] Expression of Dishevelled-1 in wound healing after acute myocardial infarction: possible involvement in myofibroblast proliferation and migrationJOURNAL OF CELLULAR AND MOLECULAR MEDICINE, Issue 2 2004Lijun Chen Abstract One of our previous studies indicated that the expression of ,-catenin, which is the key factor of wnt-frizzled pathway, increased significantly in the ischemic area of the rat heart 7 days after myocardial infarction (MI). Together with the results of other recent studies, we made an assumption that wnt-frizzled pathway may be involved in the controlled cell proliferation and migration during repair processes after MI. To verify this assumption we tried to investigate the expression of another signal transduction molecule called Dishevelled in wnt-frizzled pathway during the wound healing process after MI. The left descending coronary arteries of rats were ligated to induce MI. Immunohistochemistry SABC method and in situ hybridization were performed to detect the expression of Dishevelled-1. The results showed, that one day after MI, Dishevelled-1 mRNA but not protein expression was detected in the cells at the border zone of the infarction area; 4 days after MI the expression of Dishevelled-1 increased exclusively and cytoplasmic Dishevelled-1 was observed not only at the border zone but also in the infarct area; 7 days after MI, it seems that the expression reached its peak, the positive staining even spread into the endothelial and smooth muscle cells of the newly formed and pre-existing blood vessels in the infarction area; after that the Dishevelled-1 expression decreased abruptly and could hardly be detected 28 days after MI. Thus cytoplasmic Dishevelled-1 may be involved in the controlled proliferation and migration of myofibroblasts and vascular endothelial cells, hence play a role during the wound healing process after MI. [source] Nicotine inhibits myofibroblast differentiation in human gingival fibroblastsJOURNAL OF CELLULAR BIOCHEMISTRY, Issue 6 2005Yiyu 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] Enamel matrix derivative exhibits angiogenic effect in vitro and in a murine modelJOURNAL OF CLINICAL PERIODONTOLOGY, Issue 8 2003Kuo Yuan Abstract Objectives: Angiogenesis is one of the most critical events in the wound healing process. Any increase in angiogenesis could result in more rapid and complete healing. A recent study found that enamel matrix derivative (EMD) could accelerate early periodontal wound healing. We wanted to clarify whether EMD caused an angiogenic effect and, thus, possibly enhanced wound healing. Methods: We performed in vitro proliferation and chemotaxis assays on human umbilical vein endothelial cell (HUVEC) cultures, and a tissue culture assay using blood vessel fragments in fibrin gel. Collagen membranes soaked with EMD were implanted subcutaneously in mice to test the in vivo angiogenic effect. Results: While there were no significant differences between the negative control and EMD groups in the proliferation assay, EMD treatment did exhibit a significantly greater dose-dependent chemotactic effect on HUVEC than control group treatments. The tissue culture in fibrin gel showed new blood vessel outgrowths in the EMD groups, but none in the negative control group. In the animal studies, significantly more endothelial cells were detected in the EMD group of mice. Conclusions: Our findings show that EMD does exhibit some angiogenic effects. However, the underlying molecules and mechanisms are still unidentified. We discuss several possibilities. Zusammenfassung Ziele: Die Angiogenese gehört zu den kritischsten Ereignissen bei der Wundheilung. Eine Erhöhung der Angiogenese könnte zu einer rascheren und kompletteren Wundheilung führen. Kürzlich zeigte eine Studie, dass Schmelzmatrixderivate (EMD) die frühe parodontale Wundheilung beschleunigen könnte. Wir wollten klären, ob EMD einen angiogenetischen Effekt verursacht und dies möglicherweise die Wundheilung verbessert. Methoden: Wir führten in vitro Proliferations- und Chemotaxis-Assays an menschlichen Umbilicalvenen-Endothelzellen (HUVEC)Kulturen durch und studierten eine Gewebekultur unter Nutzung von Blutgefäßfragmenten in Fibringel. Kollagenmembranen mit EMD getränkt wurden subkutan in Mäuse implantiert, um den angiogenetischen Effekt in vivo zu testen. Ergebnisse: Während es keine signifikanten Differenzen zwischen den negativen Kontrollen und den EMD Gruppen in dem Proliferationsassay gab, zeigte die EMD Behandlung einen signifikant größeren, dosisabhängigen chemotaktischen Effekt auf HUVEC verglichen mit den Kontrollen. Die Gewebekultur im Fibringel zeigte neue Blutgefäßbildungen in den EMD-Gruppen, aber keine bei den Negativkontrollen. Bei den Tierstudien wurden signifikant mehr Endothelzellen in den EMD Mäusegruppen entdeckt. Schlussfolgerungen: Unsere Ergebnisse zeigen, dass EMD einige angiogenetische Effekte zeigt. Jedoch sind die zugrunde liegenden Moleküle und die Mechanismen noch nicht geklärt. Wir diskutieren verschiedene Möglichkeiten. Résumé Objectifs: L'Angiogenèse est un des plus critiques éléments lors du processus de cicatrisation. La moindre augmentation de l'angiogenèse peut entraîner une cicatrisation plus rapide et plus complète. Une récente étude a montré que les dérivés de la matrice amellaire (EMD) pouvait accélérer plus tôt la cicatrisation parodontale. Nous voulions clarifier la possible responsabilité de l'EMD dans l'angiogenèse et si oui, l'amélioration de la cicatrisation. Méthodes: Nous avons réalisé in vitro la prolifération et un essai de chimiotactisme sur des cultures de cellules endothéliales de la veine ombilicale humaine (HUVEC), et un essai de culture tissulaire en utilisant des fragments de vaisseaux sanguins dans un gel de fibrine. Des membranes de collagène gorgées d'EMD furent implantées en sous-cutanée chez des souris pour tester l'effet angiogénique in vivo. Résultats: Bien qu'il n'y eut pas de différences significatives entre le contrôle négatif et le groupe EMD pour le test de prolifération, le traitement par EMD présentait un effet chimiotactique dose- dépendant significativement plus élevé sur les HUVEC. La culture tissulaire sur gel de fibrine présentait une surcroissance de nouveaux vaisseaux sanguins pour le groupe EMD, mais pas dans le groupe contrôle. Plus de cellules endothéliales furent en outre détectées lors de l'étude animale, pour le groupe de souris traitées par EMD. Conclusions: Nos données montrent que l'EMD présente quelques effets angiogéniques. Cependant, les molécules et les mécanismes responsables ne sont toujours pas identifiés. Nous discutons quelques possibilités. [source] Meal patterns and meal quality in patients with leg ulcersJOURNAL OF HUMAN NUTRITION & DIETETICS, Issue 1 2000U. Wissing Background Wound healing is a complex process, which requires adequate energy sources, proteins, and specific minerals and vitamins. If an individual is unable to get or to eat the nutrients required, the wound healing process might be disrupted. The aim of this study was to investigate food-related factors, meal patterns and meal quality in relation to nutritional status in elderly out-patients with leg ulcers. Methods Nutritional status was assessed by use of the Mini Nutritional Assessment in 70 patients living in their own homes. Fifty-six of the patients recorded actual meals and snacks over four consecutive days. Meal patterns and meal quality were evaluated with the help of a qualitative classification system, the Food Based Concept for Classification of Eating Episodes. Results Thirty-six patients were classified as well-nourished, 32 were at risk of malnutrition and two were malnourished. More patients in the risk group for malnutrition did not buy their own food, and usually ate alone. Incomplete Meals and Low Quality Snacks were the most common eating types. The patients at risk of malnutrition had significantly fewer prepared Complete Meals than the well-nourished patients. Conclusion The results show a diet and meal quality which hardly meets the requirements for nutrients that are important in wound healing, especially for those patients assessed at risk of malnutrition. [source] Temporal expression of growth factors and matrix molecules in healing tendon lesionsJOURNAL OF ORTHOPAEDIC RESEARCH, Issue 1 2005Linda A. Dahlgren Abstract Overuse tendon injuries are common among elite and recreational athletes. Tendon healing may be enhanced at the cellular level through the use of exogenous growth factors; however, little is known about the endogenous expression of growth factors in healing tendon. This study describes the temporal expression of insulin-like growth factor-I (IGF-I), transforming growth factor-,1 (TGF-,1), and collagen types I and III in healing tendon lesions. Collagenase-induced lesions were created in the tensile region of the flexor digitorum superficialis tendon of both forelimbs of 14 horses. Tendons were harvested from euthanatized horses 1, 2, 4, 8 or 24 weeks following injury. Gene expression was evaluated using Northern blot analysis (collagen types I and III), real time PCR (IGF-I and TGF-,1), and in situ hybridization. Protein content was assayed by dye-binding assay (collagen types I and III), radioimmunoassay (IGF-I), ELISA (TGF-,1), and immunohistochemistry. Samples were also processed for differential collagen typing. DNA and glycosaminoglycan content, and routine H&E staining. Microscopically, lesions progressed from an amorphous, acellular lesion soon after injury to scar tissue filled with collagen fibers and mature fibroblasts organized along lines of tension. Early lesions were characterized by immediate increases in expression of growth factors and collagen. Message levels for TGF-,1 peaked early in the wound healing process (1 week), while IGF-I peaked later (4 weeks), as the regenerative phase of healing was progressing. In the first 2 weeks after lesion induction, tissue levels of IGF-I protein actually decreased approximately 40% compared to normal tendon. By 4 weeks, these levels had exceeded those of normal tendon and remained elevated through 8 weeks. Message expression for collagen types I and III increased by 1 week following injury and remained elevated throughout the course of the study. Collagen type I represented the major type of collagen in healing tendon at all time points of the study. Based on these results, IGF-I, administered exogenously during the first 2 weeks following injury, may provide a therapeutic advantage by bolstering low endogenous tissue levels and enhancing the metabolic response of individual tendon fibroblasts. © 2004 Orthopaedic Research Society. Published by Elsevier Ltd. All rights reserved. [source] Epithelial,mesenchymal interactions in keloid pathogenesis modulate vascular endothelial growth factor expression and secretion,THE JOURNAL OF PATHOLOGY, Issue 1 2007CT Ong Abstract Vascular endothelial growth factor (VEGF) plays an important role in angiogenesis during the wound healing process. As epithelial,mesenchymal interactions have been shown to regulate a plethora of genes in wound healing, we hypothesized that these interactions might have a role in modulating VEGF expression and angiogenesis. A two chamber co-culture model was used, wherein normal and keloid keratinocytes and fibroblasts were physically separated by membrane inserts while allowing cytokine diffusion. Cell lysates obtained from keratinocytes co-cultured with fibroblasts demonstrated increased expression of VEGF. An enzyme-linked immunosorbent assay (ELISA) showed significant increase in VEGF expression in co-culture conditioned media compared with controls. Additionally, the conditioned medium from keloid keratinocyte and fibroblast co-cultures increased proliferation and formation of complex three-dimensional capillary-like structures in human umbilical vein endothelial cells, emphasising the importance of epithelial,mesenchymal interactions in the angiogenic process. Immunostaining of keloid tissue localized VEGF in the basal layer of the epidermis and also demonstrated higher blood vessel density than normal skin. Keloid tissue extract also demonstrated increased expression of VEGF compared with normal skin. It is likely that epidermal VEGF exerts significant paracrine control over the dynamics and expression profile of underlying dermal fibroblasts. Addition of the inhibitors WP631, mitoxantrone, and Rapamycin to keloid keratinocyte and fibroblast co-cultures, downregulated secreted VEGF expression in a dose-dependent manner, suggesting therapeutic potential for these compounds in the treatment of keloid scars. Copyright © 2006 Pathological Society of Great Britain and Ireland. Published by John Wiley & Sons, Ltd. [source] Prostaglandin E2 is activated by airway injury and regulates fibroblast cytoskeletal dynamics,THE LARYNGOSCOPE, Issue 7 2009Vlad C. Sandulache MD Abstract Objectives/Hypothesis: To characterize the activation of cyclooxygenase (COX)-2/prostaglandin (PG) E2 signaling during airway mucosal repair and its subsequent role during the wound healing process. Study Design: Prospective animal study. Methods: The subglottis was approached via cricothyroidotomy. Sham airways were closed, and wounded airways were subjected to laser injury and closed. Subglottic tissue was harvested at 12 hours, 24 hours, 48 hours, and 72 hours postinjury. Secretions were collected preoperatively and at time of sacrifice. Inflammatory gene expression was analyzed using quantitative reverse transcriptase polymerase chain reaction. Subglottic/tracheal explants were exposed to exogenous IL-1, in the presence or absence of COX inhibitors. Explant-produced PGE2 levels were assayed using enzyme linked immunoassays. Human airway fibroblast migration and collagen contraction were assayed in the presence or absence of prostaglandin E2. Results: Laser injury triggers a rapid, dose-dependent increase in mucosal IL-1, and COX-2 gene expression, with an anatomical distribution proportional to the distance from the site of injury. Gene upregulation correlates with dose-dependent increases in PGE2 mucosal secretion levels. Ex vivo analysis indicates IL-1, is responsible for the activation of the COX-2 / PGE2 pathway. Prostaglandin E2 differentially inhibits airway fibroblast migration and contraction in a specific, dose-dependent manner. Conclusions: PGE2 is activated during mucosal inflammation and acts to decrease fibroplastic activity in the mucosal wound bed. During subglottic stenosis (SGS) development, the levels of PGE2 generated in response to injury may be insufficient to blunt the intrinsically fibroplastic phenotype of SGS fibroblasts, resulting in excessive scarring. Laryngoscope, 2009 [source] Nanostructured Biomaterials for Regeneration,ADVANCED FUNCTIONAL MATERIALS, Issue 22 2008Guobao Wei Abstract Biomaterials play a pivotal role in regenerative medicine, which aims to regenerate and replace lost/dysfunctional tissues or organs. Biomaterials (scaffolds) serve as temporary 3D substrates to guide neo tissue formation and organization. It is often beneficial for a scaffolding material to mimic the characteristics of extracellular matrix (ECM) at the nanometer scale and to induce certain natural developmental or/and wound healing processes for tissue regeneration applications. This article reviews the fabrication and modification technologies for nanofibrous, nanocomposite, and nanostructured drug-delivering scaffolds. ECM-mimicking nanostructured biomaterials have been shown to actively regulate cellular responses including attachment, proliferation, differentiation, and matrix deposition. Nanoscaled drug delivery systems can be successfully incorporated into a porous 3D scaffold to enhance the tissue regeneration capacity. In conclusion, nanostructured biomateials are a very exciting and rapidly expanding research area, and are providing new enabling technologies for regenerative medicine. 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