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Wound Contraction (wound + contraction)
Selected AbstractsNitric oxide synthesis inhibition alters rat cutaneous wound healingJOURNAL OF CUTANEOUS PATHOLOGY, Issue 7 2006Thaís P. Amadeu Background:, Nitric oxide (NO) is an important molecule that participates in wound repair, but its effects on cutaneous wound healing are not well understood. The aim of this study was to investigate the effects of NO synthesis blockade on rat cutaneous wound healing by the administration of NG -nitro- l -arginine methyl ester (l -NAME), a non-selective inhibitor of NO synthases. Methods:, NO synthesis was inhibited by administration of l -NAME (20 mg/kg/day) in drinking water. An excisional wound was done, and the animals were killed 7, 14, and 21 days later. Wound contraction and blood pressure were evaluated. The lesion and adjacent skin were formalin fixed and paraffin embedded. Mast cells were quantified, and vessels were evaluated using stereological methods. Results:,l -NAME-treated animals presented delayed wound contraction, alterations in collagen organization, and neoepidermis thickness. The inhibition of NO synthesis increased mast cell migration 7 days after wounding, but decreased 21 days after wounding. Volume density of vessels was decreased in l -NAME-treated animals, 21 days after lesion. Surface density of vessels was frequently smaller in l -NAME-treated animals than in controls. Conclusion:, The blockade of NO synthesis impaired cutaneous wound healing, acting in early and late phases of wound repair. [source] Curcumin-induced fibroblast apoptosis and in vitro wound contraction are regulated by antioxidants and heme oxygenase: implications for scar formationJOURNAL OF CELLULAR AND MOLECULAR MEDICINE, Issue 4 2009A. Scharstuhl Abstract Fibroblast apoptosis plays a crucial role in normal and pathological scar formation and therefore we studied whether the putative apoptosis-inducing factor curcumin affects fibroblast apoptosis and may function as a novel therapeutic. We show that 25-,M curcumin causes fibroblast apoptosis and that this could be inhibited by co-administration of antioxidants N -acetyl- l -cysteine (NAC), biliverdin or bilirubin, suggesting that reactive oxygen species (ROS) are involved. This is supported by our observation that 25-,M curcumin caused the generation of ROS, which could be completely blocked by addition of NAC or bilirubin. Since biliverdin and bilirubin are downstream products of heme degradation by heme oxygenase (HO), it has been suggested that HO-activity protects against curcumin-induced apoptosis. Interestingly, exposure to curcumin maximally induced HO-1 protein and HO-activity at 10,15 ,M, whereas, at a concentration of >20-,M curcumin HO-1-expression and HO-activity was negligible. NAC-mediated inhibition of 25-,M curcumin-induced apoptosis was demonstrated to act in part via restored HO-1-induction, since the rescuing effect of NAC could be reduced by inhibiting HO-activity. Moreover pre-induction of HO-1 using 5-,M curcumin protected fibroblasts against 25-,M curcumin-induced apoptosis. On a functional level, fibroblast-mediated collagen gel contraction, an in vitro wound contraction model, was completely prevented by 25-,M curcumin, while this could be reversed by co-incubation with NAC, an effect that was also partially HO-mediated. In conclusion, curcumin treatment in high doses (>25 ,M) may provide a novel way to modulate pathological scar formation through the induction of fibroblast apoptosis, while antioxidants, HO-activity and its effector molecules act as a possible fine-tuning regulator. [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] Inflammatory cytokines induce the transformation of human dermal microvascular endothelial cells into myofibroblasts: a potential role in skin fibrogenesisJOURNAL OF CUTANEOUS PATHOLOGY, Issue 2 2007V. Chaudhuri Background:, The myofibroblast plays a central role in wound contraction and in the pathology of fibrosis. The origin(s) of this important cell type in skin has not been firmly established. Methods:, Human epithelioid dermal microvascular endothelial cells (HDMEC) were isolated from foreskin tissue and maintained in cell culture. The transformation of epithelioid HDMEC into myofibroblasts (EMT) was induced by the inflammatory cytokines interleukin-1, (IL-1,) or tumour necrosis factor-, (TNF-,), and the transformed cells were characterized by electron microscopy, immunohistochemistry and quantitative RT-PCR. Results:, After short-term exposure to IL-1, or TNF-, (<3 days), EMT was reversible; after long-term exposure (>10 days), EMT was permanent. The transformed cells were identified as myofibroblasts by cytoplasmic microfilaments with dense bodies and attachment plaques, by the expression of ,-smooth muscle actin, type I collagen and calponin, and by quantitative RT-PCR gene expression of type I collagen and ,-smooth muscle actin. Conclusions:, Long-term exposure to TNF-, or IL-1, induced the permanent transformation of HDMEC into myofibroblasts in cell culture. A similar transformation following chronic inflammatory stimulation in vivo may explain one source of myofibroblasts in skin fibrogenesis. [source] Nitric oxide synthesis inhibition alters rat cutaneous wound healingJOURNAL OF CUTANEOUS PATHOLOGY, Issue 7 2006Thaís P. Amadeu Background:, Nitric oxide (NO) is an important molecule that participates in wound repair, but its effects on cutaneous wound healing are not well understood. The aim of this study was to investigate the effects of NO synthesis blockade on rat cutaneous wound healing by the administration of NG -nitro- l -arginine methyl ester (l -NAME), a non-selective inhibitor of NO synthases. Methods:, NO synthesis was inhibited by administration of l -NAME (20 mg/kg/day) in drinking water. An excisional wound was done, and the animals were killed 7, 14, and 21 days later. Wound contraction and blood pressure were evaluated. The lesion and adjacent skin were formalin fixed and paraffin embedded. Mast cells were quantified, and vessels were evaluated using stereological methods. Results:,l -NAME-treated animals presented delayed wound contraction, alterations in collagen organization, and neoepidermis thickness. The inhibition of NO synthesis increased mast cell migration 7 days after wounding, but decreased 21 days after wounding. Volume density of vessels was decreased in l -NAME-treated animals, 21 days after lesion. Surface density of vessels was frequently smaller in l -NAME-treated animals than in controls. Conclusion:, The blockade of NO synthesis impaired cutaneous wound healing, acting in early and late phases of wound repair. [source] Evaluation of wound healing activity of Lantana camara L. , a Preclinical studyPHYTOTHERAPY RESEARCH, Issue 2 2009B. Shivananda Nayak Abstract Lantana camara is used in herbal medicine for the treatment of skin itches, as an antiseptic for wounds, and externally for leprosy and scabies. The objective of our study was to investigate excision wound healing activity of the leaf extract of L. camara in rats. The animals were divided into two groups of 12 each in both the models. The test group animals were treated with the aqueous extract of L. camara (100 mg/kg/day) topically and the control group animals were left untreated. Wound healing efficacy was measured by determining the morphological and biochemical parameters. Wound healing time, wound contraction and synthesis of collagen were monitored periodically. Antimicrobial activities of the extract against the microorganisms were also assessed. Treatment of the wounds with extract enhanced significantly the rate of wound contraction (98%), synthesis of collagen and decreased mean wound healing time. These studies demonstrate that L. camara is effective in healing excision wounds in the experimental animal and could be evaluated as a therapeutic agent in tissue repair processes associated with skin injuries. Copyright © 2008 John Wiley & Sons, Ltd. [source] Wound healing properties of Hylocereus undatus on diabetic ratsPHYTOTHERAPY RESEARCH, Issue 8 2005R. M. Perez G. Abstract Aqueous extracts of leaves, rind, fruit pulp and flowers of Hylocereus undatus were studied for their wound healing properties. Wound healing effects were studied on incision (skin breaking strength), excision (percent wound contraction) and the nature of wound granulation tissues, which were removed on day 7 and the collagen, hexosamine, total proteins and DNA contents were determined, in addition to the rates of wound contraction and the period of epithelialization. In streptozotocin diabetic rats, where healing is delayed, topical applications of H. undatus produced increases in hydroxyproline, tensile strength, total proteins, DNA collagen content and better epithelization thereby facilitating healing. H. undatus had no hypoglycemic activity. Copyright © 2005 John Wiley & Sons, Ltd. [source] A novel model of wound healing in the SCID mouse using a cultured human skin substituteAUSTRALASIAN JOURNAL OF DERMATOLOGY, Issue 1 2009Martin L Windsor SUMMARY Studies of skin graft behaviour in rodent excisional wound models are limited by the dominance of wound contracture and graft sloughing as primary healing responses. To slow skin contraction, polytetrafluoroethylene (Teflon) rings were inserted into dorso-lateral full-thickness wounds in SCID mice. Cultured skin substitutes (OrCel), composed of cultured human keratinocytes and fibroblasts in a bovine collagen sponge, were implanted within the rings. Examination and histology of grafts 14 days later showed graft take in four of six recipients, with 90% epithelialization and wound contraction of 31,47%. Immunohistochemical studies, using human-specific antisera to distinguish graft from host tissues, showed that regenerated tissue was predominantly human. Staining with anticytokeratin, revealed a multilayered, stratified neoepidermis. HBG were identified in keratinocytes in all epidermal layers. Langerhans cells were absent. Antihuman vimentin, used as a fibroblast marker, confirmed that cells of the neodermis were primarily of human origin. Neoepidermal keratinocytes, primarily in the basal and suprabasal layers, were also stained. Results suggest that the poly(tetrafluoroethylene) ring inhibited graft sloughing and provided a more favourable environment for the skin substitute to regenerate a substantially normal human skin. [source] | ||||||||||