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Normal skin and hypertrophic scar fibroblasts differentially regulate collagen and fibronectin expression as well as mitochondrial membrane potential in response to basic fibroblast growth factor
Song, Rui;Bian, Hui-Ning;Lai, Wen;Chen, Hua-De;Zhao, Ke-Seng;
Brazilian Journal of Medical and Biological Research , 2011, DOI: 10.1590/S0100-879X2011007500041
Abstract: basic fibroblast growth factor (bfgf) regulates skin wound healing; however, the underlying mechanism remains to be defined. in the present study, we determined the effects of bfgf on the regulation of cell growth as well as collagen and fibronectin expression in fibroblasts from normal human skin and from hypertrophic scars. we then explored the involvement of mitochondria in mediating bfgf-inducedeffects on the fibroblasts. we isolated and cultivated normal and hypertrophic scar fibroblasts from tissue biopsies of patients who underwent plastic surgery for repairing hypertrophic scars. the fibroblasts were then treated with different concentrations of bfgf (ranging from 0.1 to 1000 ng/ml). the growth of hypertrophic scar fibroblasts became slower with selective inhibition of type i collagen production after exposure to bfgf. however, type iii collagen expression was affected in both normal and hypertrophic scar fibroblasts. moreover, fibronectin expression in the normal fibroblasts was up-regulated after bfgf treatment. bfgf (1000 ng/ml) also induced mitochondrial depolarization in hypertrophic scar fibroblasts (p < 0.01). the cellular atp level decreased in hypertrophic scar fibroblasts (p < 0.05), while it increased in the normal fibroblasts following treatment with bfgf (p < 0.01). these data suggest that bfgf has differential effects and mechanisms on fibroblasts of the normal skin and hypertrophic scars, indicating that bfgf may play a role in the early phase of skin wound healing and post-burn scar formation.
Anti-Fibrotic Actions of Interleukin-10 against Hypertrophic Scarring by Activation of PI3K/AKT and STAT3 Signaling Pathways in Scar-Forming Fibroblasts  [PDF]
Jihong Shi, Jun Li, Hao Guan, Weixia Cai, Xiaozhi Bai, Xiaobing Fang, Xiaolong Hu, Yaojun Wang, Hongtao Wang, Zhao Zheng, Linlin Su, Dahai Hu, Xiongxiang Zhu
PLOS ONE , 2014, DOI: 10.1371/journal.pone.0098228
Abstract: Background The hypertrophic scar (HS) is a serious fibrotic skin condition and a major clinical problem. Interleukin-10 (IL-10) has been identified as a prospective scar-improving compound based on preclinical trials. Our previous work showed that IL-10 has anti-fibrotic effects in transforming growth factor (TGF)-β1-stimulated fibroblasts, as well as potential therapeutic benefits for the prevention and reduction of scar formation. However, relatively little is known about the mechanisms underlying IL-10-mediated anti-fibrotic and scar-improvement actions. Objective To explore the expression of the IL-10 receptor in human HS tissue and primary HS fibroblasts (HSFs), and the molecular mechanisms contributing to the anti-fibrotic and scar-improvement capabilities of IL-10. Methods Expression of the IL-10 receptor was assessed in HS tissue and HSFs by immunohistochemistry, immunofluorescence microscopy, and polymerase chain reaction analysis. Primary HSFs were treated with IL-10, a specific phosphatidylinositol 3 kinase (PI3K) inhibitor (LY294002) or a function-blocking antibody against the IL-10 receptor (IL-10RB). Next, Western blot analysis was used to evaluate changes in the phosphorylation status of AKT and signal transducers and activators of transcription (STAT) 3, as well as the expression levels of fibrosis-related proteins. Results HS tissue and primary HSFs were characterized by expression of the IL-10 receptor and by high expression of fibrotic markers relative to normal controls. Primary HSFs expressed the IL-10 receptor, while IL-10 induced AKT and STAT3 phosphorylation in these cells. In addition, LY294002 blocked AKT and STAT phosphorylation, and also up-regulated expression levels of type I and type III collagen (Col 1 and Col 3) and alpha-smooth muscle actin (α-SMA) in IL-10-treated cells. Similarly, IL-10RB reduced STAT3/AKT phosphorylation and blocked the IL-10-mediated mitigation of fibrosis in HSFs. Conclusion IL-10 apparently inhibits fibrosis by activating AKT and STAT3 phosphorylation downstream of the IL-10 receptor, and by facilitating crosstalk between the PI3K/AKT and STAT3 signal transduction pathways.
Investigating the Role of P311 in the Hypertrophic Scar  [PDF]
Jianglin Tan,Xu Peng,Gaoxing Luo,Bing Ma,Chuan Cao,Weifeng He,Shunzong Yuan,Shirong Li,John A. Wilkins,Jun Wu
PLOS ONE , 2012, DOI: 10.1371/journal.pone.0009995
Abstract: The mechanisms of hypertrophic scar formation are not fully understood. We previously screened the differentially expressed genes of human hypertrophic scar tissue and identified P311 gene as upregulated. As the activities of P311 in human fibroblast function are unknown, we examined the distribution of it and the effects of forced expression or silencing of expression of P311. P311 expression was detected in fibroblast-like cells from the hypertrophic scar of burn injury patients but not in peripheral blood mononuclear cells, bone marrow mesenchymal stem cells, epidermal cells or normal skin dermal cells. Transfection of fibroblasts with P311 gene stimulated the expression of alpha-smooth muscle actin (α-SMA), TGF-β1 and α1(I) collagen (COL1A1), and enhanced the contraction of fibroblast populated collagen lattices (FPCL). In contrast, interference of fibroblast P311 gene expression decreased the TGF-β1 mRNA expression and reduced the contraction of fibroblasts in FPCL. These results suggest that P311 may be involved in the pathogenesis of hypertrophic scar via induction of a myofibroblastic phenotype and of functions such as TGF-β1 expression. P311 could be a novel target for the control of hypertrophic scar development.
Treatment of a Pigmented Hypertrophic Scar by Low-Level Laser Therapy (LLLT): a Case Report
Hamideh Moravvaej,Lisa Daneshvar,Mohammad Saeedi,Mohammad Reza Barzegar
Journal of Lasers in Medical Sciences , 2011,
Abstract: A hypertrophic scar is defined as an excess healing response that is a dilemma for physicians. Several therapies are available: intralesional corticosteroids, topical treatments, cryotherapy, surgery, radiation, silicone gel dressing and laser therapy.Pulsed-dye, Nd-Yag and CO2 lasers have been used for treatment of keloids and hypertrophic scars but recurrence is common. Recently Low-Level Laser Therapy(aluminum-gallium-arsenide (AlGaAs) Diode 980nm, red light (Mustung, KLO4,Helium Neon 630 nm) and blue light LED lasers have been used for closure of wounds. The aim of this report is to show the effectiveness of these lasers for the treatment of a hypertrophic scar on the forearm of a 40 year-old woman due to burning by gas explosion.
Management of Unilateral Masseter Hypertrophy and Hypertrophic Scar—A Case Report
Naresh Shetty,Rajanikanth K. Malaviya,M. K. Gupta
Case Reports in Dentistry , 2012, DOI: 10.1155/2012/521427
Abstract: Masseter muscle hypertrophy is a rare condition of idiopathic cause. It clinically presents as an enlargement of one or both masseter muscles. Most patients complain of facial asymmetry; however, symptoms such as trismus, protrusion, and bruxism may also occur. Several treatment options reported for masseter hypertrophy are present, which range from simple pharmacotherapy to more invasive surgical reduction. Keloid scar with unilateral masseter hypertrophy is a rarely seen in clinical practice. This paper reports a case of unilateral masseter hypertrophy with keloid scar in the angle of the mandible for which surgical treatment was rendered to the patient by using a single approach.
eb病毒和人巨细胞病毒感染对儿童急性淋巴细胞白血病pten及htert基因甲基化的影响  [PDF]
祁新坤,舒逸,秦茹,邹琳
南方医科大学学报 , 2013,
Abstract: 目的探讨eb病毒(ebv)与人巨细胞病毒(hcmv)感染对儿童急性淋巴细胞白血病(all)相关基因pten及htert甲基化的影响及其意义。方法收集初发儿童all患者外周血标本100例,取血浆进行病毒感染血清学检测,据血清学结果分为ebv单独感染组(20例),hcmv单独感染组(14例)ebv、hcmv联合感染组(41例)及全阴性对照组(15例)。从外周血标本分离单个核细胞,提取dna,亚硫酸氢钠盐修饰后,采用甲基化特异性(ms)-pcr法检测各组pten及htert基因dna启动子区甲基化水平的变化。结果ebv、hcmv联合感染组与对照组及单独感染组相比pten基因甲基化水平明显降低(p<0.05),htert甲基化水平有明显升高(p<0.05)。结论在儿童急性淋巴细胞白血病中,ebv和hcmv病毒联合感染使肿瘤相关基因pten及htert的甲基化水平改变,提示病毒感染可参与到基因表观遗传学调控,后续的研究还需进一步证明。
Management of Unilateral Masseter Hypertrophy and Hypertrophic Scar—A Case Report  [PDF]
Naresh Shetty,Rajanikanth K. Malaviya,M. K. Gupta
Case Reports in Dentistry , 2012, DOI: 10.1155/2012/521427
Abstract: Masseter muscle hypertrophy is a rare condition of idiopathic cause. It clinically presents as an enlargement of one or both masseter muscles. Most patients complain of facial asymmetry; however, symptoms such as trismus, protrusion, and bruxism may also occur. Several treatment options reported for masseter hypertrophy are present, which range from simple pharmacotherapy to more invasive surgical reduction. Keloid scar with unilateral masseter hypertrophy is a rarely seen in clinical practice. This paper reports a case of unilateral masseter hypertrophy with keloid scar in the angle of the mandible for which surgical treatment was rendered to the patient by using a single approach. 1. Introduction Masseter hypertrophy is usually an asymptomatic enlargement of one or both masseter muscles. In majority of the cases, the etiology is idiopathic. The highest incidence for this condition is in the second and third decades of life, with no gender predilection. A congenital variety also exists, but acquired masseter hypertrophy is more common. Unilateral occurrence can be seen when patients chew or clench primarily on one side. Muscle function may also be impaired, thus causing conditions such as trismus, protrusion, and bruxism. Numerous factors such as malocclusion, bruxism, clenching, or temporomandibular joint disorders, have been cited. The accurate diagnosis is more difficult in unilateral cases. A hypertrophied masseter will alter facial lines, cause generating discomfort, and negative cosmetic impacts in many patients. Masseter hypertrophy leads to the prominent mandibular angle which is aesthetically unacceptable to the patient. The differential diagnosis includes parotid tumor, lipoma, benign or malignant muscle tumors, and vascular tumors. 2. Case Report A 28-year-old male patient reported to the department of oral and maxillofacial surgery at people’s dental academy complaining of asymmetry of the face and scar in the mandibular angle region on the left side since 3 years. The patient gave a history that he had tripped and fallen down 3 years back and he had a laceration on the left side of the face that developed in to a scar. The patient’s chief complaint was left side facial growth without pain. The patient had no history of systemic diseases. Extraoral examination showed an obvious unilateral swelling centered over the mandibular angle. Palpation indicated that the swollen tissue was normal in tone and nontender. Mandibular movements were in the normal range. When the patient was asked to clench, the swelling became more prominent and firm. The
Are TNF-α and IL-1β the cause of post-burn hypertrophic scar tissue one year later?  [cached]
Patricia Mercadillo,Miguel Moreno,Adriana Rodriguez-Mendoza,Marco Cerbón
Medwave , 2011,
Abstract: Introduction. Post-burn hypertrophic scar tissue (H) is characterized by increased collagen synthesis, cellular growth and cell turnover. Its clinical characteristics exhibit aspects of chronic local inflammation, but the mechanism of its pathogenesis has not been clearly elucidated. In chronic skin inflammation, proinflammatory and profibrogenic cytokines play an important role in producing skin dysfunction. In this study, we examined changes in tumor necrosis factor (TNF)-α and interleukin (IL)-1β mRNA expression and its presence in post-burn hypertrophic scars. Results obtained in normotrophic scar tissue (N) were compared to results obtained in normal skin (NS). Materials and Methods. Skin biopsies were obtained from 15 patients with (H) who presented burns on over 10% of their skin surface, more than a year post-injury. N were obtained from 17 patients who experienced scarring in optimal conditions. NS were obtained from 11 patients who underwent cosmetic or reconstructive surgery. We performed histopathologic analysis with routine processing. TNF-α and IL-1β mRNA expression levels on all three types of biopsy were obtained by RT-PCR and in situ hybridization. Results. TNF-α and IL-1β mRNA expression was highly coordinated and was very similar in all the tissues processed and our histopathologic analysis yielded relatively low inflammatory infiltrate cell. But according to a semiquantitative analysis RT-PCR, TNF-α and IL-1β mRNA expression was significantly decreased in hypertrophic scars when they were compared to NS and N. Conclusions. These results suggest, that there not a differential expression TNF-α and IL-1β mRNA in hypertrophic scars a one year post injury. Interestingly, the keratinocytes showed minus expression of IL-1β mRNA compared to other cell types, which suggests that they may play an important role in post-burn skin repair processes.
The Effect of p38MAPK on Cyclic Stretch in Human Facial Hypertrophic Scar Fibroblast Differentiation  [PDF]
Qi-cui Du, Dai-zun Zhang, Xiu-juan Chen, Gui Lan-Sun, Min Wu, Wen-lin Xiao
PLOS ONE , 2013, DOI: 10.1371/journal.pone.0075635
Abstract: Hypertrophic scars (HTS), the excessive deposition of scar tissue by fibroblasts, is one of the most common skin disorders. Fibroblasts derived from surgical scar tissue produce high levels of α-smooth muscle actin (α-SMA) and transforming growth factor-β1 (TGF-β1). However, the molecular mechanisms for this phenomenon is poorly understood. Thus, the purpose of this study was to evaluate the molecular mechanisms of HTS and their potential therapeutic implications. Fibroblasts derived from skin HTS were cultured and characterized in vitro. The fibroblasts were synchronized and randomly assigned to two groups: cyclic stretch and cyclic stretch pre-treated with SB203580 (a p38MAPK inhibitor). Cyclic stretch at 10% strain was applied at a loading frequency of 10 cycles per minute (i.e. 5 seconds of tension and 5 seconds of relaxation) for 0 h, 6 h and 12 h. Cyclic stretch on HTS fibroblasts led to an increase in the expression of α-SMA and TGF-β1 mRNA and protein and the phosphorylation of p38MAPK. SB203580 reversed these effects and caused a decrease in matrix contraction. Furthermore, HTS fibroblast growth was partially blocked by p38MAPK inhibition. Therefore, the mechanism of cyclic stretch involves p38 MAPK, and its inhibition is suggested as a novel therapeutic strategy for HTS.
Texture Analysis on Two-photon Excited Microscopic Images of Human Skin Hypertrophic Scar Tissue
皮肤增生性疤痕组织的双光子显微图像纹理分析

XIE Zhi-ming,CHEN Guan-nan,CHEN Jian-xin,YANG Kun-tao,CHEN Rong,
谢志明 陈冠楠
,陈建新 杨坤涛 陈荣

中国图象图形学报 , 2009,
Abstract: According to the pathological characteristics of skin hypertrophic scar tissue, texture features on the edge direction, density distribution and geometric morphology are extracted from two-photon excited microscopic images of scar tissue and used to distinguish the normal tissue from scar tissue. Algorithms of mean-shift are applied to analyze the extracted texture features. Finally, a compositive formula is presented for quantitatively analyzing images. 118 two-photon excited microscopic images originated from human hypertrophic scar tissue are statistically analyzed based on this formula and the inaccuracy rate is 5.1%. These results indicate that texture features and analytic methods proposed in this paper are effective on distinguishing the normal tissue from scar tissue and accurately fixing on their border.
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