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Condition: Keloids

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Total 29 results found since Jan 2013.

The mechanisms of β-catenin on keloid fibroblast cells proliferation and apoptosis.
CONCLUSIONS: Knockdown of β-catenin significantly decreased the proliferation and increased apoptosis of KFB, which could inhibit the formation of pathological scar. PMID: 29509234 [PubMed - in process]
Source: European Review for Medical and Pharmacological Sciences - March 8, 2018 Category: Drugs & Pharmacology Tags: Eur Rev Med Pharmacol Sci Source Type: research

Role of Homeodomain-Interacting Protein Kinase 2 in the Pathogenesis of Tissue Fibrosis in Keloid-Derived Keratinocytes
Abstract: Epithelial-mesenchymal transition (EMT) plays a critical role in fibrotic keloid formation, which is characterized by excessive collagen and extracellular matrix synthesis and deposition. Growing evidence suggests that the serine/threonine kinase homeodomain-interacting protein kinase 2 (HIPK2) acts upstream of several major fibrosis signaling pathways; however, the role of HIPK2 in the keloid fibrogenesis remains unknown. In the current study, we investigated the roles of HIPK2 in the pathogenesis of keloids. Primary normal skin and keloid keratinocytes were cultured and pretreated with transforming growth facto...
Source: Annals of Plastic Surgery - November 11, 2017 Category: Cosmetic Surgery Tags: Burn Surgery and Research Source Type: research

Transforming growth factor-beta inducible early gene-1 (TIEG1) represses Smad7-mediated activation of TGF- β1/Smad signaling in keloid pathogenesis
Transforming growth factor β (TGF-β)/Smad signaling plays a key role in excessive fibrosis and keloid formations. Smad7 is a negative feedback regulator that prevents activation of TGF-β/Smad signaling. However, the regulatory mechanism for Smad7 in the keloid pathogenic process remains elusive. Here, we show that expressi on of TGF-β inducible early gene-1 (TIEG1) is markedly higher in keloid fibroblasts (KFs), while protein, mRNA, and promoter activity levels of Smad7 are decreased. When TIEG1 was knocked down with small interfering RNA (siRNA), both the promoter activity and protein expression of Smad7 were increa s...
Source: Journal of Investigative Dermatology - January 16, 2017 Category: Dermatology Authors: Zhi-Cheng Hu, Fen Shi, Peng Liu, Jian Zhang, Dong Guo, Xiao-ling Cao, Chu-Fen Chen, Shanqiang Qu, Jia-Yuan Zhu, Bing Tang Tags: Original Article Source Type: research

A Role for Neuregulin-1 in Promoting Keloid Fibroblast Migration via ErbB2-mediated Signaling.
Abstract Keloid disease is a fibroproliferative tumour characterised by aggressive local invasion, evident from a clinically and histologically active migrating margin. During combined laser capture microdissection and microarray analysis-based in situ gene expression profiling, we identified upregulation of the polypeptide growth factor neuregulin-1 (NRG1) and ErbB2 oncogene in keloid margin dermis, leading to the hypothesis that NRG1 contributed to keloid margin migration through ErbB2-mediated signalling. The aim of this study was to probe this hypothesis through functional in vitro studies. Exogenous NRG1 addi...
Source: Acta Dermato-Venereologica - November 23, 2016 Category: Dermatology Authors: Jumper N, Hodgkinson T, Paus R, Bayat A Tags: Acta Derm Venereol Source Type: research

miR-21 promotes collagen production in keloid via Smad7
Conclusions miR-21 promoted collagen production in keloid by negatively regulating the expression of the Smad7.
Source: Burns - October 4, 2016 Category: Dermatology Source Type: research

Peroxisome proliferator-activated receptor- γ agonist troglitazone suppresses transforming growth factor-β1 signalling through miR-92b upregulation-inhibited Axl expression in human keloid fibroblasts in vitro.
This study explored the underlying mechanisms. Fibroblasts isolated from 25 keloid patients (KFs) and fibroblasts isolated from healthy controls (NSFBs) were also subjected to treatment with PPAR-γ agonist troglitazone and antagonist GW9662 or for transfection with miR-92 mimics or inhibitor, Axl siRNA, and miR-92b or Axl promoter constructs, as well as being subjected to qRT-PCR, ELISA, Western blot, protein array, luciferase, and ChIP assays. The data demonstrated that TGF-β1 and Axl proteins were significantly elevated in samples from keloid patients, while troglitazone treatment significantly reduced levels of TGF-β...
Source: American Journal of Translational Research - September 22, 2016 Category: Research Tags: Am J Transl Res Source Type: research

Oxidative Damage and Nuclear Factor Erythroid 2-Related Factor 2 Protein Expression in Normal Skin and Keloid Tissue.
CONCLUSION: Collectively, our data indicate that Nrf2 expression is downregulated in keloid tissues, and that Nrf2 is involved in the development of apoptosis in Nrf2 siRNA-transfected fibroblasts. We propose that a defective antioxidant system and apoptotic dysregulation may participate in keloid pathogenesis. PMID: 26512164 [PubMed]
Source: Annals of Dermatology - October 31, 2015 Category: Dermatology Tags: Ann Dermatol Source Type: research

Hsp70 Knockdown by siRNA Decreased Collagen Production in Keloid Fibroblasts.
CONCLUSION: Hsp70 overexpression likely plays an important role in the excessive collagen production by keloid fibroblasts. RNA interference has therapeutic potential for the treatment of keloids. PMID: 26446645 [PubMed - in process]
Source: Yonsei Medical Journal - October 9, 2015 Category: Universities & Medical Training Authors: Shin JU, Lee WJ, Tran TN, Jung I, Lee JH Tags: Yonsei Med J Source Type: research

2ME2 increase radiation‐induced apoptosis of keloid fibroblasts by targeting HIF‐1α in vitro
ConclusionsThe present study indicates that HIF‐1α might serve as a therapeutic target for keloids. Furthermore, suppression of HIF‐1α by 2ME2 may be a promising therapeutic adjuvant in radiation therapy for keloids.
Source: Australasian Journal of Dermatology - April 15, 2015 Category: Dermatology Authors: Fei Long, Loubin Si, Xiao Long, Bob Yang, Xiaojun Wang, Fuquan Zhang Tags: Original Research Source Type: research

2ME2 increase radiation ‐induced apoptosis of keloid fibroblasts by targeting HIF‐1α in vitro
ConclusionsThe present study indicates that HIF‐1α might serve as a therapeutic target for keloids. Furthermore, suppression of HIF‐1α by 2ME2 may be a promising therapeutic adjuvant in radiation therapy for keloids.
Source: Australasian Journal of Dermatology - April 14, 2015 Category: Dermatology Authors: Fei Long, Loubin Si, Xiao Long, Bob Yang, Xiaojun Wang, Fuquan Zhang Tags: Original Research Source Type: research

Keloid-derived keratinocytes acquire a fibroblast-like appearance and an enhanced invasive capacity in a hypoxic microenvironment in vitro.
In conclusion, the present findings demonstrate that the hypoxia/HIF‑1α microenvironment provides a favorable environment for keloid‑derived keratinocytes to adopt a fibroblast‑like appearance through EMT. This transition may be responsible for the enhanced capacity of keloid keratinocytes to invade, allowing the keloids to extend beyond the wound margin. PMID: 25777304 [PubMed - as supplied by publisher]
Source: International Journal of Molecular Medicine - March 13, 2015 Category: Molecular Biology Authors: Ma X, Chen J, Xu B, Long X, Qin H, Zhao RC, Wang X Tags: Int J Mol Med Source Type: research

NADPH oxidase‐2 is a key regulator of human dermal fibroblasts: a potential therapeutic strategy for the treatment of skin fibrosis
This article is protected by copyright. All rights reserved.
Source: Experimental Dermatology - June 30, 2014 Category: Dermatology Authors: Guo‐You Zhang, Liang‐Cai Wu, Tao Dai, Shi‐Yi Chen, An‐Yuan Wang, Kang Lin, Da‐Mu Lin, Jing‐Quan Yang, Biao Cheng, Li Zhang, Wei‐Yang Gao, Zhi‐Jie Li Tags: Regular Article Source Type: research

Ex vivo evaluation of antifibrotic compounds in skin scarring: EGCG and silencing of PAI-1 independently inhibit growth and induce keloid shrinkage
& Ardeshir Bayat
Source: Laboratory Investigation AOP - July 8, 2013 Category: Laboratory Medicine Authors: Farhatullah SyedRania A BagabirRalf PausArdeshir Bayat Tags: dexamethasone EGCG immunohistochemistry keloid organ culture PAI-1 siRNA Source Type: research

Is survivin a novel pathway for the treatment and pathogenesis of keloid?
Abstract: Keloids behave like benign tumors as they grow beyond the boundaries of the original wound margin, do not regress spontaneously, and recur despite treatments. Recently, accumulating evidences showed that survivin played an important role in cell growth, apoptotic resistance, and cell cycle control. More than that, survivin was confirmed to be associated with tumor angiogenesis and chemoresistance. Survivin blocker therapy has been proved to be a novel treatment in some kinds of tumors. Our preliminary work showed that survivin expression was significantly higher in keloids than in normal skin. The mRNA and protei...
Source: Medical Hypotheses - June 19, 2013 Category: Biomedical Science Authors: Yongqian Cao, Rui Zhang, Xiawei Wang, Ran Huo, Fagang Wang, Li Lin, Qiang Li, Yibing Wang Tags: Articles Source Type: research