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Condition: Keloids

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Total 29 results found since Jan 2013.

Keloid Core Factor CTRP3 Overexpression Significantly Controlled TGF- < em > β < /em > 1-Induced Propagation and Migration in Keloid Fibroblasts
CONCLUSION: CTRP3 exerted an antifibrotic role through inhibiting proliferation, migration, and ECM accumulation of KFs via regulating TGF-β1/Smad signal path.PMID:37091895 | PMC:PMC10115533 | DOI:10.1155/2023/9638322
Source: Disease Markers - April 24, 2023 Category: Laboratory Medicine Authors: Lin He Chan Zhu Huicong Dou Xueyuan Yu Jing Jia Maoguo Shu 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

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

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

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

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

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

Syndecan-1 regulates extracellular matrix expression in keloid fibroblasts via TGF-β1/Smad and MAPK signaling pathways
Publication date: Available online 15 January 2020Source: Life SciencesAuthor(s): Jing Cui, Shan Jin, Chenglong Jin, Zhehu JinAbstractAimsThe present study aimed to explore the effect of syndecan-1 on keloid fibroblasts.Main methodsImmunohistochemistry and Western blot were employed to assess the expression of syndecan-1. Primary cultured keloid fibroblasts were transfected with syndecan-1 siRNA. The function of syndecan-1 on the proliferation of keloid fibroblasts was investigated through Cell Counting Kit-8 (CCK-8) and flow cytometry. Extracellular matrix, TGF-β1/Smad, and MAPK related proteins were evaluated by Western...
Source: Life Sciences - January 17, 2020 Category: Biology Source Type: research

Resveratrol inhibits proliferation and promotes apoptosis of keloid fibroblasts by targeting HIF-1 α.
In this study, keloid-derived fibroblasts were cultured under hypoxia environment and was treated by resveratrol. CCK-8 assay and Annexin V-FITC were used to evaluate cell activity and apoptosis level. Western blot and RT-qPCR were also used to assess the expression of HIF-α, Collagen I and Collagen III. Besides, siRNA was also used to explore the mechanisms of resveratrol's effect. In this study, hypoxia promotes proliferation and inhibits apoptosis of keloid fibroblasts. These findings highlight the potential obstacle in treating keloids. Furthermore, we demonstrated that resveratrol could reverse the effect of hypoxia ...
Source: Journal of Plastic Surgery and Hand Surgery - June 6, 2020 Category: Surgery Tags: J Plast Surg Hand Surg Source Type: research

Impaired collagen fibril assembly in keloids with enhanced expression of lumican and collagen V.
In conclusion, this study demonstrates impaired collagen assembly along with enhanced expression of lumican and collagen V, both are known for interfering with collagen fibril assembly. PMID: 33188736 [PubMed - as supplied by publisher]
Source: Archives of Biochemistry and Biophysics - November 11, 2020 Category: Biochemistry Authors: Zhou B, Tu T, Gao Z, Wu X, Wang W, Liu W Tags: Arch Biochem Biophys Source Type: research

Association between MeCP2 and Smad7 in the pathogenesis and development of pathological scars.
Authors: Li D, Yang E, Zhao J, Zhang H Abstract To explore the relationship between methylated binding protein 2 (MeCP2) and mothers against decapentaplegic homolog 7 (Smad7) in the pathogenesis and development of pathological scars. Immunohistochemistry, Western blot and real-time polymerase chain reaction (RT-PCR) were used to detect the expression of MeCP2 in different types of human scars and hypertrophic scars at different growth times. The methylation status of Smad7 gene promoter in different scar tissues was determined by methylation-specific PCR. After transfection with MeCP2-siRNA (small interfering RNA) ...
Source: Journal of Plastic Surgery and Hand Surgery - January 23, 2021 Category: Surgery Tags: J Plast Surg Hand Surg Source Type: research