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Background: Auricular keloids are difficult to treat, and recurrent keloids are more aggressive and more likely to develop aural deformities. Surgical excision, injections, or radiotherapy alone have high recurrence rates. An algorithmic approach of auricular keloid remains to be explored., Aims: To investigate the sequential treatment protocol for the treatment of auricle keloids to maintain auricle morphology and reduce the postoperative recurrence rate., Patients/methods: A retrospective analysis of 42 patients who attended the scar minimally invasive treatment center of the Hospital of Plastic Surgery, Chinese Academy of Medical Sciences for serial treatment from January 2019 to June 2021. According to the size and involvement of the keloid, the core excision of the scar was excised under the condition of ensuring the priority of the auricular contour, and the scar flap was repaired to reconstruct the auricular appearance, and electron beam treatment was performed within 24 h after the operation, ray energy: 6-7 MeV, dose: Dt18Gy/2f; regular trimethoprim combined with 5-Fu injection treatment and the application of silicone ear clips for local compression treatment were performed 1 month after the operation., Results: Thirty-five patients were followed up from 12 to 40 months after surgery, and three of them showed a tendency of recurrence, and early local treatment with trimethoprim and 5-Fu injection achieved favorable results., Conclusion: A standardized and sequential treatment plan for keloids with different morphology and anatomical locations can achieve remodeling of the auricular morphology and maintain long-term results., (© 2022 The Authors. Journal of Cosmetic Dermatology published by Wiley Periodicals LLC.)

Keloid is the abnormal wound healing puzzled by the aggressive growth and high recurrence rate due to its unrevealed key pathogenic mechanism. MicroRNAs contribute to a series of biological processes including epithelial-mesenchymal transition (EMT) and cells stemness involved in fibrotic disease. Here, using microRNAs microarray analysis we found mir-21-5p was significantly up-regulated in keloid epidermis. To investigate the role of miR-21-5p in keloid pathogenesis, we transfected miR-21-5p mimic or inhibitor in keloid keratinocytes and examined the abilities of cell proliferation, apoptosis, migration and invasion, the expressions of EMT-related markers vimentin and E-cadherin and stem-like cells-associated markers CD44 and ALDH1, and the involvement of PTEN and the signaling of AKT and ERK. Our results demonstrated that up-regulation or knockdown of miR-21-5p significantly increased or decreased the migration, invasion and sphere-forming abilities of keloid keratinocytes, and the phenotype of EMT and cells stemness were enhanced or reduced as well. Furthermore, PTEN and p-AKT were shown to participate in the regulation of miR-21-5p on EMT phenotypes and stemness signatures of keloid keratinocytes, which might account for the invasion and recurrence of keloids. This molecular mechanism of miR-21-5p on keloid keratinocytes linked EMT with cells stemness and implicated novel therapeutic targets for keloids.

Keloid is a skin fibrotic disease with the characteristics of recurrence and invasion, its pathogenesis still remains unrevealed. The epithelial-mesenchymal transition (EMT) is critical for wound healing, fibrosis, recurrence, and invasion of cancer. We sought to investigate the EMT in keloid and the mechanism through which the EMT regulates keloid formation. In keloid tissues, the expressions of EMT-associated markers and transforming growth factor (TGF)-β1/Smad3 signaling were examined by immunohistochemistry. In the keloid epidermis and dermal tissue, the expressions of genes related to the regulation of skin homeostasis, fibroblast growth factor receptor 2 (FGFR2) and p63, were analyzed using quantitative real-time polymerase chain reaction. The results showed that accompanying the loss of the epithelial marker E-cadherin and the gain of the mesenchymal markers fibroblast-specific protein 1 (FSP1) and vimentin in epithelial cells from epidermis and skin appendages, and in endothelial cells from dermal microvessels, enhanced TGF-β1 expression and Smad3 phosphorylation were noted in keloid tissues. Moreover, alternative splicing of the FGFR2 gene switched the predominantly expressed isoform from FGFR2-IIIb to -IIIc, concomitant with the decreased expression of ΔNp63 and TAp63, which changes might partially account for abnormal epidermis and appendages in keloids. In addition, we found that TGF-β1-induced hair follicle outer root sheath keratinocytes (ORSKs) and normal skin epithelial cells underwent EMT in vitro with ORSKs exhibiting more obvious EMT changes and more similar expression profiles for EMT-associated and skin homeostasis-related genes as in keloid tissues, suggesting that ORSKs might play crucial roles in the EMT in keloids. Our study provided insights into the molecular mechanisms mediating the EMT pathogenesis of keloids., (© 2015 by the Wound Healing Society.)

Objective: To construct and characterize the TGF-β1, induced epithelial-mesenchymal transition (EMT) model of keloid epithelial cells in vitro, and to investigate the expression of epithelial stem cells related surface markers in keloid epithelial cells during EMT induction., Methods: The epithelial cells from 3 keloid samples of ears were cultured in vitro and induced by transforming growth factor betal (TGF-β1, 1 ng/ml) for 5 days, which was the experimental group, the same cells untreated were considered as the negative control group. The expressions of EMT-associated markers and regulative genes were detected using immunofluorescence staining, real-time PCR and western blot analysis. Then the surface markers of epithelial stem cells were detected using real-time PCR. Statistical significance was determined using Independent-Samples t Test, a p value less than 0. 05 was considered statistically significant., Results: The mRNA expression of transcription factor snail2 and mesenchymal-specific marker vimentin increased significantly in TGF-β1, induced keloid epithelial cells (P < 0. 05), in which snail2 increasing from 0. 91 ± 0. 23 to 1. 69 ± 0. 10, and vimentin from 5. 86 ± 2. 07 to 24. 29 ± 5. 39. Whereas the mRNA expression of epithelial-specific marker E-cadherin decreased from 1. 06 ± 0. 19 to 0. 65 ± 0. 09. The mRNA expression of CD29 and Lgr6, two surface markers of epithelial stem cells, significantly increased after induction of the TGF-β1, (P < 0. 05), from 0. 55 ± 0. 14 and 1. 61 ± 0. 31 to 1. 19 ± 0. 12 and 3. 84 t 0. 62 respectively. In induced cells, the immunofluorescence results showed staining of E- cadherin became faint, but the number of positive staining cells of vimentin increased. Western blot confirmed the protein expression of E-cadherin weakened, and the vimentin and p-Smad3 enhanced (P < 0. 05)., Conclusions: TGF-β1, initiated EMT in keloid epithelial cells by inducing the up-regulation of snail2, and TGF-β1,/Smad3 signaling pathway was involved in EMT. EMT could change the phenotype of epithelial stem cells in keloid.

Background: The high recurrence rate after nonsurgical treatment of keloid is a major challenge for clinicians. Although there are many existing treatment options, how to optimize and upgrade the existing options and make a reasonable combination of utilization is our concern. The aim of this study is to provide a comprehensive non‐surgical treatment for keloid—cocktail therapy. Methods: According to the different changes of keloid with treatment, the treatment was divided into four stages, and different treatment schemes were adopted for each stage. The incidence of side effects of keloid at each stage and the effective rate and cure rate 16 months after the end of treatment were analyzed. Results: All patients completed this study on time, and were followed up 16 months after the end of treatment, the treatment effective rate was 100%, and the cure rate was up to 92.8%. Conclusion: Cocktail therapy can achieve a higher cure rate of keloid, and is worthy of clinical promotion. [ABSTRACT FROM AUTHOR]