Identification and integrated analysis of microRNA expression profiles in keloid

Zhong, Lianmei; Bian, Ligong; Lyu, Jing; Jin, Hailing; Liu, Zijie; Lyu, Lechun; Lü, Di

doi:10.1111/jocd.12706

Cited by 24 publications

(21 citation statements)

References 25 publications

(41 reference statements)

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Section: Mirna Expression Profiles In Keloidmentioning

confidence: 99%

“…Through applying the same approach, Zhong et al revealed that 264 miRNAs were significantly altered in keloid [32]. The miRNA-199a-5p, miRNA-21-5p, miRNA-214-5p, miRNA-424-5p, and miRNA-205-5p, were the high-frequency DE miRNAs and were mainly associated with MAPK and HIF-1 signaling pathway by KEGG enrichment analysis [32]. Besides, it was very meaningful that Luan et al characterized the miRNA expression profiling in the sera from 9 keloid patients and 7 normal controls, identifying the 37 DE miRNA [33].…”

Section: Mirna Expression Profiles In Keloidmentioning

confidence: 99%

See 1 more Smart Citation

Epigenetic modification mechanisms involved in keloid: current status and prospect

Ren

Hou

et al. 2020

Clin Epigenet

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Keloid, a common dermal fibroproliferative disorder, is benign skin tumors characterized by the aggressive fibroblasts proliferation and excessive accumulation of extracellular matrix. However, common therapeutic approaches of keloid have limited effectiveness, emphasizing the momentousness of developing innovative mechanisms and therapeutic strategies. Epigenetics, representing the potential link of complex interactions between genetics and external risk factors, is currently under intense scrutiny. Accumulating evidence has demonstrated that multiple diverse and reversible epigenetic modifications, represented by DNA methylation, histone modification, and non-coding RNAs (ncRNAs), play a critical role in gene regulation and downstream fibroblastic function in keloid. Importantly, abnormal epigenetic modification manipulates multiple behaviors of keloid-derived fibroblasts, which served as the main cellular components in keloid skin tissue, including proliferation, migration, apoptosis, and differentiation. Here, we have reviewed and summarized the present available clinical and experimental studies to deeply investigate the expression profiles and clarify the mechanisms of epigenetic modification in the progression of keloid, mainly including DNA methylation, histone modification, and ncRNAs (miRNA, lncRNA, and circRNA). Besides, we also provide the challenges and future perspectives associated with epigenetics modification in keloid. Deciphering the complicated epigenetic modification in keloid is hopeful to bring novel insights into the pathogenesis etiology and diagnostic/therapeutic targets in keloid, laying a foundation for optimal keloid ending.

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Section: Mirna Expression Profiles In Keloidmentioning

confidence: 99%

Section: Mirna Expression Profiles In Keloidmentioning

confidence: 99%

Epigenetic modification mechanisms involved in keloid: current status and prospect

Ren

Hou

et al. 2020

Clin Epigenet

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“…Noticeably, Chao et al . (8) reported 264 miRNAs were significantly altered in keloid lesions compared with normal skin tissue. For example, miR-21 (9) and miR-199a-5p (10) were shown to participate in keloid proliferation, migration and apoptosis.…”

Section: Introductionmentioning

confidence: 99%

MicroRNA-152-5p inhibits proliferation and migration and promotes apoptosis by regulating expression of Smad3 in human keloid fibroblasts

Pang

Wang

et al. 2019

BMB Rep.

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Keloids are the most common pathological form of trauma healing, with features that seriously affect appearance and body function, are difficult to treat and have a high recurrence rate. Emerging evidence suggests that miRNAs are involved in a variety of pathological processes and play an important role in the process of fibrosis. In this study, we investigated the function and regulatory network of miR-152-5p in keloids. The miRNA miR-152-5p is frequently downregulated in keloid tissue and primary cells compared to normal skin tissue and fibroblasts. In addition, the downregulation of miR-152-5p is significantly associated with the proliferation, migration and apoptosis of keloid cells. Overexpression of miR-152-5p significantly inhibits the progression of fibrosis in keloids. Smad3 is a direct target of miR-152-5p, and knockdown of Smad3 also inhibits fibrosis progression, consistent with the overexpression of miR-152-5p. The interaction between miR-152-5p and Smad3 occurs through the Erk1/2 and Akt pathways and regulates collagen3 production. In summary, our study demonstrates that miR-152-5p/Smad3 regulatory pathways involved in fibrotic progression may be a potential therapeutic target of keloids.

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“…In this study, analysis of the KEGG pathway between I group and N group revealed that all of the DEGs were primarily enriched in cytokine−cytokine receptor interaction and viral protein interaction with cytokine and cytokine receptor, re ecting that these pathways may affect keloid formation. A study by Zhong L et al identi ed that target genes were associated with the MAPK signaling pathway and HIF-1 signaling pathway [31]. Our study provides a new eld for the molecular study of keloids.…”

Section: Discussionmentioning

confidence: 63%

“…In all, 8 patients (5 keloid patients without in ammation other than the keloid mass and 3 keloid patients with in ammation besides the keloid mass) were randomly selected from the department of plastic surgery at Peking Union Medical College Hospital between January 2019 and March 2020. The information of keloid patients (gender, age) was collected, and the keloid's condition was assessed by modi ed Vancouver scar scale (mVSS) 31 according to the pigmentation, vascularity, pliability and height of the keloid lesions (Table 1). There were 4 male patients and 4 female patients in each group; their ages ranged from 18 to 37 years.…”

Section: Patients and Groupingmentioning

confidence: 99%

Characteristics of Tumor Immune Gene and Immune Cell Infiltration during Keloid Formation

Líu

Shan

Wang

et al. 2020

Preprint

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Background: Keloids are benign fibroproliferative skin tumors that can cause disfigurement and disability. Although current research has sought to examine keloids from the perspectives of genetics, inflammation, immunity, and tumorigenesis, their pathological mechanisms remain unclear. Methods: In this study, we used three datasets of tumor immune gene expression profiling from the normal skin tissue of keloid patients (N group), inflammation tissue of keloid patients (I group), and keloid tissue of keloid patients (K group) to describe the occurrence and characteristics of keloid development. Tumor immune-related genes were analyzed, and the differentially expressed genes (DEGs) between the three groups were compared. Gene Ontology (GO) categories and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway enrichment analysis were carried out to determine the main functions of the differentially expressed genes and keloid-related pathways. Results: We identified several genes that may play an important role in keloid development. These genes are CCR1, SELL, CCR7, CD40LG, CD69, CXCL8, ITGAM, ITGAX, CD86, and CXCL9. GO analysis revealed that there were variations in biological processes (BP) between I group and N group, including regulation of lymphocyte activation and T-cell activation. Similar variations were also found between I group and K group, which may play an important role in keloid initiation and formation. Variations in molecular function (MF) were markedly enriched in cytokine receptor binding and receptor ligand activity. Analysis of the KEGG pathway between I group and N group revealed that DEGs were primarily enriched in cytokine−cytokine receptor interaction and viral protein interaction with cytokine and cytokine receptor. We identified a higher proportion of M2 macrophages in N group than in I group, although the difference was not obvious. M1 macrophage production differed significantly between I group and K group. The proportions of CD8+T cells varied significantly between N group and K group. We traced multiple tumor immune-related hub genes from keloid formation and analyzed immune cell subsets in keloid development. Possible molecular mechanisms were described in this study using bioinformatics. Conclusions: These results provide another possibility to elucidate keloid pathogenesis and therapeutic targets in terms of tumor immune gene expression.

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Identification and integrated analysis of microRNA expression profiles in keloid

Abstract: This study revealed the profiling of miRNAs in keloid that are potentially implicated in the development of this disease and could serve as novel diagnostic and therapeutic target of keloid.

Cited by 24 publications

References 25 publications

Epigenetic modification mechanisms involved in keloid: current status and prospect

Epigenetic modification mechanisms involved in keloid: current status and prospect

MicroRNA-152-5p inhibits proliferation and migration and promotes apoptosis by regulating expression of Smad3 in human keloid fibroblasts

Characteristics of Tumor Immune Gene and Immune Cell Infiltration during Keloid Formation

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