MicroRNA Expression Abnormalities in Limited Cutaneous Scleroderma and Diffuse Cutaneous Scleroderma

Zhu, Honglin; Li, Yisha; Qu, Shunlin; Luo, Hui; Zhou, Yujun; Wang, Yanping; Zhao, Hongjun; You, Yun; Xiao, Xianzhong; Zuo, Xiaoxia

doi:10.1007/s10875-011-9647-y

Cited by 138 publications

(108 citation statements)

References 22 publications

(24 reference statements)

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“…Independently, the down-regulation of miR-29 is confirmed along with miR-145 and the up-regulation of miR-21 [42]. miR-29 targets collagen [22,42] and is shown to be down-regulated in response to TGF-b1 and platelet derivative growth factor. miR-196a is down-regulated in explanted KFs and directly targets transcripts of collagens genes (COL1A1 and COL3A1) [34].…”

Section: Discussionmentioning

confidence: 87%

“…miR-29 is down-regulated in scleroderma biopsy specimens, explanted fibroblasts, and bleomycin-induced skin fibrosis [22]. Independently, the down-regulation of miR-29 is confirmed along with miR-145 and the up-regulation of miR-21 [42]. miR-29 targets collagen [22,42] and is shown to be down-regulated in response to TGF-b1 and platelet derivative growth factor.…”

Section: Discussionmentioning

confidence: 92%

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Comparative study of microRNA profiling in keloid fibroblast and annotation of differential expressed microRNAs

Li¹,

Bai²,

Liu³

et al. 2013

ABBS

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Keloids are tumor-like skin scars that grow as a result of the aberrant healing of skin injuries, with no effective treatment. The molecular mechanism underlying keloid pathogenesis is still largely unknown. In this study, we compared microRNA (miRNA) expression profiles between keloidderived fibroblasts and normal fibroblasts (including fetal and adult dermal fibroblasts) by miRNA microarray analysis. We found that the miRNA profiles in keloid-derived fibroblasts are different with those in normal fibroblasts. Nine miRNAs were differentially expressed, six of which were significantly up-regulated in keloid fibroblasts (KFs), including miR-152, miR-23b-3p, miR-31-5p, miR-320c, miR-30a-5p, and hsv1-miR-H7, and three of which were significantly down-regulated, including miR-4328, miR-145-5p, and miR-143-3p. Functional annotations of differentially expressed miRNA targets revealed that they were enriched in several signaling pathways important for scar wound healing. In conclusion, we demonstrate that the miRNA expression profile is altered in KFs compared with in fetal and adult dermal fibroblasts, and the expression profile may provide a useful clue for exploring the pathogenesis of keloids. miRNAs might partially contribute to the etiology of keloids by affecting several signaling pathways relevant to scar wound healing.

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Section: Discussionmentioning

confidence: 87%

Section: Discussionmentioning

confidence: 92%

Comparative study of microRNA profiling in keloid fibroblast and annotation of differential expressed microRNAs

Li¹,

Bai²,

Liu³

et al. 2013

ABBS

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“…Zhu and colleagues identified an upregulation of miR-21 in SSc-FB and skin [56]. The putative targets for miR-21 are SMAD7 and COL1A1.…”

Section: Mir-21mentioning

confidence: 99%

Epigenetics and systemic sclerosis

Altorok

Kahaleh

2015

Semin Immunopathol

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Systemic sclerosis (SSc) is an autoimmune connective tissue disease characterized by vascular injury, activation of the immune system, and diffuse tissue fibrosis. The precise etiology of SSc is undetermined, but there is evidence suggestive of a connection between environmental factors and SSc pathogenesis. In general, harmful environmental factors are sensed by the epigenetic regulatory mechanisms that alter host gene expression leading to the emergence of disease-specific phenotype. There are three epigenetic mechanisms involved in gene regulation: DNA methylation, histone modifications, and microRNAs. Although there is evidence that SSc phenotype could be, to a some degree, determined by genetic variants, it is clear now that non-genetic factors outweigh the genetic risk in SSc. Accordingly, the environment can trigger epigenetic regulation that in turn establishes a molecular framework linking environmental exposures to genetics, leading to the disease process, possibly in a genetically predisposed host. Although we have just begun to appreciate the potential role of epigenetics in SSc, many important and promising clues have been observed. In this review, we will summarize the work that has been done in the field of epigenetic regulation in SSc, and we will discuss possible factors and mechanisms that may lead to epigenetic dysregulation in SSc.

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“…A beneficial effect of intravenously administered miR-29 in the mouse model of pulmonary fibrosis has been demonstrated [130]. miR-29a is strongly downregulated in SSc fibroblasts and skin sections compared with healthy controls [131]. let-7d miRNA is consistently downregulated in IPF lungs and is believed to play a crucial role in inhibiting epithelial-mesenchymal differentiation [132].…”

Section: Epigenetic Biomarkers (Micrornas)mentioning

confidence: 99%

Personalised medicine in interstitial lung diseases

2018

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Interstitial lung diseases in general, and idiopathic pulmonary fibrosis in particular, are complex disorders with multiple pathogenetic pathways, various disease behaviour profiles and different responses to treatment, all facets that make personalised medicine a highly attractive concept. Personalised medicine is aimed at describing distinct disease subsets taking into account individual lifestyle, environmental exposures, genetic profiles and molecular pathways. The cornerstone of personalised medicine is the identification of biomarkers that can be used to inform diagnosis, prognosis and treatment stratification. At present, no data exist validating a personalised approach in individual diseases. However, the importance of the goal amply justifies the characterisation of genotype and pathway signatures with a view to refining prognostic evaluation and trial design, with the ultimate aim of selecting treatments according to profiles in individual patients.

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MicroRNA Expression Abnormalities in Limited Cutaneous Scleroderma and Diffuse Cutaneous Scleroderma

Cited by 138 publications

References 22 publications

Comparative study of microRNA profiling in keloid fibroblast and annotation of differential expressed microRNAs

Comparative study of microRNA profiling in keloid fibroblast and annotation of differential expressed microRNAs

Epigenetics and systemic sclerosis

Personalised medicine in interstitial lung diseases

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