Serum microRNA screening and functional studies reveal miR-483-5p as a potential driver of fibrosis in systemic sclerosis

Abstract

Our findings showed that miR-483-5p is up-regulated in the serum of SSc patients, from the early stages of the disease onwards, and indicated its potential function as a fine regulator of fibrosis in SSc.

MicroRNA in localized scleroderma: a review of literature

“…These results indicate that miRNA-483-5p may be distinctive for conditions characterized by fibrosis of the skin [7]. Furthermore, researchers exhibited that miRNA-483-5p overexpression in endothelial cells increased the transcriptional levels of α-SMA (alpha-smooth muscle actin) and SM22A (smooth muscle protein 22-alpha)-indicators of myofibroblast differentiation [7]. Additionally, miRNA-483-5p decreased the level of Fli-1 (friend leukemia virus integration 1)-a negative regulator of extracellular matrix [7].…”

“…MicroRNA-483-5p is a molecule supposed to be a specific marker for skin fibrosis. Chouri and co-workers demonstrated that miRNA-483-5p was upregulated both in localized scleroderma (22) and systemic scleroderma (107) serum samples, unlike other autoimmunologic diseases [systemic lupus erythematosus (33), Sjögren's syndrome (23)] [7]. These results indicate that miRNA-483-5p may be distinctive for conditions characterized by fibrosis of the skin [7].…”

“…Chouri and co-workers demonstrated that miRNA-483-5p was upregulated both in localized scleroderma (22) and systemic scleroderma (107) serum samples, unlike other autoimmunologic diseases [systemic lupus erythematosus (33), Sjögren's syndrome (23)] [7]. These results indicate that miRNA-483-5p may be distinctive for conditions characterized by fibrosis of the skin [7]. Furthermore, researchers exhibited that miRNA-483-5p overexpression in endothelial cells increased the transcriptional levels of α-SMA (alpha-smooth muscle actin) and SM22A (smooth muscle protein 22-alpha)-indicators of myofibroblast differentiation [7].…”

“…Furthermore, researchers exhibited that miRNA-483-5p overexpression in endothelial cells increased the transcriptional levels of α-SMA (alpha-smooth muscle actin) and SM22A (smooth muscle protein 22-alpha)-indicators of myofibroblast differentiation [7]. Additionally, miRNA-483-5p decreased the level of Fli-1 (friend leukemia virus integration 1)-a negative regulator of extracellular matrix [7]. In previous studies, miRNA-483-5p was revealed to target Matn3 (matrillin 3) and TIMP2 (tissue inhibitor of metalloproteinase 2) to enhance extracellular matrix degradation, chondrocyte hypertrophy and cartilage angiogenesis [32].…”

Using Machine Learning to Molecularly Classify Systemic Sclerosis Patients

“…Surprisingly, despite laying a strong foundation for molecular SSc classification, these genes did not contain some of the crucial SSc‐associated genes, such as CD247 , STAT4 , TLR8 , IRF5 , IRF4 , and IRF7 . Several recent studies have shown that genetic and epigenetic profiling of specific cell types provides more information on disease mechanisms and phenotypes than whole tissue or peripheral blood mononuclear cell profiling . For example, CXCL4 has been shown to be a predictive biomarker for SSc progression and was captured by independent dendritic cell profiling or by proteomic profiling of blood and skin .…”