Aberrantly expressed long noncoding RNAs in hypertrophic scar fibroblasts in vitro: A microarray study

Abstract

A hypertrophic scar is the result of abnormal repair of the body after trauma. Histopathologically, it is mostly the result of the excessive proliferation of fibroblasts and the accumulation of extracellular matrix. Accumulating evidence has demonstrated that long non-coding RNAs (lncRNAs) have a critical role in the regulation of gene expression and in the pathogenesis of diseases. However, the roles of lncRNAs in hypertrophic scars have remained elusive. The present study investigated the profiles of differentially expressed lncRNAs between fibroblasts derived from a hypertrophic scar and normal skin, and explored the possible mechanisms underlying the development of hypertrophic scars. Microarray data indicated that 6,104 lncRNAs and 2,952 mRNAs were differentially expressed. A set of differentially expressed transcripts as confirmed by reverse transcription-quantitative polymerase chain reaction. Gene Ontology and Kyoto Encyclopedia of Genes and Genomes pathway enrichment analyses were performed to determine the principal functions of the significantly deregulated genes. Furthermore, associated expression networks, including subgroup analysis, competing endogenous RNAs (ceRNAs) and coding-noncoding co-expression networks were constructed using bioinformatics methods. The homology between differentially expressed lncRNAs and mRNAs was assessed and two exon lncRNA were selected to explore their regulatory mechanisms. The ceRNA network inferred that NR_125715 acted as a competing endogenous RNA, bound to microRNA (miR)-141-3p, miR-200a-3p and miR-29 to regulate the expression of the miRs' targets, including transforming growth factor β2 (TGFB2). Similarly, NR_046402 acted as a competing endogenous RNA, which bound to miR-133a-3p.1 and miR-4469 to then regulate the expression of the miRs' targets, including DNA polymerase δ1, catalytic subunit (POLD1). In addition, co-expression analysis indicated that the expression of lncRNAs NR_125715 and NR_046402 was correlated with that of TGFB2 and POLD1 mRNA. The identification of these differentially expressed lncRNAs in the hypertrophic scar-derived fibroblasts in the present study, may provide novel insight into the functional interactions of lncRNA, miRNA and mRNA, and lead to novel theories for the pathogenesis and treatment of hypertrophic scars.

Effects of photoelectric therapy on proliferation and apoptosis of scar cells by regulating the expression of microRNA‐206 and its related mechanisms

“…The mean CT values of MIR‐206 in the three groups were 22.33, 20.95, and 20.11, respectively. According to the formula for calculating the relative expression of each sample, as far as the relative expression of mTOR is concerned, cells without laser irradiation showed the highest expression, cells irradiated by high‐energy laser had the lowest expression (0.56), and the expression in cells irradiated by low‐energy laser was 0.83 (Figure B). In contrast, the relative expression of miR‐206 was the lowest in non‐laser irradiated samples .…”

“…In contrast, the relative expression of miR-206 was the lowest in non-laser irradiated samples. 1 With the increase of laser energy, the relative expression of miR-206 increased. The relative expression of miR-206 in the high-energy laser irradiated group was 2.01 ( Figure 5C).…”

“…It mainly includes hypertrophic scar and keloid. 1 It is a kind of pathological repair with the imbalance of extracellular matrix synthesis and decomposition caused by excessive proliferation of fibroblasts and large amount of collagen synthesis and disorder of collagen fibre arrangement, which are the main histological manifestations. [2][3][4] PS mainly occurs secondary to burns, trauma, surgery, infection, and so on.…”

Serum coding and non‐coding RNAs as biomarkers of NAFLD and fibrosis severity

“…It has been reported that TGFB2‐OT1 is involved in the negative regulation of apoptosis and positive regulation of autophagy and inflammation in vascular endothelial cells . Long Xiang Tu and colleagues reported the up‐regulation of TGFB2‐OT1 in fibroblasts derived from hypertrophic scars, suggesting its involvement in excessive proliferation of fibroblasts and accumulation of extracellular matrix . As concerns TGFB2, its pro‐fibrogenic role and/or its increased gene or protein expression has been reported in lens fibrosis, kidney fibrosis, cardiac fibrosis and liver fibrosis …”

“…31,44 Long Xiang Tu and colleagues reported the up-regulation of TGFB2-OT1 in fibroblasts derived from hypertrophic scars, suggesting its involvement in excessive proliferation of fibroblasts and accumulation of extracellular matrix. 45 As concerns TGFB2, its pro-fibrogenic role and/or its increased gene or protein expression has been reported in lens fibrosis, kidney fibrosis, cardiac fibrosis and liver fibrosis. 46 Several studies reported the involvement of BNIP3L in the regulation of pathways associated with NASH pathogenesis, specifically, apoptosis, necrosis, autophagy and fibrosis.…”