Abstract
BackgroundLong noncoding RNAs (lncRNAs) have been reported to be associated with dermis process during burn wound healing. This study aimed to investigate the role of lncRNA X-inactive specific transcript (XIST) in human skin fibroblasts (HSF) and extracellular matrix (ECM) as well as the regulatory network of XIST/microRNA-29b-3p (miR-29b-3p)/collagen 1 alpha 1 (COL1A1).MethodsThe wound samples were collected from 25 patients with deep partial thickness burn at day 5 after burn. The thermal injured model was established using HSF cells. The expressions of XIST, miR-29b-3p and COL1A1 were measured by quantitative real-time polymerase chain reaction and western blot. ECM synthesis, cell proliferation and migration were detected by western blot, cell counting kit-8 and trans-well assays, respectively. The interaction between miR-29b-3p and XIST or COL1A1 was explored by bioinformatics analysis and luciferase reporter assay.ResultsThe expressions of XIST and COL1A1 were enhanced but miR-29b-3p expression was decreased after thermal injury. XIST overexpression promoted ECM synthesis, cell proliferation and migration in thermal injured HSF cells. However, XIST knockdown played an opposite effect. miR-29b-3p overexpression inhibited ECM synthesis, cell proliferation and migration, which was reversed by XIST. COL1A1 silence suppressed ECM synthesis, cell proliferation and migration by miR-29b-3p targeting. Moreover, COL1A1 up-regulation weakened the effect of XIST silence on ECM synthesis and HSF cell function.ConclusionXIST promoted ECM synthesis, cell proliferation and migration by sponging miR-29b-3p and targeting COL1A1 in HSF cells after thermal injury, indicating the promoting role of XIST in wound healing.
Highlights
The therapy of deep burn wound is challenged because of the scar formation and poor function after wound healing
The expressions of X-inactive specific transcript (XIST), miR‐29b‐3p and Collagen 1 alpha 1 (COL1A1) are altered during wound healing To explore the potential role of XIST, miR-29b-3p and COL1A1 in wound healing, their expression levels were measured in burn wounds
XIST promotes extracellular matrix (ECM) synthesis, cell proliferation and migration in thermal injured‐human skin fibroblasts (HSF) cells To investigate the biological role of XIST during wound healing, HSF cells were transfected with si-NC, si-XIST, pcDNA or XIST, followed by treatment of thermal injury
Summary
The therapy of deep burn wound is challenged because of the scar formation and poor function after wound healing. The dermis plays an essential role in wound repair through maintaining human skin fibroblast function and extracellular matrix (ECM) synthesis to improve scar quality [1]. Long noncoding RNAs (lncRNAs) exert their functions by acting as sponges of microRNAs (miRNAs) or competing endogenous RNAs (ceRNAs) for miRNAs to derepress mRNAs [3]. LncRNAs have been suggested to play vital roles in wound healing after thermal injury. Long noncoding RNAs (lncRNAs) have been reported to be associated with dermis process during burn wound healing. This study aimed to investigate the role of lncRNA X-inactive specific transcript (XIST) in human skin fibroblasts (HSF) and extracellular matrix (ECM) as well as the regulatory network of XIST/microRNA-29b-3p (miR29b-3p)/collagen 1 alpha 1 (COL1A1)
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