BACKGROUND 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 (miR-29b-3p)/collagen 1 alpha 1 (COL1A1). METHODS The 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. RESULTS The 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. CONCLUSION XIST 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.

中文翻译：

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LncRNA XIST通过靶向热损伤后人皮肤成纤维细胞中的miR-29b-3p / COL1A1来促进细胞外基质合成，增殖和迁移。

背景技术据报道，长的非编码RNA（lncRNA）与烧伤创面愈合过程中的真皮过程有关。这项研究旨在调查lncRNA X失活特异性转录本（XIST）在人皮肤成纤维细胞（HSF）和细胞外基质（ECM）中的作用，以及XIST / microRNA-29b-3p（miR-29b-3p ）/胶原蛋白1 alpha 1（COL1A1）。方法烧伤后第5天从25例深部较厚烧伤患者中收集伤口样本。使用HSF细胞建立热损伤模型。采用定量实时聚合酶链反应和western blot检测XIST，miR-29b-3p和COL1A1的表达。ECM合成，细胞增殖和迁移分别通过蛋白质印迹，细胞计数试剂盒8和trans-well分析来检测。通过生物信息学分析和荧光素酶报告基因分析探讨了miR-29b-3p与XIST或COL1A1之间的相互作用。结果热损伤后XIST和COL1A1表达增强，而miR-29b-3p表达降低。XIST的过表达促进了热损伤的HSF细胞中ECM的合成，细胞增殖和迁移。但是，XIST组合键起到相反的作用。miR-29b-3p过表达抑制ECM合成，细胞增殖和迁移，这被XIST逆转。COL1A1沉默通过miR-29b-3p靶向抑制ECM合成，细胞增殖和迁移。此外，COL1A1上调减弱了XIST沉默对ECM合成和HSF细胞功能的影响。结论XIST促进了ECM合成，