Cyclic tensile strain promotes the ECM synthesis of cranial base synchondrosis chondrocytes by upregulating miR‐140‐5p. (30th September 2019)

• Record Type: Journal Article
• Authors: Cheng, Mingjia; Chu, Fengting; Feng, Qiping; Shen, Gang
• Is Part Of: Orthodontics and craniofacial research. Volume 23:Number 1(2020)
• Page Start: 44
• Page End: 49
• Publication Date: 2019-09-30
• Subjects: Bloc1s -- cranial base synchondrosis -- cyclic tensile strain -- MiR‐140‐5p; Skull -- Growth -- Periodicals; Facial bones -- Growth -- Periodicals; Orthodontics -- Periodicals; Orthodontics, Corrective -- Periodicals; Orthodontic appliances -- Periodicals; 617.51
• DOI: 10.1111/ocr.12341
• Languages: English
• ISSNs: 1601-6335

Abstract

Abstract: Objective: This study aimed to explore the role of miR‐140‐5p in cranial base synchondrosis chondrocytes (CBSCs) under cyclic tensile strain (CTS). Setting and Sample Population: A total of 25 1‐week‐old Sprague Dawley rats from Shanghai Laboratory Animal Center, Chinese Academy of Sciences, were used. Material and Methods: The second passage of CBSCs was applied with CTS at 10% elongation (1 Hz) for 24 hours. MiR‐140‐5p levels in CBSCs were detected by qRT‐PCR. The role of miR‐140‐5p in CBSCs was evaluated by transfection of mimics and inhibitor. RNA sequencing and online search of miRNA databases (TargetScan, miRDB and miRanda) were used in prediction of miR‐140‐5p targets. A luciferase reporter assay was applied to identify the target gene of miR‐140‐5p. Results: Compared with the control, the expression of Col2a1 and Sox9 was significantly higher after CTS ( P < .05). Also, CBSCs demonstrated higher expression of miR‐140‐5p after CTS loading for 24 hours ( P < .05). Overexpression of miR‐140‐5p promoted ECM synthesis under CTS loading environment, while suppression of miR‐140‐5p inhibited the effect. Bloc1s2 was a putative target gene of miR‐140‐5p. Conclusions: The expression of ECM in CBSCs could be promoted by CTS and miR‐140‐5p might play a role in this process through targeting Bloc1s2.