Endo 180 participates in collagen remodeling of the periodontal ligament during orthodontic tooth movement

• Published in: BMC oral health 2024-12, Vol.24 (1), p.1576-10, Article 1576
• Main Authors: Chen, Liyuan, He, Danqing, Li, Zixin, Cui, Shengjie, Yu, Min, Zhao, Zimo, Chen, Yuetong, Song, Jiayi, Jiang, Nan, Yu, Huajie, Liu, Yan
• Format: Article
• Language: English
• Subjects: Alveolar bone; Animals; Antibodies; Atomic force microscopy; Bone remodeling; Cell surface receptors; Collagen; Collagen (type I); Collagen (type III); Collagen - metabolism; Collagen remodeling; Collagen Type I - metabolism; Collagen Type III - metabolism; Computed tomography; Down-regulation; Electrons; Endo180; Fibroblasts; Gene expression; Immunofluorescence; Ligaments; Male; Mechanical force; Mechanical properties; Microscopy; Microscopy, Atomic Force; Orthodontic tooth movement; Orthodontics; Pancreatic cancer; Periodontal ligament; Periodontal Ligament - metabolism; Periodontal ligament cell; Protein structure; Rats; Rats, Sprague-Dawley; siRNA; Software; Structure-function relationships; Teeth; Therapeutic targets; Thrombolytic drugs; Tooth Movement Techniques - methods; U-Plasminogen activator; X-Ray Microtomography
• ISSN: 1472-6831; 1472-6831
• DOI: 10.1186/s12903-024-05362-8

Orthodontic tooth movement (OTM) relies on the remodeling of periodontal tissues, including the periodontal ligament (PDL) and alveolar bone. Collagen remodeling plays a crucial role during this process, allowing for the necessary changes in the PDL's structure and function. Endo180, an urokinase plasminogen activator receptor-associated protein, is a transmembrane receptor regulated collagen remodeling. This study aims to investigate whether and how Endo180 participates in collagen remodeling within the PDL during OTM. A mechanical force-induced OTM rat model was established using a closed coiled spring to mesially move the right maxillary first molar. The distance of OTM was examined by micro-computed tomography (micro-CT). The collagen remodeling within the PDL was assessed using atomic force microscope (AFM), Hematoxylin-Eosin (HE) staining and Masson staining. Protein expressions of Endo180, collagen I (COL I) and collagen III (COL III) were analyzed via immunofluorescence staining. Additionally, the mRNA expressions of Endo180, COL I, and COL III in force-induced PDL cells were examined by RT-qPCR in vitro. To further illustrate the role of Endo180 in regulating COL I and COL III expressions, Endo180 siRNA (siEndo) was applied to force-stimulated PDL cells. Force application increased OTM distance and disrupted collagen fiber organization, with a greater decrease in collagen elastic modulus on the mesial side than on the distal side of the PDL. After 7 days of force application, Endo180 and COL III expressions significantly increased in PDL tissues, while COL I expression decreased in PDL tissues. Compressive force loading in vitro upregulated the mRNA expressions of Endo180 and COL III, but downregulated COL I mRNA expression. Notably, Endo180 knockdown using siRNA suppressed force-induced COL III expression while restoring the downregulated COL I expression under compressive force stimuli. Force-induced Endo180 expression modulates collagen remodeling in PDL during OTM by upregulating COL III and downregulating COL I. This collagen reorganization facilitates efficient tooth movement, highlighting Endo180 as a potential therapeutic target to optimize orthodontic treatment outcomes.