Accelerated flexor tendon repair in superhealer mice reflects alterations in TGFB1 regulated expression programs linked to inflammatory, fibrosis and cell cycle control

Purpose: The goal of this study is to compare transcriptional profiles of flexor tendon healing in wild-type (WT, C57Bl/6J) to superhealer (MRL/MpJ) mice to gain insights in the biological drivers of the tendon injury response between the C57 and MRL mice. Methods: RNA was isolated from partially lacerated or uninjured flexor tendon 7 days post-injury. Results: Transcriptional analysis of biological drivers showed positive enrichment of TGFB1 in both C57 and MRL healing tendons. only MRL tendons exhibited downstream transcriptional effects of cell cycle regulatory genes, with negative enrichment of the cell senescence-related regulators, compared to the positively-enriched inflammatory and ECM organization pathways in the C57 tendons. Conclusions: There is altered TGFB1 regulated inflammatory, fibrosis, and cell cycle pathways in flexor tendon repair. Tendon mRNA profiles of 7 days post-injury with C57Bl/6J and MRL/MpJ mice研究目的：本研究旨在对比野生型（wild-type, WT, C57Bl/6J）小鼠与超愈型（superhealer, MRL/MpJ）小鼠的屈肌腱愈合转录谱，以解析C57与MRL小鼠肌腱损伤应答的生物学驱动因子。 实验方法：于损伤后7天，从部分撕裂或未受损的屈肌腱中提取核糖核酸（RNA）。 实验结果：针对生物学驱动因子的转录组分析显示，转化生长因子β1（TGFB1）在C57与MRL小鼠的愈合肌腱中均呈现正向富集。仅MRL肌腱表现出细胞周期调控基因的下游转录效应，相较于C57肌腱中正向富集的炎症及细胞外基质（ECM）组织通路，MRL肌腱内细胞衰老相关调控因子呈现负向富集。 研究结论：屈肌腱修复过程中，转化生长因子β1（TGFB1）所调控的炎症、纤维化及细胞周期通路存在异常改变。 本数据集包含C57Bl/6J与MRL/MpJ小鼠损伤后7天的肌腱mRNA转录谱。