前列腺素E2
感觉系统
粘附
化学
细胞生物学
髓系细胞
医学
生物
内分泌学
神经科学
生物化学
细胞
有机化学
作者
Xinshu Zhang,Yao Xiao,Zaijin Tao,Yizhe Zhang,Xuan Cheng,Xuanzhe Liu,Yanhao Li,Weiguang Yin,Jian Tian,Shuo Wang,Tianyi Zhang,Xiao Yang,Shen Liu
标识
DOI:10.1002/advs.202405367
摘要
Peritendinous adhesion that forms after tendon injury substantially limits daily life. The pathology of adhesion involves inflammation and the associated proliferation. However, the current studies on this condition are lacking, previous studies reveal that cyclooxygenase-2 (COX2) gene inhibitors have anti-adhesion effects through reducing prostaglandin E2 (PGE2) and the proliferation of fibroblasts, are contrary to the failure in anti-adhesion through deletion of EP4 (prostaglandin E receptor 4) gene in fibroblasts in mice of another study. In this study, single-cell RNA sequencing analysis of human and mouse specimens are combined with eight types of conditional knockout mice and further reveal that deletion of COX2 in myeloid cells and deletion of EP4 gene in sensory nerves decrease adhesion and impair the biomechanical properties of repaired tendons. Furthermore, the COX2 inhibitor parecoxib reduces PGE2 but impairs the biomechanical properties of repaired tendons. Interestingly, PGE2 local treatment improves the biomechanical properties of the repaired tendons. These findings clarify the complex role of PGE2 in peritendinous adhesion formation (PAF) and tendon repair.
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