• 文献检索
  • 文档翻译
  • 深度研究
  • 学术资讯
  • Suppr Zotero 插件Zotero 插件
  • 邀请有礼
  • 套餐&价格
  • 历史记录
应用&插件
Suppr Zotero 插件Zotero 插件浏览器插件Mac 客户端Windows 客户端微信小程序
定价
高级版会员购买积分包购买API积分包
服务
文献检索文档翻译深度研究API 文档MCP 服务
关于我们
关于 Suppr公司介绍联系我们用户协议隐私条款
关注我们

Suppr 超能文献

核心技术专利：CN118964589B侵权必究
粤ICP备2023148730 号-1Suppr @ 2026

文献检索

告别复杂PubMed语法，用中文像聊天一样搜索，搜遍4000万医学文献。AI智能推荐，让科研检索更轻松。

立即免费搜索

文件翻译

保留排版，准确专业，支持PDF/Word/PPT等文件格式，支持 12+语言互译。

免费翻译文档

深度研究

AI帮你快速写综述，25分钟生成高质量综述，智能提取关键信息，辅助科研写作。

立即免费体验

髓样细胞和感觉神经通过前列腺素 E2 介导腱周粘连的形成。

Myeloid Cells and Sensory Nerves Mediate Peritendinous Adhesion Formation via Prostaglandin E2.

机构信息

Department of Orthopaedics, Shanghai Sixth People's Hospital Affiliated to Shanghai Jiao Tong University School of Medicine, Shanghai, 200233, P. R. China.

State Key Laboratory of Proteomics, Beijing Proteome Research Center, National Center for Protein Sciences (Beijing), Beijing Institute of Lifeomics, Beijing, 102206, P. R. China.

出版信息

Adv Sci (Weinh). 2024 Oct;11(40):e2405367. doi: 10.1002/advs.202405367. Epub 2024 Aug 29.

DOI:10.1002/advs.202405367
PMID:39207041
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11516151/
Abstract

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.

摘要

腱损伤后形成的腱周粘连极大地限制了日常生活。粘连的病理学涉及炎症和相关的增殖。然而，目前对此类疾病的研究还很缺乏，先前的研究表明，环氧化酶-2（COX2）基因抑制剂通过减少前列腺素 E2（PGE2）和纤维母细胞的增殖来发挥抗粘连作用，与另一项研究中通过删除纤维母细胞中的 EP4（前列腺素 E 受体 4）基因导致抗粘连失败的结果相反。在这项研究中，对人类和小鼠标本进行单细胞 RNA 测序分析，并结合八种类型的条件性敲除小鼠，进一步表明髓样细胞中 COX2 的缺失和感觉神经中 EP4 基因的缺失可减少粘连并损害修复后的肌腱的生物力学特性。此外，COX2 抑制剂帕瑞昔布可减少 PGE2，但会损害修复后的肌腱的生物力学特性。有趣的是，PGE2 局部治疗可改善修复后的肌腱的生物力学特性。这些发现阐明了 PGE2 在腱周粘连形成（PAF）和肌腱修复中的复杂作用。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2cef/11516151/5c4d0d6f21db/ADVS-11-2405367-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2cef/11516151/c2617b2f4a58/ADVS-11-2405367-g009.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2cef/11516151/0b855f8ccd57/ADVS-11-2405367-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2cef/11516151/47af74a87736/ADVS-11-2405367-g010.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2cef/11516151/f2af2bbc22ee/ADVS-11-2405367-g008.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2cef/11516151/82b65cf2c8d3/ADVS-11-2405367-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2cef/11516151/1390b84c8243/ADVS-11-2405367-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2cef/11516151/ded64fc97797/ADVS-11-2405367-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2cef/11516151/bf1e08963d9f/ADVS-11-2405367-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2cef/11516151/5c4d0d6f21db/ADVS-11-2405367-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2cef/11516151/c2617b2f4a58/ADVS-11-2405367-g009.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2cef/11516151/0b855f8ccd57/ADVS-11-2405367-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2cef/11516151/47af74a87736/ADVS-11-2405367-g010.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2cef/11516151/f2af2bbc22ee/ADVS-11-2405367-g008.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2cef/11516151/82b65cf2c8d3/ADVS-11-2405367-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2cef/11516151/1390b84c8243/ADVS-11-2405367-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2cef/11516151/ded64fc97797/ADVS-11-2405367-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2cef/11516151/bf1e08963d9f/ADVS-11-2405367-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2cef/11516151/5c4d0d6f21db/ADVS-11-2405367-g006.jpg

相似文献

1
Myeloid Cells and Sensory Nerves Mediate Peritendinous Adhesion Formation via Prostaglandin E2.髓样细胞和感觉神经通过前列腺素 E2 介导腱周粘连的形成。
Adv Sci (Weinh). 2024 Oct;11(40):e2405367. doi: 10.1002/advs.202405367. Epub 2024 Aug 29.
2
Statins enhance rotator cuff healing by stimulating the COX2/PGE2/EP4 pathway: an in vivo and in vitro study.他汀类药物通过刺激COX2/PGE2/EP4途径促进肩袖愈合：一项体内和体外研究。
Am J Sports Med. 2014 Dec;42(12):2869-76. doi: 10.1177/0363546514545856. Epub 2014 Sep 2.
3
Protective Role of mPGES-1 (Microsomal Prostaglandin E Synthase-1)-Derived PGE (Prostaglandin E) and the Endothelial EP4 (Prostaglandin E Receptor) in Vascular Responses to Injury.mPGES-1（微粒体前列腺素 E 合酶-1）衍生的 PGE（前列腺素 E）和血管内皮细胞 EP4（前列腺素 E 受体）在血管损伤反应中的保护作用。
Arterioscler Thromb Vasc Biol. 2018 May;38(5):1115-1124. doi: 10.1161/ATVBAHA.118.310713. Epub 2018 Mar 29.
4
Prostaglandin E2 mediates sensory nerve regulation of bone homeostasis.前列腺素 E2 介导感觉神经对骨稳态的调节。
Nat Commun. 2019 Jan 14;10(1):181. doi: 10.1038/s41467-018-08097-7.
5
Deletion of EP4 in S100a4-lineage cells reduces scar tissue formation during early but not later stages of tendon healing.删除 S100a4 谱系细胞中的 EP4 可减少早期但不减少晚期肌腱愈合过程中的疤痕组织形成。
Sci Rep. 2017 Aug 17;7(1):8658. doi: 10.1038/s41598-017-09407-7.
6
Systemic EP4 Inhibition Increases Adhesion Formation in a Murine Model of Flexor Tendon Repair.全身性EP4抑制增加屈肌腱修复小鼠模型中的粘连形成。
PLoS One. 2015 Aug 27;10(8):e0136351. doi: 10.1371/journal.pone.0136351. eCollection 2015.
7
Sensory nerves regulate mesenchymal stromal cell lineage commitment by tuning sympathetic tones.感觉神经通过调节交感神经张力来调节间充质基质细胞谱系的决定。
J Clin Invest. 2020 Jul 1;130(7):3483-3498. doi: 10.1172/JCI131554.
8
T cell-intrinsic prostaglandin E-EP2/EP4 signaling is critical in pathogenic T17 cell-driven inflammation.T 细胞内在的前列腺素 E-EP2/EP4 信号在致病性 T17 细胞驱动的炎症中至关重要。
J Allergy Clin Immunol. 2019 Feb;143(2):631-643. doi: 10.1016/j.jaci.2018.05.036. Epub 2018 Jun 20.
9
Myeloid Cell Prostaglandin E2 Receptor EP4 Modulates Cytokine Production but Not Atherogenesis in a Mouse Model of Type 1 Diabetes.髓样细胞前列腺素E2受体EP4调节1型糖尿病小鼠模型中的细胞因子产生，但不影响动脉粥样硬化的发生。
PLoS One. 2016 Jun 28;11(6):e0158316. doi: 10.1371/journal.pone.0158316. eCollection 2016.
10
Concerted EP2 and EP4 Receptor Signaling Stimulates Autocrine Prostaglandin E Activation in Human Podocytes.协同的 EP2 和 EP4 受体信号刺激人足细胞自分泌前列腺素 E 的激活。
Cells. 2020 May 19;9(5):1256. doi: 10.3390/cells9051256.

本文引用的文献

1
Multi-omics analysis of human tendon adhesion reveals that ACKR1-regulated macrophage migration is involved in regeneration.人类肌腱粘连的多组学分析表明，ACKR1 调节的巨噬细胞迁移参与了再生。
Bone Res. 2024 May 7;12(1):27. doi: 10.1038/s41413-024-00324-w.
2
Unidirectional gene delivery electrospun fibrous membrane via charge repulsion for tendon repair.通过电荷排斥实现单向基因递送的电纺纤维膜用于肌腱修复。
Bioact Mater. 2024 Mar 21;37:191-205. doi: 10.1016/j.bioactmat.2024.03.008. eCollection 2024 Jul.
3
Targeted Macrophage CRISPR-Cas13 mRNA Editing in Immunotherapy for Tendon Injury.
靶向巨噬细胞 CRISPR-Cas13 mRNA 编辑在肌腱损伤免疫治疗中的应用。
Adv Mater. 2024 May;36(19):e2311964. doi: 10.1002/adma.202311964. Epub 2024 Feb 11.
4
A single-cell atlas depicting the cellular and molecular features in human anterior cruciate ligamental degeneration: A single cell combined spatial transcriptomics study.人类前交叉韧带退变的细胞和分子特征图谱：单细胞联合空间转录组学研究。
Elife. 2023 Nov 16;12:e85700. doi: 10.7554/eLife.85700.
5
Unloading-Induced Skeletal Interoception Alters Hypothalamic Signaling to Promote Bone Loss and Fat Metabolism.负荷诱导的骨骼内感受改变下丘脑信号促进骨丢失和脂肪代谢。
Adv Sci (Weinh). 2023 Dec;10(35):e2305042. doi: 10.1002/advs.202305042. Epub 2023 Oct 25.
6
Inflammation-related signaling pathways in tendinopathy.肌腱病中与炎症相关的信号通路。
Open Life Sci. 2023 Sep 20;18(1):20220729. doi: 10.1515/biol-2022-0729. eCollection 2023.
7
Neutralization of excessive levels of active TGF-β1 reduces MSC recruitment and differentiation to mitigate peritendinous adhesion.中和过量的活性转化生长因子-β1可减少间充质干细胞的募集和分化，以减轻腱周粘连。
Bone Res. 2023 May 8;11(1):24. doi: 10.1038/s41413-023-00252-1.
8
Origin and Heterogeneity of Tissue Myeloid Cells: A Focus on GMP-Derived Monocytes and Neutrophils.组织髓样细胞的起源与异质性：聚焦于粒-单核祖细胞衍生的单核细胞和中性粒细胞
Annu Rev Immunol. 2023 Apr 26;41:375-404. doi: 10.1146/annurev-immunol-081022-113627.
9
Tenolysis and Salvage Procedures.松解和挽救手术。
Hand Clin. 2023 May;39(2):203-214. doi: 10.1016/j.hcl.2022.08.021. Epub 2023 Feb 14.
10
Therapy after Flexor Tendon Repair.屈肌腱修复术后的治疗。
Hand Clin. 2023 May;39(2):181-192. doi: 10.1016/j.hcl.2022.08.019.