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Tendon-targeted knockout of collagen XI disrupts patellar and Achilles tendon structure and mechanical properties during murine postnatal development.在小鼠出生后的发育过程中,靶向腱的胶原蛋白XI基因敲除会破坏髌腱和跟腱的结构及力学性能。
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本文引用的文献

1
Collagen XI regulates the acquisition of collagen fibril structure, organization and functional properties in tendon.胶原 XI 调节肌腱中胶原纤维结构、组织和功能特性的获得。
Matrix Biol. 2020 Dec;94:77-94. doi: 10.1016/j.matbio.2020.09.001. Epub 2020 Sep 17.
2
A novel dominant COL11A1 mutation in a child with Stickler syndrome type II is associated with recurrent fractures.一个新的显性 COL11A1 突变与 II 型 Stickler 综合征患儿的复发性骨折有关。
Osteoporos Int. 2018 Jan;29(1):247-251. doi: 10.1007/s00198-017-4229-3. Epub 2017 Oct 3.
3
Decorin and biglycan are necessary for maintaining collagen fibril structure, fiber realignment, and mechanical properties of mature tendons.腱组织中的核心蛋白聚糖和 biglycan 对于维持胶原纤维结构、纤维重排以及成熟腱组织的力学性能是必需的。
Matrix Biol. 2017 Dec;64:81-93. doi: 10.1016/j.matbio.2017.08.004. Epub 2017 Sep 5.
4
Collagen V haploinsufficiency in a murine model of classic Ehlers-Danlos syndrome is associated with deficient structural and mechanical healing in tendons.在典型埃勒斯-当洛综合征的小鼠模型中,胶原蛋白V单倍体不足与肌腱结构和机械愈合缺陷有关。
J Orthop Res. 2017 Dec;35(12):2707-2715. doi: 10.1002/jor.23571. Epub 2017 Apr 24.
5
Joint loads resulting in ACL rupture: Effects of age, sex, and body mass on injury load and mode of failure in a mouse model.导致前交叉韧带断裂的关节负荷:年龄、性别和体重对小鼠模型中损伤负荷及失效模式的影响。
J Orthop Res. 2017 Aug;35(8):1754-1763. doi: 10.1002/jor.23418. Epub 2016 Sep 19.
6
Mutation survey and genotype-phenotype analysis of COL2A1 and COL11A1 genes in 16 Chinese patients with Stickler syndrome.16例中国Stickler综合征患者COL2A1和COL11A1基因的突变检测及基因型-表型分析
Mol Vis. 2016 Jun 23;22:697-704. eCollection 2016.
7
Multiscale regression modeling in mouse supraspinatus tendons reveals that dynamic processes act as mediators in structure-function relationships.小鼠冈上肌腱的多尺度回归建模表明,动态过程在结构-功能关系中起中介作用。
J Biomech. 2016 Jun 14;49(9):1649-1657. doi: 10.1016/j.jbiomech.2016.03.053. Epub 2016 Apr 2.
8
Semantic interrogation of a multi knowledge domain ontological model of tendinopathy identifies four strong candidate risk genes.对肌腱病多知识领域本体模型的语义询问识别出四个强有力的候选风险基因。
Sci Rep. 2016 Jan 25;6:19820. doi: 10.1038/srep19820.
9
Regulatory role of collagen V in establishing mechanical properties of tendons and ligaments is tissue dependent.胶原蛋白V在建立肌腱和韧带机械性能方面的调节作用因组织而异。
J Orthop Res. 2015 Jun;33(6):882-8. doi: 10.1002/jor.22893. Epub 2015 Apr 27.
10
Targeted deletion of collagen V in tendons and ligaments results in a classic Ehlers-Danlos syndrome joint phenotype.在肌腱和韧带中靶向删除胶原蛋白V会导致典型的埃勒斯-当洛综合征关节表型。
Am J Pathol. 2015 May;185(5):1436-47. doi: 10.1016/j.ajpath.2015.01.031. Epub 2015 Mar 20.

胶原 XI 在小鼠肌腱和韧带机械性能建立中的调控作用具有组织依赖性。

Regulatory Role of Collagen XI in the Establishment of Mechanical Properties of Tendons and Ligaments in Mice Is Tissue Dependent.

机构信息

McKay Orthopaedic Research Laboratory, University of Pennsylvania, Philadelphia, PA 19104; Department of Orthopedics, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, Hubei 430030, China.

McKay Orthopaedic Research Laboratory, University of Pennsylvania, Philadelphia, PA 19104.

出版信息

J Biomech Eng. 2025 Jan 1;147(1). doi: 10.1115/1.4066570.

DOI:10.1115/1.4066570
PMID:39297758
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11500803/
Abstract

Collagen XI is ubiquitous in tissues such as joint cartilage, cancellous bone, muscles, and tendons and is an important contributor during a crucial part in fibrillogenesis. The COL11A1 gene encodes one of three alpha chains of collagen XI. The present study elucidates the role of collagen XI in the establishment of mechanical properties of tendons and ligaments. We investigated the mechanical response of three tendons and one ligament tissues from wild type and a targeted mouse model null for collagen XI: Achilles tendon (ACH), the flexor digitorum longus tendon (FDL), the supraspinatus tendon (SST), and the anterior cruciate ligament (ACL). Area was substantially lower in Col11a1ΔTen/ΔTen ACH, FDL, and SST. Maximum load and maximum stress were significantly lower in Col11a1ΔTen/ΔTen ACH and FDL. Stiffness was lower in Col11a1ΔTen/ΔTen ACH, FDL, and SST. Modulus was reduced in Col11a1ΔTen/ΔTen FDL and SST (both insertion site and midsubstance). Collagen fiber distributions were more aligned under load in both wild type group and Col11a1ΔTen/ΔTen groups. Results also revealed that the effect of collagen XI knockout on collagen fiber realignment is tendon-dependent and location-dependent (insertion versus midsubstance). In summary, this study clearly shows that the regulatory role of collagen XI on tendon and ligament is tissue specific and that joint hypermobility in type II Stickler's Syndrome may in part be due to suboptimal mechanical response of the soft tissues surrounding joints.

摘要

胶原 XI 普遍存在于关节软骨、松质骨、肌肉和肌腱等组织中,是原纤维生成过程中的一个重要贡献者。COL11A1 基因编码胶原 XI 的三个α链之一。本研究阐明了胶原 XI 在肌腱和韧带机械性能建立中的作用。我们研究了三种肌腱和一种韧带组织的力学响应,这些组织来自野生型和靶向胶原 XI 缺失的小鼠模型:跟腱(ACH)、指深屈肌腱(FDL)、冈上肌腱(SST)和前交叉韧带(ACL)。Col11a1ΔTen/ΔTen ACH、FDL 和 SST 的面积明显较低。Col11a1ΔTen/ΔTen ACH 和 FDL 的最大载荷和最大应力显著降低。Col11a1ΔTen/ΔTen ACH、FDL 和 SST 的刚度降低。Col11a1ΔTen/ΔTen FDL 和 SST 的模量降低(均为插入部位和中间部位)。在两种野生型和 Col11a1ΔTen/ΔTen 组中,在载荷下胶原纤维的分布更趋于一致。结果还表明,胶原 XI 缺失对胶原纤维重新排列的影响是肌腱依赖性和位置依赖性的(插入部位与中间部位)。总之,本研究清楚地表明,胶原 XI 对肌腱和韧带的调节作用具有组织特异性,II 型斯提克勒综合征的关节过度活动可能部分是由于关节周围软组织的机械反应不佳。