Long noncoding RNAs (lncRNAs), as a novel regulatory factor, are considered to play a vital role in various biological processes and diseases.However, the overall expression profile and biological functions of lncRNAs in the partially injured anterior cruciate ligament(ACL) and medial collateral ligament(MCL) have not been clearly explored.Partially injured models of ACL and MCL were established in 3-month-old healthy male New Zealand white rabbits.Expression of lncRNAs and mRNAs in the ligament tissue was detected by highthroughput sequencing technology, and biological functions of differentially expressed RNAs were evaluated by Gene Ontology(GO) and Kyoto Encyclopedia of Genes and Genomes(KEGG) analysis.Validation of several differentially expressed RNAs was performed using quantitative real-time PCR(qRT-PCR).Protein-protein interaction (PPI) analysis and competitive endogenous RNA (ceRNA) prediction were used to identify interactions among hub genes and the interaction among lncRNAs, miRNAs, and mRNAs.The results showed that compared with the normal group, there were 267 mRNAs and 329 lncRNAs differentially expressed in ACL and 726 mRNAs and 609 lncRNAs in MCL in the injured group.Compared with MCL, 420 mRNAs and 470 lncRNAs were differentially expressed in ACL in the normal group; 162 mRNAs and 205 lncRNAs were differentially expressed in ACL in the injured group.Several important lncRNAs and genes were identified, namely, COL7A1, LIF, FGFR2, EPHA2, CSF1, MMP2, MMP9, SOX5, LOX, MSTRG.1737.1,MSTRG.26038.25,MSTRG.20209.5,MSTRG.22764.1, and MSTRG.18113.1, which are closely related to inflammatory response, tissue damage repair, cell proliferation, differentiation, migration, and apoptosis.Further study of the functions of these genes may help to better understand the specific molecular mechanisms underlying the occurrence of endogenous repair disorders in ACL, which may provide new ideas for further exploration of effective means to promote endogenous repair of ACL injury.

Long noncoding RNAs (lncRNAs), as a novel regulatory factor, are considered to play a vital role in various biological processes and diseases.However, the overall expression profile and biological functions of lncRNAs in the partially injured anterior cruciate ligament(ACL) and medial collateral ligament(MCL) have not been clearly explored.Partially injured models of ACL and MCL were established in 3-month-old healthy male New Zealand white rabbits.Expression of lncRNAs and mRNAs in the ligament tissue was detected by highthroughput sequencing technology, and biological functions of differentially expressed RNAs were evaluated by Gene Ontology(GO) and Kyoto Encyclopedia of Genes and Genomes(KEGG) analysis.Validation of several differentially expressed RNAs was performed using quantitative real-time PCR(qRT-PCR).Protein-protein interaction (PPI) analysis and competitive endogenous RNA (ceRNA) prediction were used to identify interactions among hub genes and the interaction among lncRNAs, miRNAs, and mRNAs.The results showed that compared with the normal group, there were 267 mRNAs and 329 lncRNAs differentially expressed in ACL and 726 mRNAs and 609 lncRNAs in MCL in the injured group.Compared with MCL, 420 mRNAs and 470 lncRNAs were differentially expressed in ACL in the normal group; 162 mRNAs and 205 lncRNAs were differentially expressed in ACL in the injured group.Several important lncRNAs and genes were identified, namely, COL7A1, LIF, FGFR2, EPHA2, CSF1, MMP2, MMP9, SOX5, LOX, MSTRG.1737.1,MSTRG.26038.25,MSTRG.20209.5,MSTRG.22764.1, and MSTRG.18113.1, which are closely related to inflammatory response, tissue damage repair, cell proliferation, differentiation, migration, and apoptosis.Further study of the functions of these genes may help to better understand the specific molecular mechanisms underlying the occurrence of endogenous repair disorders in ACL, which may provide new ideas for further exploration of effective means to promote endogenous repair of ACL injury.

目的:交叉对比兔前交叉韧带(ACL)与内侧副韧带(MCL)部分损伤前后环状RNA表达差异,并进行功能分析,探讨ACL内源性修复障碍可能的分子机制.方法:对兔ACL及MCL组织环状RNA建库测序,筛选符合标准的差异环状RNA,并用qRT-PCR验证,对筛选的差异环状RNA进行京都基因和基因组百科全书(KEGG)和基因本体论(GO)分析,并构建其ceRNA网络.结果:各组中共筛选出308个差异环状RNA,GO和KEGG分析表明,ACL与MCL损伤后的差异环状RNA在血管生成、炎症反应、细胞增殖与凋亡及mRNA转录与蛋白翻译方面均存在较大差异.ACL与MCL损伤后的ceRNA网络差异显著.结论:环状RNA在ACL与MCL损伤后的差异表达谱中存在明显差异,为进一步研究ACL损伤内源性修复障碍的机制提供了新思路.

Long noncoding RNAs (lncRNAs), as a novel regulatory factor, are considered to play a vital role in various biological processes and diseases. However, the overall expression profile and biological functions of lncRNAs in the partially injured anterior cruciate ligament (ACL) and medial collateral ligament (MCL) have not been clearly explored. Partially injured models of ACL and MCL were established in 3-month-old healthy male New Zealand white rabbits. Expression of lncRNAs and mRNAs in the ligament tissue was detected by high-throughput sequencing technology, and biological functions of differentially expressed RNAs were evaluated by Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) analysis. Validation of several differentially expressed RNAs was performed using quantitative real-time PCR (qRT-PCR). Protein-protein interaction (PPI) analysis and competitive endogenous RNA (ceRNA) prediction were used to identify interactions among hub genes and the interaction among lncRNAs, miRNAs, and mRNAs. The results showed that compared with the normal group, there were 267 mRNAs and 329 lncRNAs differentially expressed in ACL and 726 mRNAs and 609 lncRNAs in MCL in the injured group. Compared with MCL, 420 mRNAs and 470 lncRNAs were differentially expressed in ACL in the normal group; 162 mRNAs and 205 lncRNAs were differentially expressed in ACL in the injured group. Several important lncRNAs and genes were identified, namely, COL7A1, LIF, FGFR2, EPHA2, CSF1, MMP2, MMP9, SOX5, LOX, MSTRG.1737.1, MSTRG.26038.25, MSTRG.20209.5, MSTRG.22764.1, and MSTRG.18113.1, which are closely related to inflammatory response, tissue damage repair, cell proliferation, differentiation, migration, and apoptosis. Further study of the functions of these genes may help to better understand the specific molecular mechanisms underlying the occurrence of endogenous repair disorders in ACL, which may provide new ideas for further exploration of effective means to promote endogenous repair of ACL injury.