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2型糖尿病合并下肢动脉粥样硬化闭塞症的转录组学分析

Transcriptomic Analysis of Type 2 Diabetes Mellitus Combined with Lower Extremity Atherosclerotic Occlusive Disease.

作者信息

Zeng Guang, Jin Yong-Zhi, Huang Yi, Hu Jun-Sheng, Li Meng-Fan, Tian Ming, Lu Jun, Huang Rong

机构信息

Department of General Surgery, Putuo Hospital Shanghai University of Traditional Chinese Medicine, Shanghai, 200062, People's Republic of China.

Department of General Surgery, LiQun Hospital, Shanghai, 200333, People's Republic of China.

出版信息

Diabetes Metab Syndr Obes. 2024 Feb 28;17:997-1011. doi: 10.2147/DMSO.S432698. eCollection 2024.

DOI:10.2147/DMSO.S432698
PMID:38435631
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC10909374/
Abstract

BACKGROUND

The pathological damage mechanism of type 2 diabetes (T2D) and macroangiopathy is extremely complex, and T2D and arteriosclerosis obliterans have different biological behaviors and clinical features. To explore the mechanism of lower extremity arteriosclerosis occlusion (LEAOD) in T2D patients, we utilized RNA-seq to identify unique gene expression signatures of T2D and LEAOD through transcriptomic analysis.

METHODS

We obtained blood samples and performed RNA sequencing from four patients with T2D, five of whom had LEAOD. Another six age- and gender-matched blood samples from healthy volunteers were used for control. By exploring the general and specific differential expression analysis after transcriptome sequencing, specific gene expression patterns of T2D and LEAOD were verified.

RESULTS

Transcriptome analysis found differentially expressed genes in T2D, and T2D + LEAOD (vs normal) separately, of which 35/486 (T2D/T2D + LEAOD) were up-regulated and 1290/2970 (T2D/T2D + LEAOD) were down-regulated. A strong overlap of 571 genes across T2D, LEAOD, and coexisting conditions was mainly involved in extracellular exosomes and the transcription process. By exploring the sex difference gene expression features between T2D, T2D + LEAOD, and healthy controls, we noticed that sex chromosome-associated genes do not participate in the sexual dimorphism gene expression profiles of T2D and LEAOD. Protein-Protein Interaction Network analysis and drug target prediction provided the drug candidates to treat T2D and LEAOD.

CONCLUSION

This study provides some evidence at the transcript level to uncover the association of T2D with LEAOD. The screened hub genes and predicted target drugs may be therapeutic targets.

摘要

背景

2型糖尿病（T2D）与大血管病变的病理损伤机制极为复杂，且T2D与动脉硬化闭塞症具有不同的生物学行为和临床特征。为探究T2D患者下肢动脉硬化闭塞症（LEAOD）的发病机制，我们利用RNA测序技术通过转录组分析来识别T2D和LEAOD独特的基因表达特征。

方法

我们采集了4例T2D患者的血样并进行RNA测序，其中5例患有LEAOD。另外选取6例年龄和性别匹配的健康志愿者血样作为对照。通过对转录组测序后的一般和特异性差异表达分析，验证了T2D和LEAOD的特定基因表达模式。

结果

转录组分析分别在T2D以及T2D + LEAOD（与正常对照相比）中发现了差异表达基因，其中35/486（T2D/T2D + LEAOD）个基因上调，1290/2970（T2D/T2D + LEAOD）个基因下调。T2D、LEAOD及共存疾病中571个基因的强烈重叠主要涉及细胞外囊泡和转录过程。通过探究T2D、T2D + LEAOD与健康对照之间的性别差异基因表达特征，我们注意到性染色体相关基因不参与T2D和LEAOD的性别二态性基因表达谱。蛋白质-蛋白质相互作用网络分析和药物靶点预测提供了治疗T2D和LEAOD的候选药物。

结论

本研究在转录水平上提供了一些证据，以揭示T2D与LEAOD之间的关联。筛选出的关键基因和预测的靶向药物可能成为治疗靶点。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e67a/10909374/1c47c457c85d/DMSO-17-997-g0006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e67a/10909374/4054e94fc786/DMSO-17-997-g0001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e67a/10909374/8428fdbf8739/DMSO-17-997-g0002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e67a/10909374/6ad15919124a/DMSO-17-997-g0003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e67a/10909374/273dc78d5ba2/DMSO-17-997-g0004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e67a/10909374/c6d6add32e36/DMSO-17-997-g0005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e67a/10909374/1c47c457c85d/DMSO-17-997-g0006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e67a/10909374/4054e94fc786/DMSO-17-997-g0001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e67a/10909374/8428fdbf8739/DMSO-17-997-g0002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e67a/10909374/6ad15919124a/DMSO-17-997-g0003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e67a/10909374/273dc78d5ba2/DMSO-17-997-g0004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e67a/10909374/c6d6add32e36/DMSO-17-997-g0005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e67a/10909374/1c47c457c85d/DMSO-17-997-g0006.jpg

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