老年急性心肌梗死病人冠状动脉的蛋白质翻译后修饰定量分析

doi:10.3969/j.issn.1003-9198.2023.04.013

Abstract

Abstract: Objective To explore the role of protein post-translational modification (PTM) in human coronary artery atherosclerosis. Methods Twenty coronary artery segments were collected from two elderly subjects dying from acute myocardium infarction. The hematoxylin and eosin (HE) staining was performed for pathological classification, and the human coronary arterial proteome and proteomics features were detected by means of mass spectrometry (MS) analysis. By means of Peaks Studio X+, further quantitative analysis was conducted. The STRING website was used for bioinformatics analysis, such as network cluster, reactome pathways and gene ontology (GO) functional enrichment analysis. Results A total of 2819 proteins and 233 types of PTM were identified in the 20 coronary artery segments. There were 123 differentially expressed proteins and 22 PTM modification sites, and the modifications of 22 sites included oxidation, acetylation and deamidation. Bioinformatics analysis showed that differential proteins and differential PTM sites were mainly highly correlated with mitochondrial energy metabolism. Cluster analysis of protein network showed that the mitochondrial adenosine triphosphate (ATP) synthesis coupled proton transport network was the most enriched, which included ATP5A1, ATP5B, ATP5H and ATP5O. The abundance of PTM of the four proteins was higher in the early stage of atherosclerosis. Conclusions Protein PTM may affect the development of human coronary atherosclerosis through mitochondrial energy metabolism and plays an important role in the early stage of atherosclerosis.

Key words: coronary heart disease, post-translational modification, acute myocardium infarction, artery atherosclerosis, bioinformatics analysis

CLC Number:

R 542.22

ZHANG Sheng, JIA En-zhi, WANG Lian-sheng. Protein post-translational modification of coronary artery in elderly patients with acute myocardium infarction[J]. Practical Geriatrics, 2023, 37(4): 373-377.

References

[1] GBD 2013 Mortality and Causes of Death Collaborators. Global, regional, and national age-sex specific all-cause and cause-specific mortality for 240 causes of death, 1990-2013: a systematic analysis for the Global Burden of Disease Study 2013[J]. Lancet, 2015, 385(9963):117-171.
[2] MALAKAR A K, CHOUDHURY D, HALDER B, et al. A review on coronary artery disease, its risk factors, and therapeutics[J]. J Cell Physiol, 2019, 234(10):16812-16823.
[3] THAL M A, KRISHNAMURTHY P, MACKIE AR, et al. Enhanced angiogenic and cardiomyocyte differentiation capacity of epigenetically reprogrammed mouse and human endothelial progenitor cells augments their efficacy for ischemic myocardial repair[J]. Circ Res, 2012, 111(2):180-190.
[4] McLENDON P M, FERGUSON B S, OSINSKA H, et al. Tubulin hyperacetylation is adaptive in cardiac proteotoxicity by promoting autophagy[J]. Proc Natl Acad Sci U S A, 2014, 111(48):E5178-E5186.
[5] ZHOU Y, YUAN J, FAN Y, et al.Proteomic landscape of human coronary artery atherosclerosis[J]. Int J Mol Med, 2020, 46(1):371-383.
[6] TRAN N H, QIAO R, XIN L, et al. Deep learning enables de novo peptide sequencing from data-independent-acquisition mass spectrometry[J]. Nature Methods, 2018, 16(1):63-66.
[7] ZHANG J, XIN L, SHAN B, et al. PEAKS DB: de novo sequencing assisted database search for sensitive and accurate peptide identification[J]. Mol Cell Proteomics, 2012, 11(4):M111.
[8] LIN H, HE L, MA B. A combinatorial approach to the peptide feature matching problem for label-free quantification[J]. Bioinformatics, 2013, 29(14):1768-1775.
[9] HAN X, HE L, XIN L, et al. PeaksPTM: mass spectrometry-based identification of peptides with unspecified modifications[J]. J Proteome Res, 2011, 10(7):2930-2936.
[10] PINA J M, REYNAGA J M, TRUONG A A M, et al. Post-translational modifications in polypyrimidine tract binding proteins PTBP1 and PTBP2[J]. Biochemistry, 2018, 57(26):3873-3882.
[11] SZKLARCZYK D, GABLE A L, LYON D, et al. STRING v11: protein-protein association networks with increased coverage, supporting functional discovery in genome-wide experimental datasets[J]. Nucleic Acids Res, 2019, 47(D1):D607-D613.
[12] SZKLARCZYK D, MORRIS J H, COOK H, et al. The STRING database in 2017: quality-controlled protein-protein association networks, made broadly accessible[J]. Nucleic Acids Res, 2017, 45(D1):D362-D368.
[13] HERON M. Deaths: leading causes for 2007[J]. Natl Vital Stat Rep, 2011, 59(8):1-95.
[14] FIELDS S. Proteomics. proteomics in genomeland[J]. Science, 2001, 291(5507):1221-1224.
[15] SILVA A M N, VITORINO R, DOMINGUES M R M, et al. Post-translational modifications and mass spectrometry detection[J]. Free Radic Biol Med, 2013, 65(1):925-941.
[16] SZKLARCZYK D, GABLE A L, LYON D, et al. STRING v11: protein-protein association networks with increased coverage, supporting functional discovery in genome-wide experimental datasets[J]. Nucleic Acids Res, 2019, 47(D1):D607-D613.
[17] SEELER J S, DEJEAN A. SUMO and the robustness of cancer[J]. Nat Rev Cancer, 2017, 17(3):184-197.
[18] LIU Y, ZHAO D, QIU F, et al. Manipulating PML SUMOylation via silencing UBC9 and RNF4 regulates cardiac fibrosis[J]. Mol Ther, 2017, 25(3):666-678.
[19] SANTOS A L, LINDNER A B. Protein posttranslational modifications: roles in aging and age-related disease[J]. Oxid Med Cell Longev, 2017. DOI: 10.1155/2017/5716409.
[20] CHEN H, XU H, POTASH S, et al. Mild metabolic perturbations alter succinylation of mitochondrial proteins[J]. J Neurosci Res, 2017, 95(11):2244-2252.
[21] GREISSEL A, CULMES M, NAPIERALSKI R, et al. Alternation of histone and DNA methylation in human atherosclerotic carotid plaques[J]. Thromb Haemost, 2015, 114(2):390-402.
[22] DA SILVA-FERRADA E, RIBEIRO-RODRIGUES T M, RODRÍGUEZ M S, et al. Proteostasis and SUMO in the heart[J]. Int J Biochem Cell Biol, 2016, 79(1):443-450.
[23] TAANMAN J W. The mitochondrial genome: structure, transcription, translation and replication[J]. Biochim Biophys Acta, 1999, 1410(1): 103-123.
[24] AIT-AISSA K, BLASZAK S C, BEUTNER G, et al. Mitochondrial oxidative phosphorylation defect in the heart of subjects with coronary artery disease[J]. Sci Rep, 2019, 9(1):7623-7623.

Protein post-translational modification of coronary artery in elderly patients with acute myocardium infarction

PDF (PC)

Knowledge

Abstract

Cite this article

share this article

References

Related Articles 5

Metrics

Recommended 10

[1]	XIANG Chao, LUO Caidong. Analysis of the diagnostic value of T wave change of avL lead for the degree of coronary artery stenosis in elderly patients with coronary heart disease [J]. Practical Geriatrics, 2024, 38(8): 788-791.
[2]	ZHANG Jingjing, ZHU Xiaoxia, YAO Chunlei, WANG Wei. Correlation between control nutritional status score and heart failure in elderly patients with coronary artery disease [J]. Practical Geriatrics, 2024, 38(7): 697-700.
[3]	ZHA Zhimin, LIU Huan, WANG Xiangming, LI Qiushuang, GUO Yan. Effect of cardiac valve calcification on prognosis of elderly patients with coronary heart disease [J]. Practical Geriatrics, 2024, 38(3): 245-250.
[4]	GU Chonghuai, XIANG Xuejun, ZHENG Yuanxi, QIAO Rui, LIN Song. Efficacy of dapagliflozin in elderly patients undergoing coronary intervention with type 2 diabetes mellitus and ejection fraction reduced heart failure [J]. Practical Geriatrics, 2024, 38(10): 1025-1029.
[5]	JI Jia-lin, LIU Jing, WANG Xue-li, FENG Hong-lin, HAN Xu. Ameta-analysis and sequential analysis of the effects of Guanxinping on coronary heart disease [J]. Practical Geriatrics, 2023, 37(2): 128-133.