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Research Article Dysregulated Circulating Apoptosis- and Autophagy-Related Lncrnas As Diagnostic Markers in Coronary Artery Disease

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Research Article Dysregulated Circulating Apoptosis- and Autophagy-Related Lncrnas As Diagnostic Markers in Coronary Artery Disease Hindawi BioMed Research International Volume 2021, Article ID 5517786, 19 pages https://doi.org/10.1155/2021/5517786 Research Article Dysregulated Circulating Apoptosis- and Autophagy-Related lncRNAs as Diagnostic Markers in Coronary Artery Disease Lijiao Zhang,1 Dayuan Lou,1 Dan He,2 Ying Wang,3 Yuhang Wu,3 Xinyang Cao,3 and Peng Qu 1 1Department of Cardiology, The Second Affiliated Hospital of Dalian Medical University, Dalian, 116027 Liaoning, China 2Department of Physiology and Pathophysiology, School of Basic Medical Sciences, Peking University, Beijing 100191, China 3Institute of Heart & Vessel Diseases, The Second Affiliated Hospital of Dalian Medical University, Dalian, 116027 Liaoning, China Correspondence should be addressed to Peng Qu; [email protected] Received 2 February 2021; Revised 3 April 2021; Accepted 16 August 2021; Published 1 September 2021 Academic Editor: Parameshachari B. D. Copyright © 2021 Lijiao Zhang et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. Objective. Increasing evidence emphasizes the implications of dysregulated apoptosis and autophagy cellular processes in coronary artery disease (CAD). Herein, we aimed to explore apoptosis- and autophagy-related long noncoding RNAs (lncRNAs) in peripheral blood of CAD patients. Methods. The mRNA and lncRNA expression profiles were retrieved from the Gene Expression Omnibus (GEO) database. With ∣fold change∣ >1:5 and adjusted p value < 0.05, differentially expressed apoptosis- and autophagy-related mRNAs were screened between CAD and healthy blood samples. Also, differentially expressed lncRNAs were identified for CAD. Using the psych package, apoptosis- and autophagy-related lncRNAs were defined with Spearson’s correlation analysis. Receiver operating characteristic (ROC) curves were conducted for the assessment of the diagnosed efficacy of these apoptosis- and autophagy-related lncRNAs. Results. Our results showed that 24 apoptosis- and autophagy- related mRNAs were abnormally expressed in CAD than normal controls. 12 circulating upregulated and 1 downregulated apoptosis- and autophagy-related lncRNAs were identified for CAD. The ROCs confirmed that AC004485.3 (AUC = 0:899), AC004920.3 (AUC = 0:93), AJ006998.2 (AUC = 0:776), H19 (AUC = 0:943), RP5-902P8.10 (AUC = 0:956), RP5-1114G22.2 (AUC = 0:883), RP11-247A12.1 (AUC = 0:885), RP11-288L9.4 (AUC = 0:928), RP11-344B5.2 (AUC = 0:858), RP11-452C8.1 (AUC = 0:929), RP11-565A3.1 (AUC = 0:893), and XXbac-B33L19.4 (AUC = 0:932) exhibited good performance in differentiating CAD from healthy controls. Conclusion. Collectively, our findings proposed that circulating apoptosis- and autophagy-related lncRNAs could become underlying diagnostic markers for CAD in clinical practice. 1. Introduction angiography, and a peripheral blood biochemical test is only used for evaluating the risk factors of CAD. Increasing evi- Coronary artery disease (CAD), as a commonly diagnosed dence highlights that circulating biomarkers that can be heart disease, contributes to the dominant cause of detected in peripheral blood can be applied for early detec- cardiovascular-related deaths [1]. This disease mainly occurs tion in patients with high-risk CAD [5]. The noninvasive when the myocardial blood supply decreases [2]. It is com- early diagnosis may prevent the progression of CAD, thereby posed of myocardial infarction and stable and unstable validly lowering its mortality [6]. Nevertheless, there is still angina, as well as sudden cardiac death [3]. The etiology of lack of circulating markers with high diagnostic value for CAD remains little understood due to complex causes such CAD in clinical practice [7]. as environmental or genetic risk factors [4]. Hence, it Apoptosis and autophagy, as two types of programmed requires exploring in depth for the pathogenesis of CAD. cellular deaths, are both involved in the development of Despite much progress in CAD management, the prevalence CAD [8]. Undue apoptosis inevitably induces cell death is still rising and clinical outcomes are unsatisfactory. Cur- under oxidative stress, ischemia conditions, and the like rently, the gold standard for diagnosing CAD is still coronary [9]. Meanwhile, autophagy is an evolutionarily conserved 2 BioMed Research International CAD vs healthy GSE113079 and GSE113079 dataset GES69587 datasets > p < FC 1.5 and 0.05 FC >1.5 and p < 0.05 Differentially Differentially expressed circulating expressed circulating mRNAs IncRNAs Autophagy-and apoptosis-related circulating mRNAs Spearson correlation Protein-protein analysis with psych interaction network package Evaluation of the diagnostic efficacy Autophagy- and with ROC curves Hub genes apoptosis-related circulating IncRNAs External validation in the GSE169256 dataset Figure 1: The workflow of this study. cellular process that participates in degrading and recycling cesses that occurred in CAD, which could provide a novel the redundant or useless protein constituents, organelles, insight into the diagnosis and management of CAD. and the like [10]. This process is fundamental for maintain- ing intracellular homeostasis. Hence, its disorder in cardiac 2. Materials and Methods cells exerts destructive impacts on the cardiovascular system [11]. Currently, activation of autophagy has been a thera- 2.1. Datasets and Preprocessing. The mRNA and lncRNA fi peutic approach for heart diseases [12]. Increasing evidence expression pro les of CAD patients and healthy controls emphasizes the implications of the interplay between were searched from the Gene Expression Omnibus (GEO; autophagy and apoptosis in CAD [13]. The balance between https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi) according — the two decides cell survival. Both serum levels in CAD to the following criteria: organism Homo sapiens; experi- — fi patients are higher than healthy controls [14]. lncRNAs with ment type noncoding RNA pro ling by array; and disea- — >200 nucleotides may participate in the pathophysiological se CAD. As a result, two datasets including GSE113079 processes of CAD including autophagy and apoptosis [15]. and GSE69587 datasets were obtained for this study. The On account of their tissue and cell specificity, circulating GSE113079 dataset included 93 CAD and 48 healthy blood lncRNAs are promising diagnostic markers for various dis- samples based on the GPL20115 platform [19]. The eases [15]. A previous study has identified three lncRNAs GSE69587 dataset was composed of 3 CAD and 3 healthy including Chast, HULC, and DICER1-AS1 that are distinctly blood specimens on the platform of GPL15314 [20]. The related to autophagy in blood circulation of CAD patients microarray data were normalized to quartile by the normal- [16]. Among them, HULC and DICER1-AS1 may properly izeBetweenArrays in the limma package [21]. If the same differentiate CAD individuals from healthy individuals. It gene corresponded to multiple IDs, the average value was has been demonstrated that apoptosis and autophagy may calculated as the expression level of the gene. be mediated by several common lncRNAs in CAD. For 2.2. Differential Expression Analysis. Differentially expressed example, lncRNA MALAT1 [17] or THRIL [18] inhibits mRNAs or lncRNAs were screened between CAD and autophagy and apoptosis of endothelial progenitor cells in healthy groups with the cutoff of ∣fold change ðFCÞ ∣ >1:5 CAD. However, it remains unclear what the clinical implica- and adjusted p value < 0.05 via the limma package, which tions of autophagy- and apoptosis-related lncRNAs in CAD were visualized into volcano and heatmaps [21]. are. Herein, we firstly screened circulating dysregulated apo- ptosis- and autophagy-related mRNAs in CAD. Secondly, 2.3. Autophagy- and Apoptosis-Related mRNAs. Genes in fi circulating abnormally expressed lncRNAs were identi ed autophagy (entry: map04140) and apoptosis (entry: ’ in CAD compared to healthy subjects. Thirdly, Spearson s map04210) were obtained from the Kyoto Encyclopedia of correlation analysis was employed for identifying circulating Genes and Genomes database (KEGG; https://www.kegg apoptosis- and autophagy-related lncRNAs, and ROC curves .jp/) [22]. They were overlapped by differentially expressed ffi were conducted for evaluating their diagnostic e cacy for mRNAs called differentially expressed autophagy- and fi CAD. Finally, their expression was externally veri ed in apoptosis-related mRNAs. blood specimens of CAD and healthy subjects. Figure 1 showed the workflow of this study. These lncRNAs proposed 2.4. Protein-Protein Interaction (PPI). Physical or functional by our findings may reflect the pathologically relevant pro- interactions between specified proteins were analyzed via the BioMed Research International Expression − − 4 2 0 2 4 6 8 SM3095926 SM3095930 SM3095934 SM3095938 SM3095942 SM3095946 SM3095950 SM3095954 SM3095958 SM3095962 SM3095966 SM3095970 SM3095974 SM3095978 Expression − 5 SM3095982 0 5 (b) SM3095986 SM3095990 SM3095994 SM3095998 SM3095926 SM3096002 SM3095930 SM3096006 SM3095934 SM3096010 SM3095938 SM3096014 SM3095942 SM3096018 SM3095946 SM3096022 SM3095950 SM3096026 SM3095954 SM3096030 SM3095958 Figure SM3096034 SM3095962 SM3096038 SM3095966 SM3096042 SM3095970 SM3096046 SM3095974 SM3095978 2: Continued. SM3096050 SM3095982 SM3096054 (a) SM3096058 SM3095986 SM3096062 SM3095990 SM3096066 SM3095994 SM3095998 SM3096002 SM3096006 − SM3096010 CAD 10 0 5 5 SM3096014 SM3096018 NMNAT2 SM3096022
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