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Dysregulated circulating SOCS3 and HP expression associated with stable CAD and acute coronary syndrome: an integrated study based on bioinformatics analysis and case control validation [Anatol J Cardiol]
Anatol J Cardiol. Ahead of Print: AJC-56346 | DOI: 10.14744/AnatolJCardiol.2020.56346  

Dysregulated circulating SOCS3 and HP expression associated with stable CAD and acute coronary syndrome: an integrated study based on bioinformatics analysis and case control validation

Xunnan Zhang1, Xi Lv1, Xiandong Li2, Yaping Wang1, Hao-yu Lin3, Jicai Zhang2, Chunyan Peng4
1Postgraduate Training Basement of Jinzhou Medicical University, Taihe Hospital, Hubei University of Medicine, Shiyan 442000, Hubei, P.R. China
2Department of Laboratory Medicine, Taihe Hospital, Hubei University of Medicine, Shiyan 442000, Hubei, P.R. China
3Department of Breast and Thyroid Surgery, The First Affiliated Hospital of Shantou University Medical College, Shantou 515000, Guangdong, P.R. China
4Hubei Key Laboratory of Wudang Local Chinese Medicine Research, Hubei University of Medicine, Hubei Province, P.R. China
5Hubei Key Laboratory of Embryonic Stem Cell research, Hubei University of Medicine, Hubei Province, P.R. China

Objective: Blood transcriptome analysis has been extensively used to identify potential diagnostic and therapeutic targets for cardiovascular diseases. Methods: Two gene expression datasets (GSE59867 and GSE62646) were downloaded from GEO Datasets to identify altered blood transcriptomes in patients with ST-segment elevated myocardial infarction (STEMI) compared to stable CAD state. Thereafter, several computational approaches were adopted to determine functional roles and regulatory networks of differentially expressed genes (DEGs). Finally, the expression of dysregulated two hub genes-SOCS3 and HP were validated in a case-control study. Results: A total of 119 DEGs were identified in the discovery phase, consisting of 71 up-regulated genes and 48 down-regulated genes; two hub modules consisting of two hub genes-SOCS3 and HP were identified. In the validation phase, both SOCS3 and HP were significantly down-regulated in the stable CAD patients and ACS patients when compared with healthy controls. Meanwhile, HP was significant up-regulated in STEMI patients when compared with stable CAD patients (p = 0.041). Logistic regression analysis indicated that down-regulated expression of HP correlated with increased risk of CAD (odds ratio (OR) = 0.52, 95% confidence interval (CI) = 0.31~0.87, p = 0.013); down-regulated expression of SOCS3 correlated with increased risk of ACS (odds ratio (OR) = 0.66, 95% confidence interval (CI) = 0.46~0.94, p = 0.023) when age, gender, history of hyperlipidemia, diabetes and hypertension were included as covariates. Conclusion: Future clarification of how SOCS3 and HP influence the pathogenesis of disease might pave the way for the development of novel diagnostic and therapeutic methods.

Keywords: SOCS3, HP, coronary artery disease, acute coronary syndrome, differentially expressed genes, microarray analysis




Corresponding Author: Chunyan Peng, China


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