Reciprocal Changes of Circulating Long Non-Coding RNAs ZFAS1 and CDR1AS Predict Acute Myocardial Infarction

Zhang, Ying; Sun, Lihua; Xuan, Lina; Pan, Zhenwei; Li, Kang; Liu, Shuangshuang; Huang, Yuechao; Zhao, Xu-Yun; Hu, Lihua; Wang, Zhiguo; Hou, Yan; Li, Junnan; Tian, Ye; Yu, Jiahui; Han, Ho Jae; Liu, Yanhong; Gao, Fei; Zhang, Yong; Shu, Wang; Du, Zhenhong; Lu, Yanjie; Yang, Baofeng

doi:10.1038/srep22384

Cited by 115 publications

(79 citation statements)

References 36 publications

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“…Recently, few literatures have focused on the role of lncRNAs in AMI. For instance, circulating level of lncRNA ZFAS1 in AMI subjects was significantly lower than that in non-AMI subjects, whereas the level of lncRNA CDR1AS in AMI subjects was higher than that in non-AMI subjects [12]. Vausort et al studied expressions of five different lncRNAs in patients with MI, and showed that several lncRNAs were aberrantly expressed in MI patients [13].…”

Section: Introductionmentioning

confidence: 99%

Long Non-Coding RNA H19 Protects H9c2 Cells against Hypoxia-Induced Injury by Targeting MicroRNA-139

Gong¹,

Xu²,

Guo³

et al. 2017

Cell Physiol Biochem

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Background/Aims: Acute myocardial infarction (AMI) occurs when blood supply to the heart is diminished (ischemia) for long time; ischemia is primarily caused due to hypoxia. The present study evaluated the effects of long non-coding RNA H19 on hypoxic rat H9c2 cells and mouse HL-1 cells. Methods: Hypoxic injury was confirmed by measuring cell viability, migration and invasion, and apoptosis using MTT, Transwell and flow cytometry assays, respectively. H19 expression after hypoxia was estimated by qRT-PCR. We then measured the effects of non-physiologically expressed H19, knockdown of miR-139 with or without H19 silence, and abnormally expressed Sox8 on hypoxia-induced H9c2 cells. Moreover, the interacted miRNA for H19 and downstream target gene were virtually screened and verified. The involved signaling pathways and the effects of abnormally expressed H19 on contractility of HL-1 cells were explored via Western blot analysis. Results: Hypoxia induced decreases of cell viability, migration and invasion, increase of cell apoptosis and up-regulation of H19. Knockdown of H19 increased hypoxia-induced injury in H9c2 cells. H19 acted as a sponge for miR-139 and H19 knockdown aggravated hypoxia-induced injury by up-regulating miR-139. Sox8 was identified as a target of miR-139, and its expression was negatively regulated by miR-139. The mechanistic studies revealed that overexpression of Sox8 might decrease hypoxia-induced cell injury by activating the PI3K/AKT/mTOR pathway and MAPK. Besides, H19 promoted contractility of HL-1 cells. Conclusion: These findings suggest that H19 alleviates hypoxia-induced myocardial cell injury by miR-139-mediated up-regulation of Sox8, along with activation of the PI3K/AKT/mTOR pathway and MAPK.

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Section: Introductionmentioning

confidence: 99%

Long Non-Coding RNA H19 Protects H9c2 Cells against Hypoxia-Induced Injury by Targeting MicroRNA-139

Gong¹,

Xu²,

Guo³

et al. 2017

Cell Physiol Biochem

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“…ZFAS1 (zinc finger antisense 1) is one of cardiac-specific or cardiacrelated lncRNAs. Previous study observed the increased ZFAS1 level in myocardium of AMI mouse models (Zhang et al, 2016a), suggesting the potential involvement of ZFAS1 in AMI. However, its role has not been defined.…”

mentioning

confidence: 78%

Knockdown of Long Non‐Coding RNA‐ZFAS1 Protects Cardiomyocytes Against Acute Myocardial Infarction Via Anti‐Apoptosis by Regulating miR‐150/CRP

et al. 2017

J of Cellular Biochemistry

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ZFAS1 is one of cardiac-specific or cardiac-related lncRNAs. This study was to explore the functional involvement of ZFAS1 and its regulatory role in AMI. In this study, the models of AMI rat and myocardial cell cultured under hypoxia were made. The expression of ZFAS1 and miR-150 of myocardial infarction tissue or cardiac myocytes was determined by quantitative real time PCR. The regulatory role of ZFAS1 on miR-150 was examined by RNA pull down assay. The effect of miR-150 or ZFAS1 expression on cell viability was analyzed by MTT assay. The relative expression of ZFAS1 in the myocardium infracted zone and border zone was significantly upregulated at 1-48 h of AMI rats, but it downregulated at 1 week and 2 weeks; miR-150 was significantly downregulated at AMI-1-48 h and upregulated at 1 and 2 weeks after model establishment. The result of RNA pull down assay indicated that ZFAS1 could interact directly with miR-150. C-reactive protein (CRP) was regulated by ZFAS1/miR-150 axis and negatively targeted by miR-150. Hypoxia caused the decrease of cell viability and the upregulation of CRP at mRNA and protein levels; whereas this upregulation could be attenuated by miR-150 mimic or si-ZFAS1 in H9C2 cells and cardiomyocytes. Knockdown of ZFAS1 or miR-150 overexpression effectively relieved AMI-induced myocardial infarction in AMI-1 week rats. The ZFAS1/miR-150 axis was involved in the molecular mechanism of AMI induced cardiomyocytes apoptosis via regulating CRP. J. Cell. Biochem. 118: 3281-3289, 2017. © 2017 Wiley Periodicals, Inc.

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“…Serum lncRNA-RP11-445H22.4 has been confirmed as a biomarker for detecting breast cancer and exhibited AUC of 0.904 (Sp = 74%, Se = 92%) [20]. Ying Zhang revealed lncRNA-ZFAS1 and lncRNA-CDR1AS as novel predictors for acute myocardial infarction (AMI) in human whole blood; the AUC was 0.664 or 0.671 when AMI was diagnosed with lncRNA-ZFAS1 or lncRNA-CDR1AS alone and increased to 0.691 when the two lncRNAs were combined [21]. We first evaluated the diagnostic value of lncRNAs in human peripheral blood samples for IS based on lncRNA microarray screening and qRT-PCR validations.…”

Section: Cellular Physiology and Biochemistrymentioning

confidence: 99%

Identification of Novel LncRNA Biomarkers and Construction of LncRNA-Related Networks in Han Chinese Patients with Ischemic Stroke

Guo

Yang

Liang

et al. 2018

Cell Physiol Biochem

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Background/Aims: Long non-coding RNAs (lncRNAs) are potential biomarkers of tumors, cardiac disease, and cerebral disease because of their interaction with coding RNAs. This work focused on ischemic stroke (IS) and aimed to identify novel lncRNA biomarkers and construct lncRNA-related networks in IS. Methods: Differentially expressed lncRNAs were identified using Arraystar Human LncRNA Microarray v4.0, and validated with qRT-PCR. A lncRNA–mRNA co-expression network and a lncRNA–miRNA–mRNA regulatory network were constructed. Functional and pathway analyses were then performed. Results: In total, 560 up-regulated and 690 down-regulated differentially expressed lncRNAs were found (P < 0.05, false discovery rate < 0.05, absolute fold change ≥ 2). qRT-PCR results confirmed that lncRNA-ENST00000568297, lncRNA-ENST00000568243, and lncRNA-NR_046084 exhibited significant differential expression between IS and controls (all P < 0.05). Areas under the curves (AUCs) for these lncRNAs were 0.733, 0.743, and 0.690, respectively, and the combined AUC was 0.843. A coding–noncoding co-expression (CNC) network was constructed based on Pearson’s correlation coefficient. A specific lncRNA–miRNA–mRNA regulatory network of ENST00000568297, ENST00000568243, and NR_046084 was also constructed. Functional annotation of the up- and down-regulated mRNAs was performed. Pathway analysis enriched IS-related pathways with mRNAs in the lncRNA–miRNA–mRNA regulatory network. Conclusion: LncRNA and mRNA expression profiles in human peripheral blood were altered after IS. ENST00000568297, ENST00000568243, and NR_046084 were identified as novel potential diagnostic biomarkers of IS. Analysis of the CNC network and lncRNA–miRNA–mRNA regulatory network suggested that lncRNAs may participate in IS pathophysiology by regulating pivotal miRNAs, mRNAs, or IS-related pathways.

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Reciprocal Changes of Circulating Long Non-Coding RNAs ZFAS1 and CDR1AS Predict Acute Myocardial Infarction

Cited by 115 publications

References 36 publications

Long Non-Coding RNA H19 Protects H9c2 Cells against Hypoxia-Induced Injury by Targeting MicroRNA-139

Long Non-Coding RNA H19 Protects H9c2 Cells against Hypoxia-Induced Injury by Targeting MicroRNA-139

Knockdown of Long Non‐Coding RNA‐ZFAS1 Protects Cardiomyocytes Against Acute Myocardial Infarction Via Anti‐Apoptosis by Regulating miR‐150/CRP

Identification of Novel LncRNA Biomarkers and Construction of LncRNA-Related Networks in Han Chinese Patients with Ischemic Stroke

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