LncRNA ANRIL knockdown relieves myocardial cell apoptosis in acute myocardial infarction by regulating IL-33/ST2

Objective: To characterize the expression of long non-coding RNA LncRNA-FA2H-2 in coronary heart disease (CHD) and its correlation with inflammatory markers.Methods: From December 2018 to December 2020, 316 patients at Henan Provincial People's Hospital who complained of chest tightness or chest pain and had coronary angiography to clarify their coronary artery conditions for definitive diagnoses were selected as the study subjects. Plasma was collected to detect white blood cells (WBCs), total cholesterol (TG), triglyceride cholesterol (TC), low-density lipoprotein cholesterol (LDL-C), high-density lipoprotein cholesterol (HDL-C), apolipoprotein A1 (ApoA1), and C-reactive protein (CRP) levels. Tumor necrosis factor (TNF-α), monocyte chemotactic protein 1 (MCP-1), vascular cell adhesion molecule-1 (VCAM-1), intercellular cell adhesion molecule-1 (ICAM-1), and interleukin-6 (IL-6) levels were also measured using ELISA. The expression levels of lncRNA-FA2H-2 were measured using quantitative real-time PCR. The data obtained were analyzed by independent sample t-tests, rank sum tests, regression analyses, Pearson's or Spearman's correlation analyses, and receiver operating characteristic curves.Results: (1) Compared with the control group, the differences in age, sex, diabetes, smoking, drinking, body mass index (BMI), WBC, TC, and LDL-C in CHD were not statistically significant, while the differences in hypertension, TG, HDL-C, ApoA1, and CRP were statistically significant. (2) In the grouping of coronary lesion branches, patients with age, sex, hypertension, diabetes, smoking, drinking, BMI, WBC, TC, LDL-C, HDL-C, and ApoA1 differences were not statistically significant, but TG and CRP differences were statistically significant. (3) The relative expressions of TNF-α, MCP-1, VCAM-1, ICAM-1, and IL-6 were significantly upregulated in the CHD group (P < 0.001). (4) The results showed that the relative levels of TNF-α, MCP-1, VCAM-1, ICAM-1, and IL-6 between the two comparative analyses (high risk, moderate risk, and low risk groups) were statistically significant. In addition, positive correlations were found between the Gensini score and TNF-α, MCP-1, VCAM-1, ICAM-1, and IL-6 in CHD patients. (5) LncRNA-FA2H-2 relative expression in the CHD group was significantly downregulated (P < 0.001). (6) The differences in the expression levels of LncRNA-FA2H-2 were statistically significant between the two comparative analyses (P < 0.01), except between the 2-branch lesion and 3-branch lesion groups. (7) LncRNA-FA2H-2 was not associated with age, sex, hypertension, diabetes, smoking, drinking, BMI, WBC, TG, TC, LDL-C, HDL-C, and ApoA1 (P > 0.05). (8) A correlation was found between LncRNA-FA2H-2 and MCP-1, and VCAM-1, ICAM-1, IL-6, and Gensini. (9) The results indicated that the relative levels of LncRNA-FA2H-2 between the two comparative analyses (high risk, moderate risk, and low risk groups) were statistically significant. A negative correlation was found between the Gensini score and LncRNA-FA2H-2. (10) ROC curve analyses of TNF-α, MCP-1, VCAM-1, ICAM-1, and IL-6 in CHD showed the area under the curve (AUC) = 0.832 (0.77, 0.893) with a cut-off value of 290.5, a sensitivity of 73%, and a specificity of 64%; AUC = 0.731 (0.653, 0.809) with a cut-off value of 396 and with a sensitivity of 59% and specificity of 79%; AUC = 0.822 (0.757, 0.887) with a cut-off value of 264 and with a sensitivity of 72% and specificity of 83%; AUC = 0.794 (0.715, 0.874) with a cut-off value of 201.5 and with a sensitivity of 75% and specificity of 65%; AUC = 0.760 (0.685, 0.834) with a cut-off value of 328 and with a sensitivity of 55% and specificity of 90%. (11) ROC curve analysis of LncRNA-FA2H-2 in CHD patients showed AUC = 0.834 (0.688, 0.85) with a cut-off value of 3.155 and with a sensitivity of 85% and specificity of 82%. (12) Logistic analyses showed that TNF-α, MCP-1, VCAM-1, IL-6, and LncRNA-FA2H-2 were independent risk factors for CHD.Conclusions: The expression of LncRNA-FA2H-2 was reduced and inversely correlated with inflammation-related factors in CHD patients. LncRNA-FA2H-2 may have potential as an inflammatory marker for risk assessment of CHD development.

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“…Kcnq1ot1 could be used as a prognostic indicator to determine left ventricular function (33)(34)(35).…”

Section: Discussionmentioning

confidence: 99%

Correlation of Long Non-coding RNA LncRNA-FA2H-2 With Inflammatory Markers in the Peripheral Blood of Patients With Coronary Heart Disease

Guo

Sha

et al. 2021

Front. Cardiovasc. Med.

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“…Abnormal expression of ANRIL is associated with vascular endothelium injury and proliferation, migration, and apoptosis of VSMCs; which also contribute to mononuclear cell adhesion and proliferation ( 104 , 105 ). ANRIL knockdown induced cardiomyocyte apoptosis in acute MI by regulating IL-33/ST2 or Akt ( 106 , 107 ). Enhanced expression of ANRIL and suppressed expression of miR-181b, which was inhibited by ANRIL, were recorded in CAD populations and confirmed ANRIL as an independent risk factor ( 108 ).…”

Section: Predicted Lncrnas Based On Available Evidencementioning

confidence: 99%

The Role of Long Non-coding RNAs in Sepsis-Induced Cardiac Dysfunction

Zhang

et al. 2021

Front. Cardiovasc. Med.

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Sepsis is a syndrome with life-threatening organ dysfunction induced by a dysregulated host response to infection. The heart is one of the most commonly involved organs during sepsis, and cardiac dysfunction, which is usually indicative of an extremely poor clinical outcome, is a leading cause of death in septic cases. Despite substantial improvements in the understanding of the mechanisms that contribute to the origin and responses to sepsis, the prognosis of sepsis-induced cardiac dysfunction (SICD) remains poor and its molecular pathophysiological changes are not well-characterized. The recently discovered group of mediators known as long non-coding RNAs (lncRNAs) have presented novel insights and opportunities to explore the mechanisms and development of SICD and may provide new targets for diagnosis and therapeutic strategies. LncRNAs are RNA transcripts of more than 200 nucleotides with limited or no protein-coding potential. Evidence has rapidly accumulated from numerous studies on how lncRNAs function in associated regulatory circuits during SICD. This review outlines the direct evidence of the effect of lncRNAs on SICD based on clinical trials and animal studies. Furthermore, potential functional lncRNAs in SICD that have been identified in sepsis studies are summarized with a proven biological function in research on other cardiovascular diseases.

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“…In contrast to the immunomodulation effect of IL-18 which can stimulate Th1 cells to secrete a variety of cytokines and promote the proliferation of Th1 cells, IL-33/sST2 can regulate Th1/Th2 balance by promoting Th2 anti-inflammatory immunity and inhibiting Th1 immune response. 9 Emerging studies have revealed that IL-33/sST2 is closely correlated with cardiovascular diseases, autoimmune and nervous system diseases, 10–12 yet its role in the nervous system remains poorly understood. Some studies have demonstrated that serum IL-33 has a protective effect against stroke through anti-inflammatory and can improve the prognosis of stroke.…”

Section: Introductionmentioning

confidence: 99%

The Clinical Significance of Serum IL-33 and sST2 Alterations in the Post-Stroke Depression

Xu¹,

Wu²

2021

JMDH

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Introduction This study was to test whether the serum levels of IL-33 and sST2 are correlated with the development of depression after acute ischemic stroke. Methods Patients diagnosed with acute ischemic stroke were selected. This study took the 24-item Hamilton Depression Rating Scale (HAMD) (score ≥20) as the diagnostic criteria for depression. On the 21st day after admission, patients who met the depression diagnostic criteria were included in the depression group, and patients who failed to meet the diagnostic criteria were included in the non-depression group. The serum levels of IL-33, sST2 and hsCRP were measured by enzyme-linked immunosorbent assay (ELISA). Results On 1st day after stroke, compared with the non-depression group, there was no significant difference in the serum IL-33, sST2 and hsCRP levels in the depression group; on 21st day after stroke, compared with the non-depression group, the serum IL-33 and hsCRP levels were significantly increased, while the sST2 level was significantly decreased in the depression group. Correlation analysis showed that IL-33 was positively correlated with the depression quantitative score and hsCRP, while sST2 was negatively correlated with the depression quantitative score and hsCRP. Regression analysis showed that IL-33 and sST2 were independent risk factors for the depression after acute ischemic stroke. Discussion The abnormal alterations of serum IL-33 and sST2 levels in the stroke patients may serve as one of the risk factors for the occurrence and exacerbation of the depression, and its mechanism may be related to the promotion of inflammatory factor production in vivo.

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LncRNA ANRIL knockdown relieves myocardial cell apoptosis in acute myocardial infarction by regulating IL-33/ST2

Cited by 48 publications

References 28 publications

Correlation of Long Non-coding RNA LncRNA-FA2H-2 With Inflammatory Markers in the Peripheral Blood of Patients With Coronary Heart Disease

Correlation of Long Non-coding RNA LncRNA-FA2H-2 With Inflammatory Markers in the Peripheral Blood of Patients With Coronary Heart Disease

The Role of Long Non-coding RNAs in Sepsis-Induced Cardiac Dysfunction

The Clinical Significance of Serum IL-33 and sST2 Alterations in the Post-Stroke Depression

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