Plasma microRNAs reflecting cardiac and inflammatory injury in coronary artery bypass grafting surgery

Wang, Zi; Li, Xiaoye; Shen, Jie; Tian, Dan; Ji, Qiuyi; Xia, Limin; Lv, Qianzhou

doi:10.1016/j.jss.2017.11.036

Cited by 12 publications

(11 citation statements)

References 28 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Several recent studies have found that plasma levels of myogenic miRNAs were elevated after open-heart surgeries, correlated with serum levels of cardiac troponin (cTnI), and responded earlier to myocardial ischemia and infarction than cTnI [28-31]. Through passive release or active secretion, circulating miRNA levels could serve as signaling molecules and have a systemic influence [6].…”

Section: Discussionmentioning

confidence: 99%

Plasma Levels of Myocardial MicroRNA-133a Increase by Intraoperative Cytokine Hemoadsorption in the Complex Cardiovascular Operation

et al. 2019

View full text Add to dashboard Cite

BackgroundComplex cardiovascular procedures may initiate a systemic inflammatory response syndrome (SIRS) with a massive cytokine release, which is involved in postoperative myocardial injury. Intraoperative cytokine hemoadsorption (HA) mitigates the inflammatory response. Micro ribonucleic acids (miRNAs) are emerging as a marker of myocardial injury.MethodsThis study evaluated if intraoperative cytokine reduction by HA modulates SIRS and affects myocardial injury as measured by miRNA-126, 223 and miRNA-1, 133a, respectively. Twenty-eight patients were assigned into HA (n = 15) and control (C) (n = 13) groups. HA was performed by integrating CytoSorb™ into the extracorporeal circuit.ResultsMiRNA-133a plasma levels were increased postoperatively in both groups but were much higher in the HA group than in the C group at 3 h (P = 0.037) and 18 h (P = 0.017) after reperfusion. MiRNA-1 and miRNA-223 plasma levels were significantly increased postoperatively, but did not differ between groups. The vascular miRNA-126 was not affected.ConclusionIntraoperative cytokine HA in cardiovascular operations increased the plasma levels of miRNA-133a, suggesting higher myocardial injury.

show abstract

Section: Discussionmentioning

confidence: 99%

Plasma Levels of Myocardial MicroRNA-133a Increase by Intraoperative Cytokine Hemoadsorption in the Complex Cardiovascular Operation

et al. 2019

View full text Add to dashboard Cite

show abstract

“…Our results also suggested that microRNA-208a reduced inflammation and oxidative stress in vitro model. Wang et al [21] showed that microRNA-208a was significantly related to IL-6 in coronary artery bypass grafting surgery.…”

Section: Discussionmentioning

confidence: 99%

Effects of microRNA-208a on inflammation and oxidative stress in ketamine-induced cardiotoxicity through Notch/NF-κB signal pathways by CHD9

Yuan

Deng

et al. 2019

Bioscience Reports

View full text Add to dashboard Cite

Background: MicroRNA can regulate gene expression, and participate in multiple vital activities, such as inflammation, oxidative stress epigenetic modification, cell proliferation, and apoptosis. It plays an important role in the genesis and development of cardiovascular disease. Objective: To assess the role of microRNA-208a in ketamine-induced cardiotoxicity. Methods: All rats were randomly selected into two groups: sham and model groups. After fixed, all rats in the model group was intraperitoneally (IP) injected with 100 mg/kg of ketamine. Heart samples were stained with HE assay. Total RNAs from serum were used to hybridize with the SurePrint G3 Rat Whole Genome GE 8×60 K Microarray G4858A platform. Results: In the rat model with ketamine-induced cardiotoxicity, microRNA-208a expression was increased. Then, over-expression of microRNA-208a increased inflammation and oxidative stress in vitro model. However, down-regulation of microRNA-208a decreased inflammation and oxidative stress in vitro model. Over-expression of microRNA-208a suppressed CHD9 and Notch1, and induced p65 protein expression in vitro model. Overexpression of CHD9 reduced the effects of microRNA-208a on inflammation and oxidative stress in heart cell through Notch/p65 signal pathways. Notch1 activation reduced the effects of microRNA-208a on inflammation and oxidative stress in heart cell through p65 signal pathways. Conclusion: MicroRNA-208a may be a potential biomarker for ketamine-induced cardiotoxicity through inflammation and oxidative stress by Notch/NF-κB signal pathways by CHD9.

show abstract

“…The biological behavior of HUVSMcs and HUVEcs allows them to serve an important role in restenosis and long-term occlusion of vein bridges following coronary angioplasty (41)(42)(43)(44). Increasing evidence has indicated that the abnormal expression of miRNAs serves an important role in transplanted vascular diseases and they have received much interest in the research of various diseases (21,(45)(46)(47). Proliferation, migration and phenotypic transformation of SMcs or endothelial cells are associated with various miRNAs (48) including miR-145 (49,50), miR-222 (51), miR-195 (52) and miR-21 (53).…”

Section: Discussionmentioning

confidence: 99%

Upregulation of miR‑423 improves autologous vein graft restenosis via targeting ADAMTS‑7

Ren

Liang

et al. 2019

Int J Mol Med

View full text Add to dashboard Cite

coronary artery bypass graft (cABG) is one of the primary methods of treating coronary heart disease (cHd); however, vein graft restenosis is a major limiting factor of the effectiveness of cABG. Emerging evidence has indicated that miR-423 is associated with vascular diseases. Additionally, upregulation of a disintegrin and metalloproteinase with thrombospondin motifs-7 (AdAMTS-7) contributes to neointima formation by promoting the proliferation and migration of vascular smooth muscle cells and inhibiting the proliferation and migration of endothelial cells. The aim of the present study was to examine the effects of miR-423 target, AdAMTS-7, on regulating vein graft disease and identify novel biomarkers for use in therapy of vein graft failure (VGF). Aberrant expression of miR-423 in plasma of patients with CHD prior to and following CABG confirms that miR-423 may be a suitable target for preventing VGF. Furthermore, a dual-luciferase reporter gene assay indicated that miR-423 directly interacted with AdAMTS-7 and suppressed its expression. Ectopic expression of miR-423 suppressed AdAMTS-7, resulting in decreased proliferation and migration rates of human umbilical vein smooth muscle cells by targeting AdAMTS-7, but resulted in increased proliferation and migration of human umbilical vein endothelial cells in vitro. Overexpression of miR-423 also enhanced re-endothelialization and decreased neointimal formation in a rat vein graft model. In conclusion, the results of the present study demonstrated that the miR-423/AdAMTS-7 axis may possess potential clinical value for the prevention and treatment of restenosis in patients with cHd following cABG.

show abstract

Plasma microRNAs reflecting cardiac and inflammatory injury in coronary artery bypass grafting surgery

Cited by 12 publications

References 28 publications

Plasma Levels of Myocardial MicroRNA-133a Increase by Intraoperative Cytokine Hemoadsorption in the Complex Cardiovascular Operation

Plasma Levels of Myocardial MicroRNA-133a Increase by Intraoperative Cytokine Hemoadsorption in the Complex Cardiovascular Operation

Effects of microRNA-208a on inflammation and oxidative stress in ketamine-induced cardiotoxicity through Notch/NF-κB signal pathways by CHD9

Upregulation of miR‑423 improves autologous vein graft restenosis via targeting ADAMTS‑7

Contact Info

Product

Resources

About