MicroRNA-939 governs vascular integrity and angiogenesis through targeting γ-catenin in endothelial cells

Hou, Shiqiang; Fang, Ming; Zhu, Qian; Liu, Ying; Liu, Liang; Li, Xinming

doi:10.1016/j.bbrc.2017.01.085

Cited by 24 publications

(19 citation statements)

References 27 publications

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“…The results of the present study demonstrated that ulinastatin significantly inhibited NF-κB, TNF-α, IL-1β and IL-6 levels in ISO-induced CHF rats through suppression of NF-κB. Hou et al (16) posited that ulinastatin may inhibit inflammation via regulation of the 5'-AMP-activated protein kinase/NF-κB pathway in lipopolysaccharide-induced acute lung injury in mice.…”

Section: Discussionsupporting

confidence: 58%

“…Ulinastatin is a type of glycoprotein, isolated and purified from the fresh urine of healthy adult males, which acts as a broad-spectrum enzyme inhibitor and may block the release of inflammatory cytokines, prevent the initiation of the cytokine cascade, suppress excessive activation of leukocytes, and block cycle of feedback activation among cytokines, inflammatory mediators and leukocytes (16). Previous studies have demonstrated, regarding the anti-inflammatory, immunomodulatory and visceral protective effects of ulinastatin, that ulinastatin exhibits a cellular protective function in ischemia-reperfusion injury in the liver, kidney, heart and lung, and improves immune function (16)(17)(18). The present study examined the hypothesis that the cardioprotective effect of ulinastatin may prevent ISO-induced CHF, and aimed to elucidate the possible mechanism.…”

Section: Introductionmentioning

confidence: 99%

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Cardioprotective effects of ulinastatin against isoproterenol-induced chronic heart failure through the PI3K‑Akt, p38 MAPK and NF-κB pathways

Hao

Jiang

et al. 2017

Mol Med Report

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The purpose of the present study was to evaluate the cardioprotective effect of ulinastatin against isoproterenol‑induced chronic heart failure (CHF). Compared with the control group, treatment with ulinastatin decreased interventricular septal thickness and left ventricular posterior wall thickness, and improved the left ventricular ejection fraction, left ventricular fractional shortening and peak E and peak A ratio in the isoproterenol‑induced CHF rat. In addition, ulinastatin suppressed inflammation, oxidative stress and apoptosis in heart tissue from isoproterenol‑induced CHF rats. Ulinastatin induced the activation of the phosphatidylinositol 3‑kinase (PI3K)/RAC‑α serine/threonine protein kinase (Akt) signaling pathway and downregulated the p38 mitogen‑activated protein kinase (MAPK) and nuclear factor (NF)‑κB pathway in isoproterenol‑induced CHF rats. These data demonstrated the cardioprotective effect of ulinastatin against isoproterenol‑induced chronic heart failure through the PI3K‑Akt, p38 MAPK and NF‑κB pathways.

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Section: Discussionsupporting

confidence: 58%

Section: Introductionmentioning

confidence: 99%

Cardioprotective effects of ulinastatin against isoproterenol-induced chronic heart failure through the PI3K‑Akt, p38 MAPK and NF-κB pathways

Hao

Jiang

et al. 2017

Mol Med Report

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“…miRNA-939 inhibits angiogenesis by targeting human-catenin proteins, thus destroying the integrity of blood vessels. Overexpression of miRNA-939 in HUVECs can significantly inhibit cell proliferation, adhesion and angiogenesis but increase cell migration (35).…”

Section: Sequencing Samples All Clinical Samples Collectedmentioning

confidence: 99%

A novel plasma lncRNA ENST00000416361 is upregulated in coronary artery disease and is related to inflammation and lipid metabolism

Yan

et al. 2020

Mol Med Report

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coronary artery disease (cad) is a serious threat to human health and a major cause of mortality worldwide. long noncoding rnas (lncrnas) affect the occurrence and development of cad via the regulation of cell proliferation and apoptosis, inflammatory responses and lipid metabolism. Screening methods and therapeutic strategies for cad have been extensively studied. The present study analyzed clinical indexes of 187 patients with CAD and 150 healthy subjects. The data showed significant differences in diabetes mellitus, hypertension, high-density lipoprotein level and smoking history between the CAD group and the control group. A series of differentially expressed lncRNAs were detected in the plasma samples of three patients with CAD by high-throughput sequencing. reverse transcription-quantitative (rT-q)Pcr data revealed that the expression level of the novel lncRNA enST00000416361 was ~2.3-fold higher in the plasma of 50 patients with CAD compared with the 50 control subjects. receiver operating characteristic (roc) curves were generated, and the area under the roc curve was 0.7902. Knockdown of ENST00000416361 in human umbilical vein endothelial cells markedly downregulated interleukin-6 and tumor necrosis factor-α levels. In addition, sterol regulatory element binding transcription factor (SreBP)1 and SreBP2 were upregulated in patients with cad, and they were positively correlated with the expression of ENST00000416361. RT-qPCR further demonstrated that knockdown of enST00000416361 led to the downregulation of SreBP1 and SreBP2. overall, the novel lncRNA ENST00000416361 may be associated with CAD-induced inflammation and lipid metabolism, and it may serve as a potential biomarker for CAD.

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“…This mechanism plays an essential role in vascular remodeling during ischemic events [148]. Because the growth of collateral vessels offers an alternative route for irrigation when a coronary artery is blocked, angiogenesis may decrease myocardial damage and improve prognosis [149]. HUVEC models have been used to study the molecular and signaling pathways involved in this process [150][151][152][153][154].…”

Section: Angiogenesismentioning

confidence: 99%

“…Voellenkle et al identified 400 microRNAs differentially expressed in HUVEC associated with angiogenesis under hypoxic conditions [157]. MicroRNA-939 is negatively regulated in patients with coronary artery disease, and this reduced expression is associated with increased coronary collateral circulation [149]. The authors suggest these microRNAs are potential biomarkers and therapeutic targets in ischemic heart disease.…”

Section: Angiogenesismentioning

confidence: 99%

Use of Human Umbilical Vein Endothelial Cells (HUVEC) as a Model to Study Cardiovascular Disease: A Review

et al. 2020

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Cardiovascular disease (CVD) is the leading cause of death worldwide, and extensive research has been performed to understand this disease better, using various experimental models. The endothelium plays a crucial role in the development of CVD, since it is an interface between bloodstream components, such as monocytes and platelets, and other arterial wall components. Human umbilical vein endothelial cell (HUVEC) isolation from umbilical cord was first described in 1973. To date, this model is still widely used because of the high HUVEC isolation success rate, and because HUVEC are an excellent model to study a broad array of diseases, including cardiovascular and metabolic diseases. We here review the history of HUVEC isolation, the HUVEC model over time, HUVEC culture characteristics and conditions, advantages and disadvantages of this model and finally, its applications in the area of cardiovascular diseases.

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MicroRNA-939 governs vascular integrity and angiogenesis through targeting γ-catenin in endothelial cells

Cited by 24 publications

References 27 publications

Cardioprotective effects of ulinastatin against isoproterenol-induced chronic heart failure through the PI3K‑Akt, p38 MAPK and NF-κB pathways

Cardioprotective effects of ulinastatin against isoproterenol-induced chronic heart failure through the PI3K‑Akt, p38 MAPK and NF-κB pathways

A novel plasma lncRNA ENST00000416361 is upregulated in coronary artery disease and is related to inflammation and lipid metabolism

Use of Human Umbilical Vein Endothelial Cells (HUVEC) as a Model to Study Cardiovascular Disease: A Review

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