MicroRNA-26a prevents endothelial cell apoptosis by directly targeting TRPC6 in the setting of atherosclerosis

Zhang, Yong; Qin, Wei; Zhang, Longyin; Wu, Xianxian; Du, Ning; Hu, Yingying; Li, Xiaoguang; Shen, Nanping; Xiao, Dan; Zhang, Haiying; Li, Zhange; Zhang, Yue; Yang, Huan; Gao, Feng; Du, Zhenhong; Xu, Chaoqian; Yang, Baofeng

doi:10.1038/srep09401

Cited by 127 publications

(88 citation statements)

References 54 publications

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“…The cells were maintained at 37°C in a humidified atmosphere of 5% CO 2 and 95% air. Cells grown to a confluency of 80-90% were used for experimental measurements [18]. …”

Section: Methodsmentioning

confidence: 99%

“…The total protein was extracted from HAECs, following the procedures essentially the same as described in detail elsewhere [18]. Protein samples of 80 µg each were loaded to SDS polyacrylamide gel and transferred onto a nitrocellulose membrane, which was subsequently blocked by 6% non-fat milk dissolved in PBS for 2 h. The blots were probed by primary antibodies against CD31 (Cat.…”

Section: Methodsmentioning

confidence: 99%

“…#TA336621; Zhongshanjinqiao, Inc., Beijing, China) was used as an internal control. Western Blot bands were quantified using the Odyssey Infrared Imaging System (LI-COR, Lincoln, NE, USA) by measuring band intensity (Area × OD) [18, 20]. …”

Section: Methodsmentioning

confidence: 99%

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Low-Intensity Pulsed Ultrasound Prevents the Oxidative Stress Induced Endothelial-Mesenchymal Transition in Human Aortic Endothelial Cells

Zhang

Ren

et al. 2018

Cell Physiol Biochem

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Background/Aims: Endothelial-mesenchymal transition (EndMT) has been shown to take part in the generation and progression of diverse diseases, involving a series of changes leading to a loss of their endothelial characteristics and an acquirement of properties typical of mesenchymal cells. Low-intensity pulsed ultrasound (LIPUS) is a new therapeutic option that has been successfully used in fracture healing. However, whether LIPUS can inhibit oxidative stress-induced endothelial cell damages through inhibiting EndMT remained unknown. This study aimed to investigate the protective effects of LIPUS against oxidative stress-induced endothelial cell damages and the underlying mechanisms. Methods: EndMT was induced by H₂O₂ (100 µm for seven days). Human aortic endothelial cells (HAECs) were exposed to H₂O₂ with or without LIPUS treatment for seven days. The expression of EndMT markers (CD31, VE-cadherin, FSP1 and α-SMA) were analyzed. The levels of total and phosphorylated PI3K and AKT proteins were detected by Western Blot analysis. Cell chemotaxis was determined by wound healing and transwell assay. Results: LIPUS relieved EndMT by decreasing ROS accumulation and increasing activation of the PI3K signaling cascade. LIPUS alleviated the migration of EndMT-derived mesenchymal-like cells through reducing extracellular matrix (ECM) deposition that is associated with matrix metallopeptidase (MMP) proteolytic activity and collagen production. Conclusion: LIPUS produces cytoprotective effects against oxidative injuries to endothelial cells through suppressing the oxidative stress-induced EndMT, activating the PI3K/AKT pathway under oxidative stress, and limiting cell migration and excessive ECM deposition.

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“…The cells were maintained at 37°C in a humidified atmosphere of 5% CO 2 and 95% air. Cells grown to a confluency of 80-90% were used for experimental measurements [18]. …”

Section: Methodsmentioning

confidence: 99%

Section: Methodsmentioning

confidence: 99%

See 1 more Smart Citation

Low-Intensity Pulsed Ultrasound Prevents the Oxidative Stress Induced Endothelial-Mesenchymal Transition in Human Aortic Endothelial Cells

Zhang

Ren

et al. 2018

Cell Physiol Biochem

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“…Xu et al (10) suggested that miR-135b-5p and miR-499a-3p promoted cell proliferation and migration in AS. Zhang et al (11) demonstrated that miR-26a prevented endothelial cell apoptosis under AS conditions. Ouimet et al (12) found that miR-33 antagonism exerted atheroprotective roles via regulating macrophage-associated inflammation.…”

Section: Introductionmentioning

confidence: 99%

Blockade of 146b‑5p promotes inflammation in atherosclerosis‑associated foam cell formation by targeting TRAF6

Lin

2017

Exp Ther Med

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Abstract. Atherosclerosis (AS) is a chronic inflammation in response to lipid accumulation. Increasing evidence has demonstrated that numerous microRNAs (miRs) have critical roles in inflammatory responses. A previous study suggested that miR-146b-5p is possibly associated with AS; however, its exact role has remained largely elusive. The present study aimed to investigate the potential role of miR-146b-5p in AS and to explore the underlying mechanism. Fist, the levels of miR-146b-5p were determined in foam cells and clinical specimens from patients with AS by reverse-transcription quantitative PCR. The role of miR-146b-5p in AS was then investigated by using miR-146b-5p inhibitor. The results demonstrated that the expression levels of miR-146b-5p were elevated in the lesions of patients with AS. In addition, the levels of miR-146b-5p in THP-1 cells stimulated with phorbol 12-myristate 13-acetate (100 nM) to induce their differentiation into macrophages were dose-and time-dependently elevated by oxidized low-density lipoprotein treatment applied for inducing foam cell formation. miR-146b-5p was also revealed to directly target tumor necrosis factor receptor-associated factor 6 (TRAF6), which functions as a signal transducer in the nuclear factor-κB (NF-κB) pathway. Furthermore, the present study reported for the first time that miR-146b-5p inhibition promotes the inflammatory response and enhances lipid uptake during foam cell formation. In conclusion, miR-146b-5p inhibition promoted chronic inflammation and had a detrimental role during AS-associated foam cell formation by targeting TRAF6.

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“…Growing evidence has pinpointed miRNAs as important modulators of cardiovascular health and disease. For instance, miRNAs participate in vascular inflammation (8), arterial remodeling (9), smooth muscle plasticity (10), atherosclerosis (11), and endothelial cell apoptosis (12). Nevertheless, the role of miRNAs in the development of diabetic endothelial dysfunction is sparsely studied.…”

mentioning

confidence: 99%

Inhibition of miR-200c Restores Endothelial Function in Diabetic Mice Through Suppression of COX-2

Zhang

Liu

et al. 2016

Diabetes

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mice revealed that COX-2 mediated miR-200c-induced endothelial dysfunction and that miR-200c upregulated COX-2 expression in endothelial cells through suppression of ZEB1 and increased production of prostaglandin E 2 , which also reduced EDR. This study demonstrates for the first time to our knowledge that miR-200c is a new mediator of diabetic endothelial dysfunction and inhibition of miR-200c rescues EDRs in diabetic mice. These new findings suggest the potential usefulness of miR-200c as the target for drug intervention against diabetic vascular complications.

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MicroRNA-26a prevents endothelial cell apoptosis by directly targeting TRPC6 in the setting of atherosclerosis

Cited by 127 publications

References 54 publications

Low-Intensity Pulsed Ultrasound Prevents the Oxidative Stress Induced Endothelial-Mesenchymal Transition in Human Aortic Endothelial Cells

Low-Intensity Pulsed Ultrasound Prevents the Oxidative Stress Induced Endothelial-Mesenchymal Transition in Human Aortic Endothelial Cells

Blockade of 146b‑5p promotes inflammation in atherosclerosis‑associated foam cell formation by targeting TRAF6

Inhibition of miR-200c Restores Endothelial Function in Diabetic Mice Through Suppression of COX-2

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