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miR-26a inhibits atherosclerosis progression by targeting TRPC3

Overview of attention for article published in Cell & Bioscience, January 2018
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Title
miR-26a inhibits atherosclerosis progression by targeting TRPC3
Published in
Cell & Bioscience, January 2018
DOI 10.1186/s13578-018-0203-9
Pubmed ID
Authors

Min Feng, Daqian Xu, Lirui Wang

Abstract

Atherosclerosis, a chronic multi-factorial vascular disease, has become a predominant cause of a variety of cardiovascular disorders. miR-26a was previously reported to be involved in atherosclerosis progression. However, the underlying mechanism of miR-26a in atherosclerosis remains to be further explained. High-fat diet (HFD)-fed apolipoprotein E (apoE)-/- mice and oxidized low-density lipoprotein (ox-LDL)-stimulated human aortic endothelial cells (HAECs) were established as in vivo and in vitro models of atherosclerosis. RT-qPCR and western blot analysis were performed to measure the expression of miR-26a and transient receptor potential canonical 3 (TRPC3), respectively. Binding between miR-26a and TRPC3 was predicted with bioinformatics software and verified using a dual luciferase reporter assay. The effects of miR-26a on the lipid accumulation, atherosclerotic lesion, and inflammatory response in HFD-fed apoE-/- mice were investigated by a colorimetric enzymatic assay system, hematoxylin-eosin and oil-Red-O staining, and ELISA, respectively. Additionally, the effects of miR-26a or combined with TRPC3 on cell viability, apoptosis and the nuclear factor-kappa B (NF-κB) pathway in ox-LDL-stimulated HAECs were evaluated by MTT assay, TUNEL assay, and western blot, respectively. miR-26a was downregulated in HFD-fed apoE-/- mice and ox-LDL-stimulated HAECs. miR-26a overexpression inhibited the pathogenesis of atherosclerosis by attenuating hyperlipidemia, atherosclerotic lesion and suppressing inflammatory response in HFD-fed apoE-/- mice. Moreover, miR-26a overexpression suppressed inflammatory response and the NF-κB pathway, promoted cell viability and inhibited apoptosis in ox-LDL-stimulated HAECs. Additionally, TRPC3 was demonstrated to be a direct target of miR-26a. Enforced expression of TRPC3 reversed the effects of miR-26a on cell viability, apoptosis, and the NF-κB pathway in ox-LDL-treated HAECs. miR-26a alleviated the development of atherosclerosis by regulating TRPC3, providing a potential target for atherosclerosis treatment.

Twitter Demographics

The data shown below were collected from the profile of 1 tweeter who shared this research output. Click here to find out more about how the information was compiled.

Mendeley readers

The data shown below were compiled from readership statistics for 7 Mendeley readers of this research output. Click here to see the associated Mendeley record.

Geographical breakdown

Country Count As %
Unknown 7 100%

Demographic breakdown

Readers by professional status Count As %
Researcher 2 29%
Lecturer 1 14%
Other 1 14%
Student > Ph. D. Student 1 14%
Student > Master 1 14%
Other 1 14%
Readers by discipline Count As %
Agricultural and Biological Sciences 2 29%
Biochemistry, Genetics and Molecular Biology 1 14%
Unspecified 1 14%
Immunology and Microbiology 1 14%
Unknown 2 29%

Attention Score in Context

This research output has an Altmetric Attention Score of 1. This is our high-level measure of the quality and quantity of online attention that it has received. This Attention Score, as well as the ranking and number of research outputs shown below, was calculated when the research output was last mentioned on 02 February 2018.
All research outputs
#9,968,438
of 12,452,101 outputs
Outputs from Cell & Bioscience
#168
of 269 outputs
Outputs of similar age
#245,813
of 339,219 outputs
Outputs of similar age from Cell & Bioscience
#1
of 4 outputs
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So far Altmetric has tracked 269 research outputs from this source. They receive a mean Attention Score of 2.2. This one is in the 14th percentile – i.e., 14% of its peers scored the same or lower than it.
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