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Molecular regulation of the expression of leptin by hypoxia in human coronary artery smooth muscle cells

Overview of attention for article published in Journal of Biomedical Science, January 2015
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Title
Molecular regulation of the expression of leptin by hypoxia in human coronary artery smooth muscle cells
Published in
Journal of Biomedical Science, January 2015
DOI 10.1186/s12929-014-0109-8
Pubmed ID
Authors

Chiung-Zuan Chiu, Bao-Wei Wang, Kou-Gi Shyu

Abstract

BackgroundLeptin, produced mainly by white adipose tissue, is a hormone that promotes vascular smooth muscle cell (VSMC) migration and proliferation, a process involved in the pathophysiology of atherosclerosis. Leptin expression in human coronary artery smooth cell (HCASMC) is induced by hypoxia. However, our understanding of the process of atherosclerosis in HCASMC is only emerging. Since the mechanisms by which hypoxia regulates leptin in HCASMC are as yet unknown, this study aims to investigate the mechanics of molecular regulation of leptin expression in HCASMC under hypoxia. We subjected cultured HCASMCs to hypoxia for varying periods of time. Through use of different signal pathway inhibitors, we were able to sort out and identify the pathway through which hypoxia-induced leptin expression occurs.ResultsLeptin mRNA and protein levels increased after 2.5% hypoxia for 2-to-4 hours, with earlier expression of angiotensin II (AngII) and reactive oxygen species (ROS). The addition before hypoxia of the c-Jun N-terminal kinase (JNK) pathway inhibitor (SP600125), JNK small interfering RNA (siRNA), AngII receptor blockers (ARBs; losartan), or N-acetyl-L-cysteine (NAC, an ROS scavenger), had the effect of inhibiting JNK phosphorylation and leptin expression. Gel shift assay and luciferase promoter study showed that leptin/activator protein 1 (AP-1) binding and transcriptional activity to the leptin promoter increased after hypoxia, and SP600125, JNK siRNA, losartan, and NAC abolished the binding and transcriptional activity induced by hypoxia. The use of SP600125, JNK siRNA, losartan, and NAC effectively inhibited the binding and transcriptional activity induced by hypoxia. Migration and proliferation, ROS generation, and the presence of leptin in the nuclei of HCASMCs also increased under hypoxia.ConclusionHypoxia in HCASMCs increases leptin expression through the induction of AngII, ROS, and the JNK pathway to enhance atherosclerosis in HCASMCs.

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Mendeley readers

Mendeley readers

The data shown below were compiled from readership statistics for 11 Mendeley readers of this research output. Click here to see the associated Mendeley record.

Geographical breakdown

Country Count As %
United Kingdom 1 9%
Unknown 10 91%

Demographic breakdown

Readers by professional status Count As %
Student > Ph. D. Student 3 27%
Researcher 3 27%
Professor 1 9%
Student > Master 1 9%
Student > Bachelor 1 9%
Other 0 0%
Unknown 2 18%
Readers by discipline Count As %
Biochemistry, Genetics and Molecular Biology 2 18%
Medicine and Dentistry 2 18%
Agricultural and Biological Sciences 2 18%
Pharmacology, Toxicology and Pharmaceutical Science 1 9%
Environmental Science 1 9%
Other 0 0%
Unknown 3 27%
Attention Score in Context

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 14 January 2015.
All research outputs
#19,945,185
of 25,374,917 outputs
Outputs from Journal of Biomedical Science
#839
of 1,101 outputs
Outputs of similar age
#252,079
of 358,683 outputs
Outputs of similar age from Journal of Biomedical Science
#6
of 9 outputs
Altmetric has tracked 25,374,917 research outputs across all sources so far. This one is in the 18th percentile – i.e., 18% of other outputs scored the same or lower than it.
So far Altmetric has tracked 1,101 research outputs from this source. They typically receive a lot more attention than average, with a mean Attention Score of 11.0. This one is in the 20th percentile – i.e., 20% of its peers scored the same or lower than it.
Older research outputs will score higher simply because they've had more time to accumulate mentions. To account for age we can compare this Altmetric Attention Score to the 358,683 tracked outputs that were published within six weeks on either side of this one in any source. This one is in the 25th percentile – i.e., 25% of its contemporaries scored the same or lower than it.
We're also able to compare this research output to 9 others from the same source and published within six weeks on either side of this one. This one has scored higher than 3 of them.