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Original Article
 
Effects of HIF-1α on ERRα/γ protein expression in mouse skeletal muscle
Ying Zhang1, Weixiu Ji1, Lianfeng Zhang2, Sixue Liu1, Gang Liu3, Jianxiong Wang4
1Institute of Sports Science, Beijing Sport University, China.
2Key Laboratory of Human Disease Comparative Medicine, Ministry of Health, Institute of Laboratory Animal Science, Chinese Academy of Medical Sciences & Comparative Medical Center, Peking Union Medical College, China.
3Teaching Laboratory Centre, Beijing Sport University, China.
3School of Health and Wellbeing, Faculty of Health, Engineering, and Sciences, University of Southern Queensland, Australia.

Article ID: 100002B05YZ2015
doi:10.5348/B05-2015-2-OA-2

Address correspondence to:
Professor Ying Zhang
Institute of Sport Science, Beijing Sport University
Beijing 100084
China

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How to cite this article
Zhang Y, Ji W, zhang L, Liu S, Liu G, Wang J. Effects of HIF-1α on ERRα/γ protein expression in mouse skeletal muscle. Edorium J Biomed Technol 2015;1:4–10.


Abstract
Aims: HIF-1α plays an important role in the adaptive responses to hypoxia. The ERRα and γ are crucial regulators of energy metabolism in skeletal muscle. The aim of the present study was to generate the inducible HIF-1α transgenic mice and examine the effects of different HIF-1α protein expression levels on ERRα/γ in mouse skeletal muscle.
Methods: We generated the HIF-1α high-expression transgenic mice (HT) and HIF-1α low-expression transgenic mice (LT), and then compared the expressions of ERRα/γ and its target genes in skeletal muscles of three kinds of mice: HT, LT, and non-transgenic mice (NT).
Results: The results showed that (1) the double positive mice from the founder of 3# and 68# showed an obvious expression of HIF-1α induced by tamoxifen and both of them were maintained to the further research as HT and LT mice, respectively; and (2) the nucleoprotein expressions of ERRα/γ and the mRNA levels of the ERRα/γ target genes: MCAD, PPARa, NRF1 and PDK4 were higher in the LT mice than the values in the NT, but only the mRNA levels of MCAD and PPARa were significantly higher. The HT mice showed significantly lower ERRα protein content than that of the NT mice.
Conclusion: Our study was the first to report the generation of the inducible HIF-1α transgenic mice and effects of HIF-1α on ERRα/γ protein expression in mouse skeletal muscle in vivo. These data demonstrate that the low HIF-1α protein expression may associate with an up-regulation of ERRα/γ and their target genes in skeletal muscles, while the aggravated HIF-1α protein expression would reduce the effects.

Keywords: ERRα/γ,, HIF-1α, Skeletal muscle, Target genes, Transgenic mouse


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Author Contributions:
Ying Zhang – Substantial contributions to conception and design, Acquisition of data, Drafting the article, Revising it critically for important intellectual content, Final approval of the version to be published
Weixiu Ji – Substantial contributions to conception and design, Acquisition of data, Drafting the article, Revising it critically for important intellectual content, Final approval of the version to be published
Lianfeng Zhang – Substantial contributions to conception and design, Acquisition of data, Drafting the article, Final approval of the version to be published
Sixue Liu – Substantial contributions to conception and design, Acquisition of data, Drafting the article, Revising it critically for important intellectual content, Final approval of the version to be published
Gang Liu – Substantial contributions to conception and design, Acquisition of data, Drafting the article, Final approval of the version to be published
Jianxiong Wang – Substantial contributions to conception and design, Drafting the article, Revising it critically for important intellectual content, Final approval of the version to be published
Guarantor of submission
The corresponding author is the guarantor of submission.
Source of support
None
Conflict of interest
Authors declare no conflict of interest.
Copyright
© 2015 Ying Zhang et al. This article is distributed under the terms of Creative Commons Attribution License which permits unrestricted use, distribution and reproduction in any medium provided the original author(s) and original publisher are properly credited. Please see the copyright policy on the journal website for more information.