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IBC 2013, vol. 5, article no. 9 | doi: 10.4051/ibc.2013.5.4.0009
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The Establishment of Tumor Necrosis Factor Receptor-associated Protein1 (TRAP1) Transgenic Mice and Severe Fat Accumulation in the Liver of TRAP1 Mice during Liver Regeneration
Chang-Nim Im1,2,3, Ying Zheng1,2, Sun Hye Kim1,2,4, Tai-Qin Huang1,2,5, Du-Hyong Cho6 and Jeong-Sun Seo1,2,*
1
Department of Biochemistry and Molecular Biology, College of Medicine, Seoul National University, Seoul, Korea
2
ILCHUN Molecular Medicine Institute MRC, Seoul National University, Seoul, Korea
3
Division of Radiation Cancer Research, Korea Institute of Radiological and Medical Sciences, Seoul, Korea
4
Cutaneous Biology Research Center Massachusetts General Hospital, Harvard Medical School, Boston, USA
5
Department of Biochemistry and Biophysics, University of North Carolina, NC, USA
6
Department of Neurology, Konkuk University Medical Center, Konkuk University, Korea
*Corresponding author
received: November 22, 2013 ; accepted: December 23, 2013 ; published : December 24, 2013
This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License (http://creativecommons.org/licenses/by-nc/3.0/) which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited.
Synopsis

Introduction: Tumor necrosis factor receptor-associated protein 1 (TRAP1) is a mitochondrial heat shock protein (HSP), which belongs to HSP90 family. It plays important roles in regulating mitochondrial integrity, protecting against oxidative stress, and inhibiting cell death. Recent studies suggest that TRAP1 is linked to mitochondria and its metabolism. In this study, we established TRAP1 transgenic mice and performed partial hepatectomy (PH) on wild-type (WT) and TRAP1 transgenic mice to investigate the function of TRAP1 during liver regeneration.
Results and Discussion: We found that TRAP1 was highly expressed in liver as well as kidney. In addition, liver regeneration slightly decreased together with increased fatty liver and inflammation at 72 hr after PH in TRAP1 transgenic mice compared with WT control group mice. Concomitantly, we observed decreased levels of p38 protein in TRAP1 transgenic mice compared with WT control group mice. These results suggest that TRAP1 plays a critical role in liver energy balance by regulating lipid accumulation during liver regeneration.
Conclusions and Prospects: To our knowledge, we reported, for the first time, that liver regeneration slightly reduced together with increased fat accumulations after PH in TRAP1 transgenic mice compared with WT control group mice. Concomitantly, we observed decreased levels of p38 protein in TRAP1 transgenic mice compared with WT control group mice. Overexpression of TRAP1 might affect liver regeneration via disturbing mitochondrial function leading to fatty liver in vivo.

Keywords : Fatty liver, mitochondria, partial hepatectomy, p38, TRAP1
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Reviewed by
- Su Ryeon Seo
- Se Ran Yang
Edited by
- Keun Woo Lee
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