Open Access

N‑terminal truncated peroxisome proliferator‑activated receptor‑γ coactivator‑1α alleviates phenylephrine‑induced mitochondrial dysfunction and decreases lipid droplet accumulation in neonatal rat cardiomyocytes

  • Authors:
    • Zuheng Liu
    • Jinghai Hua
    • Wanqiang Cai
    • Qiong Zhan
    • Wenyan Lai
    • Qingchun Zeng
    • Hao Ren
    • Dingli Xu
  • View Affiliations

  • Published online on: June 14, 2018     https://doi.org/10.3892/mmr.2018.9158
  • Pages: 2142-2152
  • Copyright: © Liu et al. This is an open access article distributed under the terms of Creative Commons Attribution License.

Metrics: Total Views: 0 (Spandidos Publications: | PMC Statistics: )
Total PDF Downloads: 0 (Spandidos Publications: | PMC Statistics: )


Abstract

N‑terminal truncated peroxisome proliferator‑activated receptor‑γ coactivator‑1α (NT‑PGC‑1α) is an alternative splice variant of PGC‑1α. NT‑PGC‑1α exhibits stronger anti‑obesity effects in adipose tissue than PGC‑1α; however, NT‑PGC‑1α has not yet been investigated in neonatal rat cardiomyocytes (NRCMs). The present study aimed to investigate the role of NT‑PGC‑1α in mitochondrial fatty acid metabolism and its possible regulatory mechanism in NRCMs. NRCMs were exposed to phenylephrine (PE) or angiotensin II (Ang II) to induce cardiac hypertrophy. Following this, NRCMs were infected with adenovirus expressing NT‑PGC‑1α, and adenosine 5'‑triphsophate (ATP) levels, reactive oxygen species (ROS) generation and mitochondrial membrane potential were subsequently detected. In addition, western blotting, lipid droplet staining and oxygen consumption assays were performed to examine the function of NT‑PGC‑1α in fatty acid metabolism. NT‑PGC‑1α was demonstrated to be primarily expressed in the cytoplasm, which differed from full‑length PGC‑1α, which was predominantly expressed in the nucleus. NT‑PGC‑1α overexpression alleviated mitochondrial function impairment, including ATP generation, ROS production and mitochondrial membrane potential integrity. Furthermore, NT‑PGC‑1α overexpression alleviated the PE‑induced suppression of fatty acid metabolism‑associated protein expression, increased extracellular oxygen consumption and decreased lipid droplet accumulation in NRCMs. Taken together, the present study demonstrated that NT‑PGC‑1α alleviated PE‑induced mitochondrial impairment and decreased lipid droplet accumulation in NRCMs, indicating that NT‑PGC‑1α may have ameliorated mitochondrial energy defects in NRCMs, and may be considered as a potential target for the treatment of heart failure.
View Figures
View References

Related Articles

Journal Cover

August-2018
Volume 18 Issue 2

Print ISSN: 1791-2997
Online ISSN:1791-3004

Sign up for eToc alerts

Recommend to Library

Copy and paste a formatted citation
x
Spandidos Publications style
Liu Z, Hua J, Cai W, Zhan Q, Lai W, Zeng Q, Ren H and Xu D: N‑terminal truncated peroxisome proliferator‑activated receptor‑γ coactivator‑1α alleviates phenylephrine‑induced mitochondrial dysfunction and decreases lipid droplet accumulation in neonatal rat cardiomyocytes. Mol Med Rep 18: 2142-2152, 2018
APA
Liu, Z., Hua, J., Cai, W., Zhan, Q., Lai, W., Zeng, Q. ... Xu, D. (2018). N‑terminal truncated peroxisome proliferator‑activated receptor‑γ coactivator‑1α alleviates phenylephrine‑induced mitochondrial dysfunction and decreases lipid droplet accumulation in neonatal rat cardiomyocytes. Molecular Medicine Reports, 18, 2142-2152. https://doi.org/10.3892/mmr.2018.9158
MLA
Liu, Z., Hua, J., Cai, W., Zhan, Q., Lai, W., Zeng, Q., Ren, H., Xu, D."N‑terminal truncated peroxisome proliferator‑activated receptor‑γ coactivator‑1α alleviates phenylephrine‑induced mitochondrial dysfunction and decreases lipid droplet accumulation in neonatal rat cardiomyocytes". Molecular Medicine Reports 18.2 (2018): 2142-2152.
Chicago
Liu, Z., Hua, J., Cai, W., Zhan, Q., Lai, W., Zeng, Q., Ren, H., Xu, D."N‑terminal truncated peroxisome proliferator‑activated receptor‑γ coactivator‑1α alleviates phenylephrine‑induced mitochondrial dysfunction and decreases lipid droplet accumulation in neonatal rat cardiomyocytes". Molecular Medicine Reports 18, no. 2 (2018): 2142-2152. https://doi.org/10.3892/mmr.2018.9158