Next Article in Journal
Generation of Rho Zero Cells: Visualization and Quantification of the mtDNA Depletion Process
Next Article in Special Issue
Skeletal Muscle Mitochondrial Energetic Efficiency and Aging
Previous Article in Journal
Microfluidic Impedance Flow Cytometry Enabling High-Throughput Single-Cell Electrical Property Characterization
Previous Article in Special Issue
Mitochondria as Key Targets of Cardioprotection in Cardiac Ischemic Disease: Role of Thyroid Hormone Triiodothyronine
Article Menu
Issue 5 (May) cover image

Export Article

Open AccessArticle
Int. J. Mol. Sci. 2015, 16(5), 9831-9849; doi:10.3390/ijms16059831

Abnormal Mitochondrial Function and Impaired Granulosa Cell Differentiation in Androgen Receptor Knockout Mice

1
Graduate Institute of Clinical Medicine & Department of Obstetrics and Gynecology, College of Medicine, Taipei Medical University, Taipei 110, Taiwan
2
Department of Biochemistry and Molecular Cell Biology, College of Medicine, Taipei Medical University, Taipei 110, Taiwan
3
School of Medical Laboratory Science and Biotechnology, College of Medical Science and Technology, Taipei Medical University, Taipei 110, Taiwan
4
Center of General Education, Chang Gung University, Taoyuan 333, Taiwan
5
George H. Whipple Lab for Cancer Research, Departments of Pathology, Urology and Radiation Oncology, University of Rochester Medical Center, Rochester, NY 14642, USA
*
Authors to whom correspondence should be addressed.
Academic Editors: Jaime M. Ross and Giuseppe Coppotelli
Received: 31 January 2015 / Revised: 20 April 2015 / Accepted: 22 April 2015 / Published: 30 April 2015
(This article belongs to the Special Issue Mitochondrial Dysfunction in Ageing and Diseases)
View Full-Text   |   Download PDF [1892 KB, uploaded 30 April 2015]   |  

Abstract

In the ovary, the paracrine interactions between the oocyte and surrounded granulosa cells are critical for optimal oocyte quality and embryonic development. Mice lacking the androgen receptor (AR−/−) were noted to have reduced fertility with abnormal ovarian function that might involve the promotion of preantral follicle growth and prevention of follicular atresia. However, the detailed mechanism of how AR in granulosa cells exerts its effects on oocyte quality is poorly understood. Comparing in vitro maturation rate of oocytes, we found oocytes collected from AR−/− mice have a significantly poor maturating rate with 60% reached metaphase II and 30% remained in germinal vesicle breakdown stage, whereas 95% of wild-type AR (AR+/+) oocytes had reached metaphase II. Interestingly, we found these AR−/− female mice also had an increased frequency of morphological alterations in the mitochondria of granulosa cells with reduced ATP generation (0.18 ± 0.02 vs. 0.29 ± 0.02 µM/mg protein; p < 0.05) and aberrant mitochondrial biogenesis. Mechanism dissection found loss of AR led to a significant decrease in the expression of peroxisome proliferator-activated receptor γ (PPARγ) co-activator 1-β (PGC1-β) and its sequential downstream genes, nuclear respiratory factor 1 (NRF1) and mitochondrial transcription factor A (TFAM), in controlling mitochondrial biogenesis. These results indicate that AR may contribute to maintain oocyte quality and fertility via controlling the signals of PGC1-β-mediated mitochondrial biogenesis in granulosa cells. View Full-Text
Keywords: androgen receptor; granulosa cell; PGC1-β; mitochondria androgen receptor; granulosa cell; PGC1-β; mitochondria
This is an open access article distributed under the Creative Commons Attribution License which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. (CC BY 4.0).

Supplementary material

Scifeed alert for new publications

Never miss any articles matching your research from any publisher
  • Get alerts for new papers matching your research
  • Find out the new papers from selected authors
  • Updated daily for 49'000+ journals and 6000+ publishers
  • Define your Scifeed now

SciFeed Share & Cite This Article

MDPI and ACS Style

Wang, R.-S.; Chang, H.-Y.; Kao, S.-H.; Kao, C.-H.; Wu, Y.-C.; Yeh, S.; Tzeng, C.-R.; Chang, C. Abnormal Mitochondrial Function and Impaired Granulosa Cell Differentiation in Androgen Receptor Knockout Mice. Int. J. Mol. Sci. 2015, 16, 9831-9849.

Show more citation formats Show less citations formats

Related Articles

Article Metrics

Article Access Statistics

1

Comments

[Return to top]
Int. J. Mol. Sci. EISSN 1422-0067 Published by MDPI AG, Basel, Switzerland RSS E-Mail Table of Contents Alert
Back to Top