Loss of AMPK activity induces organelle dysfunction and oxidative stress during oocyte aging

• Published in: Biology direct 2024-04, Vol.19 (1), p.29-29, Article 29
• Main Authors: Hu, Lin-Lin, Liao, Mei-Hua, Liu, Ya-Xi, Xing, Chun-Hua, Nong, Lan-Lan, Yang, Feng-Lian, Sun, Shao-Chen
• Format: Article
• Language: English
• Subjects: Ageing; Aging; AMP-activated protein kinase; AMP-Activated Protein Kinases - genetics; AMP-Activated Protein Kinases - metabolism; AMPK; Analysis; Animals; Antibodies; ATP; Biological fertilization; Cells; Cellular Senescence; Copy number; Cytoplasmic organelles; Energy; Energy balance; Energy metabolism; Female; Fertilization; Gametocytes; Golgi apparatus; Health aspects; Homeostasis; Infertility; Kinases; Lasers; Lipids; Lysosomes; Maturation; Meiosis; Membranes; Metabolic diseases; Metabolism; Mice; Mitochondria; Mitochondria - metabolism; Mitochondrial DNA; Oocyte; Oocytes; Oocytes - metabolism; Organelles - metabolism; Oxidative Stress; Phosphorylation; Prevention; Protein kinases; Protein-serine/threonine kinase; Proteins; Reactive Oxygen Species - metabolism; Reproductive technologies; Risk factors; Serine; Spawning; Threonine
• ISSN: 1745-6150; 1745-6150
• DOI: 10.1186/s13062-024-00471-4

Oocyte quality is critical for the mammalian reproduction due to its necessity on fertilization and early development. During aging, the declined oocytes showing with organelle dysfunction and oxidative stress lead to infertility. AMP-activated protein kinase (AMPK) is a serine/threonine protein kinase which is important for energy homeostasis for metabolism. Little is known about the potential relationship between AMPK with oocyte aging. In present study we reported that AMPK was related with low quality of oocytes under post ovulatory aging and the potential mechanism. We showed the altered AMPK level during aging and inhibition of AMPK activity induced mouse oocyte maturation defect. Further analysis indicated that similar with its upstream regulator PKD1, AMPK could reduce ROS level to avoid oxidative stress in oocytes, and this might be due to its regulation on mitochondria function, since loss of AMPK activity induced abnormal distribution, reduced ATP production and mtDNA copy number of mitochondria. Besides, we also found that the ER and Golgi apparatus distribution was aberrant after AMPK inhibition, and enhanced lysosome function was also observed. Taken together, these data indicated that AMPK is important for the organelle function to reduce oxidative stress during oocyte meiotic maturation.