Starvation at birth impairs germ cell cyst breakdown and increases autophagy and apoptosis in mouse oocytes.
The female reproductive lifespan is largely determined by the size of primordial follicle pool, which is established following germ cell cyst breakdown around birth. Almost two-third of oocytes are lost during germ cell cysts breakdown, following autophagic and apoptosis mechanisms. To investigate a possible relationship between germ cell cyst breakdown and nutrition supply, we established a starvation model in mouse pups at birth and evaluated the dynamics of cyst breakdown during nutrient deprivation. Our results showed that after 36 h of starvation between 1.5 and 3 d.p.p., indicators of metabolism both at systemic and ovarian level were significantly altered and the germ cell cyst breakdown markedly decreased. We also found that markers of oxidative stress, autophagy and apoptosis were increased and higher number of oocytes in cyst showing autophagic markers and of TUNEL-positive oocytes and somatic cells were present in the ovaries of starved pups. Moreover, the proliferation of pre-granulosa cells and the expression of the oocyte-specific transcription factor Nobox were decreased in such ovaries. Finally, we observed that the ovaries of the starved pups could recover a normal number of follicles after about 3 weeks from re-feeding. In conclusion, these data indicate that nutrient deficiency at birth can generate a number of adaptive metabolic and oxidative responses in the ovaries causing increased apoptosis both in the somatic cells and oocyte and autophagy mainly in these latter and leading to a delay of germ cell cyst breakdown and follicle assembly.
College of Life Sciences, Qingdao Agricultural University, Qingdao 266109, China.|College of Animal Science and Technology, Institute of Reproductive Sciences, Qingdao Agricultural University, Qingdao 266109, China.
Yong-Yong
YY
Wang
College of Animal Science and Technology, Institute of Reproductive Sciences, Qingdao Agricultural University, Qingdao 266109, China.
Yuan-Chao
YC
Sun
College of Life Sciences, Qingdao Agricultural University, Qingdao 266109, China.|College of Animal Science and Technology, Institute of Reproductive Sciences, Qingdao Agricultural University, Qingdao 266109, China.
Xiao-Feng
XF
Sun
College of Animal Science and Technology, Institute of Reproductive Sciences, Qingdao Agricultural University, Qingdao 266109, China.
Shun-Feng
SF
Cheng
Chengguo Station of Animal Husbandry and Veterinary, Laizhou 261437, China.
Bo
B
Li
College of Animal Science and Technology, Institute of Reproductive Sciences, Qingdao Agricultural University, Qingdao 266109, China.
Xi-Feng
XF
Zhang
Department of Biomedicine and Prevention, University of Rome Tor Vergata, Rome 00133, Italy.
Massimo
M
De Felici
College of Animal Science and Technology, Institute of Reproductive Sciences, Qingdao Agricultural University, Qingdao 266109, China.
Wei
W
Shen
D000818:Animals; D000831:Animals, Newborn / Q000502:physiology; D017209:Apoptosis / Q000502:physiology*; D001343:Autophagy / Q000502:physiology*; D003560:Cysts / Q000473:pathology*; D005260:Female; D005854:Germ Cells / Q000473:pathology; D006107:Granulosa Cells / Q000473:pathology; D051379:Mice; D009865:Oocytes / Q000473:pathology*; D006080:Ovarian Follicle / Q000473:pathology; D015398:Signal Transduction / Q000502:physiology; D013217:Starvation / Q000503:physiopathology*