Lipid droplets synthesized during luteinization are degraded after pregnancy

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  • MITSUI Junichiro
    Laboratory Animal and Genome Sciences Section, National Institutes for Quantum Science and Technology, Chiba 263-8555, Japan Department of Comprehensive Reproductive Medicine, Graduate School of Medical and Dental Sciences, Tokyo Medical and Dental University, Tokyo 113-8519, Japan
  • IBAYASHI Megumi
    Laboratory Animal and Genome Sciences Section, National Institutes for Quantum Science and Technology, Chiba 263-8555, Japan
  • AIZAWA Ryutaro
    Laboratory Animal and Genome Sciences Section, National Institutes for Quantum Science and Technology, Chiba 263-8555, Japan
  • ISHIKAWA Tomonori
    Perinatal and Maternal Medicine (Ibaraki), Graduate School of Medical and Dental Sciences, Tokyo Medical and Dental University, Tokyo 113-8519, Japan
  • MIYASAKA Naoyuki
    Department of Comprehensive Reproductive Medicine, Graduate School of Medical and Dental Sciences, Tokyo Medical and Dental University, Tokyo 113-8519, Japan
  • TSUKAMOTO Satoshi
    Laboratory Animal and Genome Sciences Section, National Institutes for Quantum Science and Technology, Chiba 263-8555, Japan

抄録

<p> After pregnancy, the corpus luteum (CL) functions as a transient endocrine gland that produces progesterone, which is necessary to maintain pregnancy. To maintain constant progesterone production, CLs are enriched in lipids as its precursors. Lipid droplets (LDs) are organelles that originate from the endoplasmic reticulum and store neutral lipids such as triacylglycerols and cholesteryl esters. The size and number of LDs in a cell are regulated by LD-associated proteins that coat their surface. LD degradation is regulated by either neutral lipid hydrolases (lipolysis), selective autophagic mechanism (lipophagy), or both. Mammalian CLs are long known to be enriched in LDs, but LDs are rapidly depleted after pregnancy and reappear near the time of delivery. In this present study, we hypothesized that LDs synthesized by luteinization are massively degraded after pregnancy. Using mCherry-HPos mice, in which LD synthesis can be visualized in vivo, we found that LD synthesis, which was activated during luteal development, was suppressed after implantation. In CLs, LD synthesis remained low during pregnancy, but was reactivated before and after delivery. These changes in LDs were confirmed using electron microscopy and immunostaining. Furthermore, LD degradation was mediated by lipolysis rather than lipophagy. In summary, our findings indicate that luteinization-induced LD synthesis is suppressed after pregnancy onset and that CLs are lipid-poor during pregnancy because LDs stored during luteal development are extensively degraded by lipolysis.</p>

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