Journal
GENES TO CELLS
Volume 22, Issue 2, Pages 174-188Publisher
WILEY
DOI: 10.1111/gtc.12465
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Funding
- funding program for Next Generation World-Leading Researchers (NEXT Program) from the Japan Society for the Promotion of Science (JSPS)
- Ministry of Education, Culture, Sports, Science, and Technology (MEXT) of Japan, Joint Usage/Research Program of Medical Research Institute Tokyo Medical and Dental University [23221010, 16H02478]
- Grants-in-Aid for Scientific Research [23221010, 15K06815, 16H02478] Funding Source: KAKEN
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Paternally expressed 11/Retrotransposon-like 1 (Peg11/Rtl1) knockout (KO) mice show mid-to late fetal lethality or late fetal growth retardation associated with frequent neonatal lethality. The lethal phenotype is largely dependent on genetic background and becomes more severe with each succeeding generation in the course of backcross experiments to C57BL/6 (B6). We previously suggested that these lethal and growth phenotypes in the fetal stages were due to severe defects in placental fetal capillaries in the labyrinth layer. In this study, we re-examined KO fetuses and placentas and confirmed that the severe clogging of fetal capillaries was associated with KO fetuses showing mid-fetal lethality with internal bleeding. Importantly, the basal region of the fetal capillary network was specifically damaged, also leading to poor expansion of the labyrinth layer and placental size reduction in the later stage. An apparent down-regulation of transmembrane protein 100 (Tmem100), mesenchyme homeobox 2 (Meox2) and lymphatic vessel endothelial hyaluronan receptor 1 (Lyve1) expression were observed in earlier stage placentas even before apparent size reduction became, suggesting that these genes are involved in the maintenance of fetal capillaries associated with Peg11/Rtl1 during development.
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