Biological potentials for a family of disintegrin and metalloproteinase (ADAMDEC)-1 in mouse normal pregnancy
| Autor: | Orie Nagaoka, Ken Takeshi Kusakabe, Nobue Kuniyoshi, Hiroyuki Imai, Yasuo Kiso |
|---|---|
| Rok vydání: | 2021 |
| Předmět: |
Vascular Endothelial Growth Factor A
040301 veterinary sciences Disintegrins Placenta Biology 0403 veterinary science Andrology Mice 03 medical and health sciences chemistry.chemical_compound Vasculogenesis Pregnancy medicine Animals reproductive and urinary physiology 030304 developmental biology 0303 health sciences Matrigel Full Paper General Veterinary epithelial cell Uterus Decidua uterine NK cell Endothelial Cells Trophoblast 04 agricultural and veterinary sciences a disintegrin and metalloprotease-like decysin-1 Actin cytoskeleton trophoblast Mice Inbred C57BL Vascular endothelial growth factor Haematopoiesis medicine.anatomical_structure chemistry Mice Inbred DBA embryonic structures Metalloproteases Mice Inbred CBA Female Anatomy |
| Zdroj: | The Journal of Veterinary Medical Science |
| ISSN: | 1347-7439 0916-7250 |
| Popis: | Our previous research has indicated local expression of ADAMDEC-1, a family of disintegrin and metalloproteinase, was confirmed in the mouse placentas and enhancement was found in the sites for spontaneous abortion. Present study was aimed to identify biological effects of ADAMDEC-1 in pregnancy process. Syngeneic pairs of C57BL/6J mice and heterogenic mating pairs of CBA/J and DBA/2 mice were used. Pregnant mice were treated with recombinant ADAMDEC-1 protein. Vasculogenesis effects was evaluated using the Matrigel plugs including vascular endothelial growth factor singularity or combination with ADAMDEC-1. ADAMDEC-1 single effects were evaluated by tubal formation and proliferation assays using HuEht-1 endothelial cells. Expression of ADAMDEC-1 was not exactly corresponded with the time periods for miscarriage initiation. ADAMDEC-1 was distributed in normal placentas and fetuses, especially at extraembryonic ectoderm, decidua cells, uterine natural killer (uNK) cells in decidua, trophoblasts in labyrinthine zone, and hematopoietic cells in umbilical blood and fetal liver. ADAMDEC-1 treatment did not affect reproductive performances, while it elevated uNK cell recruitment in placenta and enlarged lumen sizes of the intraplacental vessels. In vitro analysis also indicated ADAMDEC-1 promoting effect on tubal formation and cell length of HuEht-1. qPCR analysis showed that ADAMDEC-1 modified placental gene expression especially for linkage of actin filament rearrangement. Our findings suggested that ADAMDEC-1 is correlated on cell shape, stability, and movement via modification of actin cytoskeleton. ADMADEC-1 suspected to regulate cellular activity of endothelial cells, trophoblasts, and uNK cells and may support normal developing of mouse placentas. |
| Databáze: | OpenAIRE |
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