The expression of the H-19 and IGF-2 genes during human embryogenesis and placental development.
The H-19 gene in mice is maternally imprinted and its ectopic expression causes prenatal lethality. We have recently identified H-19 transcript in differentiating human placental cells and showed that its expression increases concomitantly with differentiation of cytotrophoblasts in vitro. Placental and embryonal specimens were collected from conception products derived from normal first and second trimester pregnancy terminations. We investigated the abundance of H-19 mRNA throughout placental development in vivo and compared it to the expression of other genes linked to placental differentiation. Furthermore, the expression of H-19 transcript in different organs of human fetuses, aborted during the second trimester, was examined by RNA isolation from separated fetal organs. Since IGF-2 is known to play an important role in embryogenesis, identical blots were hybridized with IGF-2 probe. H-19 expression in human placenta from the different trimesters of pregnancy remains practically constant. A high amount of H-19 gene product was found in the fetoplacental unit with the highest level measured in the adrenal gland. These findings argue that H-19 gene may play a role in human embryogenesis.
Goshen
R
R
Department of Biological Chemistry, Hebrew University, Jerusalem, Israel.
Rachmilewitz
J
J
Schneider
T
T
de-Groot
N
N
Ariel
I
I
Palti
Z
Z
Hochberg
A A
AA
D000311:Adrenal Glands / Q000196:embryology / Q000378:metabolism; D005314:Embryonic and Fetal Development / Q000235:genetics*; D005260:Female; D015870:Gene Expression; D006801:Humans; D007335:Insulin-Like Growth Factor II / Q000235:genetics*; D008431:Maternal-Fetal Exchange / Q000235:genetics; D010920:Placenta / Q000378:metabolism*; D010929:Placentation; D011247:Pregnancy; D012333:RNA, Messenger / Q000235:genetics; D014018:Tissue Distribution; D000509:alpha-Fetoproteins / Q000235:genetics
D012333:RNA, Messenger; D000509:alpha-Fetoproteins; D007335:Insulin-Like Growth Factor II