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2015 Fiscal Year Final Research Report

Fetoplacental factors involved in feto-maternal communications: who and how

Research Project

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Project/Area Number 25461655
Research Category

Grant-in-Aid for Scientific Research (C)

Allocation TypeMulti-year Fund
Section一般
Research Field Embryonic/Neonatal medicine
Research InstitutionTokai University

Principal Investigator

ISHIMOTO Hitoshi  東海大学, 医学部, 教授 (10212937)

Co-Investigator(Kenkyū-buntansha) TOGO Atsuko  東海大学, 医学部, 助教 (20408024)
NISHIMURA Osamu  東海大学, 医学部, 助教 (80296657)
Project Period (FY) 2013-04-01 – 2016-03-31
Keywords胎児シグナル / 栄養膜細胞 / midkine / コルチゾール / 妊娠維持機構
Outline of Final Research Achievements

In search for factors involved in feto-maternal communications, we studied on midkine (MK) that shows fetus-specific expression. Obtained data is as follows: 1) in contrast to mice, human placental MK mRNA and immunoreactive MK intensity showed the highest level in the first trimester and decreased dramatically thereafter. MK was localized to syncytiotrophoblasts and extravillous trophoblasts; 2) in BeWo cells, MK significantly increased syncytin-2 mRNA, but not that of syncytin-1, and cAMP induced MK as well as the syncytins; 3) DNA microarrays and RNA-seq on MK-silenced JEG-3 and MK-treated BeWo cells identified novel genes likely induced or suppressed by MK; and 4) in NCI-H295A cells, MK did not decrease HSD3B2 mRNA, as opposed to fetal adrenocortical cells, but exerted similar proliferative effects. As we also observed a differential expression of putative MK receptors, the above-mentioned differential responses to MK likely reflect different MK signaling pathways.

Free Research Field

周産期医学、胎児内分泌学

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Published: 2017-05-10  

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