| Project/Area Number |
25461655
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Multi-year Fund |
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| Section | 一般 |
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| Research Field |
Embryonic/Neonatal medicine
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| Research Institution | Tokai University |
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Principal Investigator |
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| 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)
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| Project Period (FY) |
2013-04-01 – 2016-03-31
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| Project Status |
Completed (Fiscal Year 2015)
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| Budget Amount *help |
¥4,940,000 (Direct Cost: ¥3,800,000、Indirect Cost: ¥1,140,000)
Fiscal Year 2015: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
Fiscal Year 2014: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
Fiscal Year 2013: ¥2,080,000 (Direct Cost: ¥1,600,000、Indirect Cost: ¥480,000)
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| 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 |
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| 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.
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