| Budget Amount *help |
¥19,110,000 (Direct Cost: ¥14,700,000、Indirect Cost: ¥4,410,000)
Fiscal Year 2010: ¥2,340,000 (Direct Cost: ¥1,800,000、Indirect Cost: ¥540,000)
Fiscal Year 2009: ¥3,510,000 (Direct Cost: ¥2,700,000、Indirect Cost: ¥810,000)
Fiscal Year 2008: ¥13,260,000 (Direct Cost: ¥10,200,000、Indirect Cost: ¥3,060,000)
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| Research Abstract |
The ductus arteriosus (DA), a fetal arterial connection between the main pulmonary artery and the descending aorta, normally closes immediately after birth. The DA is a normal and essential fetal structure. However, it becomes abnormal if it remains patent after birth. In addition to functional closure of the DA (vasoconstriction), anatomical closure of the DA is essential for the final DA closure. The present study identified that the DA-specific downstream signals via PGE2-EP4 stimulation induced vascular remodeling of the DA to promote anatomical closure. Furthermore, we found that other factors such as calcium influx via T-type calcium channels and growth hormone play a role in vascular remodeling in the DA. Clarifying the molecular mechanism of DA closure will lead to develop a novel therapeutic strategy for patent DA.
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