| Project/Area Number |
25293125
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| Research Category |
Grant-in-Aid for Scientific Research (B)
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| Allocation Type | Partial Multi-year Fund |
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| Section | 一般 |
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| Research Field |
Applied pharmacology
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| Research Institution | University of Tsukuba |
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Principal Investigator |
SAKAI SATOSHI 筑波大学, 医学医療系, 講師 (30282362)
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| Co-Investigator(Kenkyū-buntansha) |
BUKAWA Hiroki 筑波大学, 医学医療系, 教授 (80173558)
SUMIDA Takayuki 筑波大学, 医学医療系, 教授 (00183054)
MIYAUCHI Takashi 筑波大学, 医学医療系, 教授 (60222329)
WARABI Eiji 筑波大学, 医学医療系, 講師 (70396612)
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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 |
¥18,980,000 (Direct Cost: ¥14,600,000、Indirect Cost: ¥4,380,000)
Fiscal Year 2015: ¥3,380,000 (Direct Cost: ¥2,600,000、Indirect Cost: ¥780,000)
Fiscal Year 2014: ¥6,370,000 (Direct Cost: ¥4,900,000、Indirect Cost: ¥1,470,000)
Fiscal Year 2013: ¥9,230,000 (Direct Cost: ¥7,100,000、Indirect Cost: ¥2,130,000)
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| Keywords | マイクロRNA / 肺高血圧症 / マイクロアレイ / マイクロＲＮＡ / 低酸素 |
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| Outline of Final Research Achievements |
We analyzed the expression of miRNA and mRNA in lungs of patients with pulmonary arterial hypertension (PAH) (n=3) and normal subject (n=3) using the microarray chips for miRNA and mRNA. We obtained actually decreased 81 genes among the target genes predicted from the increased miRNA in PAH lungs. These decreased 81 genes is involved in TGFb signaling pathway (ALK1, BMP2, BMPR2) and cytotoxic responses (FAS, ICAM1). It suggests that the suppression of TGFb signaling and anti-apoptosis contributes to the development of pathogenesis of PAH. Moreover, decrease in ALK1, BMP2, BMPR2 expression and inhibition of apoptosis by decreased FAS expression are partly regulated by miRNA augmentation in lungs of patients with PAH.
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