| Project/Area Number |
25293187
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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 |
Cardiovascular medicine
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| Research Institution | Nara Medical University |
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Principal Investigator |
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| Co-Investigator(Kenkyū-buntansha) |
ONOUE Kenji 奈良県立医科大学, 医学部第1内科, 助教 (90510173)
染川 智 奈良県立医科大学, 医学部, 助教 (90453167)
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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 |
¥18,850,000 (Direct Cost: ¥14,500,000、Indirect Cost: ¥4,350,000)
Fiscal Year 2015: ¥2,730,000 (Direct Cost: ¥2,100,000、Indirect Cost: ¥630,000)
Fiscal Year 2014: ¥4,550,000 (Direct Cost: ¥3,500,000、Indirect Cost: ¥1,050,000)
Fiscal Year 2013: ¥11,570,000 (Direct Cost: ¥8,900,000、Indirect Cost: ¥2,670,000)
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| Keywords | TMEM100 / 肺高血圧 / 右心不全 / BMP9/10 / IP3受容体 / ＧＰＲ78 / ALK1 / 血管新生 / BMP9 |
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| Outline of Final Research Achievements |
The mechanism for pulmonary arterial hypertension (PAH) and its complication, right-sided heart failure is unknown. Using cDNA array analyses in the right ventricular tissues in the rats with monocrotaline-induced pulmonary hypertension, we have focused TMEM100, which is 20kD protein located in endo-cyto plasmic reticulum. Interestingly, TMEM100 expression is upregulated in cultured human umbilical arterial endothelial cells by BMP9/10, specific ligands for ALK1/BMPR2 receptors, recognized as causative genes for PAH by the linkage analysis in familial PAH. Thus, it is expected that TMEM100 is involved in the pathogenesis of PAH and its complication, right-sided heart failure.
Because of mice lacking the tmem100 gene is embryonic lethal, we generated inducible knockout mice of the tmem100 gene. Unfortunately, in spite of several experimental pulmonary arterial hypertension models, we have not found the evidence that TMEM100 is involved in the pathogenesis of PAH.
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