| Project/Area Number |
25660248
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| Research Category |
Grant-in-Aid for Challenging Exploratory Research
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| Allocation Type | Multi-year Fund |
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| Research Field |
Integrative animal science
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| Research Institution | University of Tsukuba |
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Principal Investigator |
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| Project Period (FY) |
2013-04-01 – 2015-03-31
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| Project Status |
Completed (Fiscal Year 2014)
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| Budget Amount *help |
¥4,030,000 (Direct Cost: ¥3,100,000、Indirect Cost: ¥930,000)
Fiscal Year 2014: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2013: ¥2,470,000 (Direct Cost: ¥1,900,000、Indirect Cost: ¥570,000)
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| Keywords | 高血圧妊娠 / 乳腺 / レニン-アンジオテンシン系 / 授乳 / アンジオテンシンII受容体 / 妊娠 / レニン・アンジオテンシン系 / トランスジェニックマウス / ストレス妊娠 / 妊娠高血圧 / 病態モデルマウス / 乳腺発達 / アンジオテンシンII |
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| Outline of Final Research Achievements |
Angiotensin II (AngII) has critical roles in regulation of blood pressure. We previously generated pregnancy-associated hypertensive (PAH) mice by mating female human angiotensinogen transgenic mice with male human renin transgenic mice. A recent study demonstrated that angiotensin II type I receptor (AT1) is expressed in mammary epithelial cells, however, the role of AngII-AT1 signaling in the development of mammary gland during pregnancy remains unclear. In this study, we analyzed the mammary gland of PAH mice. PAH mice exhibited precocious lobuloalveolar development and increased milk protein and lipid production, indicating that mammary gland development was accelerated in PAH mice. Furthermore, AT1 blocker treatment suppressed acceleration of mammary gland development in PAH mice, while antihypertensive drug hydralazine treatment did not. These data suggest that AngII-AT1 signaling accelerates mammary gland development during pregnancy through hypertension-independent mechanism.
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