| Project/Area Number |
24591312
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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 |
Metabolomics
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| Research Institution | Chiba University |
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Principal Investigator |
KOBAYASHI Kazuki 千葉大学, 医学(系)研究科(研究院), 寄附講座教員 (30400998)
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| Co-Investigator(Kenkyū-buntansha) |
TAKEMOTO Minoru 千葉大学, 大学院医学研究院, 准教授 (60447307)
FUJIMOTO Masaki 千葉大学, 医学部附属病院, 助教 (20451742)
KAWAMURA Harukiyo 千葉大学, 大学院医学研究院, 助教 (70527902)
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| Project Period (FY) |
2012-04-01 – 2015-03-31
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| Project Status |
Completed (Fiscal Year 2014)
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| Budget Amount *help |
¥5,460,000 (Direct Cost: ¥4,200,000、Indirect Cost: ¥1,260,000)
Fiscal Year 2014: ¥1,820,000 (Direct Cost: ¥1,400,000、Indirect Cost: ¥420,000)
Fiscal Year 2013: ¥1,820,000 (Direct Cost: ¥1,400,000、Indirect Cost: ¥420,000)
Fiscal Year 2012: ¥1,820,000 (Direct Cost: ¥1,400,000、Indirect Cost: ¥420,000)
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| Keywords | セマフォリン3G / 心腎連関 / ポドサイト / 動脈硬化 / 慢性腎臓病 / Semaphorin3g |
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| Outline of Final Research Achievements |
The purpose of this study was to investigate the mechanism of cardiorenal syndrome, the association between atherosclerosis and kidney diseases, through the functional analysis of Sema3G. We found that Sema3G deficient mice showed worsening renal injury under diabetic or inflammatory condition or more progressive atheroma in atherosclerosis model. In vitro, we also revealed that Sema3G had a role in maintenance of cell shape or anti-inflammatory function in podocytes, and in suppressive mechanism for proliferation or adhesion in monocytes. Through our data, we surmise that Sema3G could be the common suppressive factor for both pathogenesis of atherosclerosis and kidney diseases.
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