Apoptosis Signal-Regulating Kinase 1 Deficiency Attenuates Vascular Injury-Induced Neointimal Hyperplasia By Suppressing Apoptosis In Smooth Muscle Cells
| Project/Area Number |
24790394
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| Research Category |
Grant-in-Aid for Young Scientists (B)
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| Allocation Type | Multi-year Fund |
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| Research Field |
Experimental pathology
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| Research Institution | University of Occupational and Environmental Health, Japan |
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Principal Investigator |
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| Research Collaborator |
TASAKI Takashi
NOGUCHI Hirotugu
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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 |
¥4,550,000 (Direct Cost: ¥3,500,000、Indirect Cost: ¥1,050,000)
Fiscal Year 2014: ¥1,300,000 (Direct Cost: ¥1,000,000、Indirect Cost: ¥300,000)
Fiscal Year 2013: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2012: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
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| Keywords | 病理学 / 動脈硬化 / アポトーシス |
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| Outline of Final Research Achievements |
We investigated neointimal remodeling in ligated carotid arteries of ASK1-deficient mice (ASK1-/-) for 3 weeks. ASK1-/- mice had significantly more suppressed intimal formation, inversely manifesting as potential anti-atherogenic aspects of ASK1 deficiency, characterized by fewer SMCs and less collagen synthesis; and fewer apoptotic SMCs, infiltrating T-lymphocytes and microvessels, associated with decreased apoptosis of luminal endothelial cells (ECs), compared to those of wild type (WT) mice. Injured arteries of ASK1-/- mice also showed significantly down-regulated expression of pro-apoptotic markers, adhesion molecules and pro-inflammatory signaling factors. Moreover, tumor necrosis factor-a-induced apoptosis was markedly suppressed in cultured aortic SMCs from ASK1-/- mice.
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Report
(4 results)
Research Products
(7 results)
