2014 Fiscal Year Final Research Report
Apoptosis Signal-Regulating Kinase 1 Deficiency Attenuates Vascular Injury-Induced Neointimal Hyperplasia By Suppressing Apoptosis In Smooth Muscle Cells
| Project/Area Number |
24790394
|
|---|
| Research Category |
Grant-in-Aid for Young Scientists (B)
|
| Allocation Type | Multi-year Fund |
|---|
| Research Field |
Experimental pathology
|
|---|
| Research Institution | University of Occupational and Environmental Health, Japan |
|---|
Principal Investigator |
|
|---|
| Research Collaborator |
TASAKI Takashi
NOGUCHI Hirotugu
|
|---|
| Project Period (FY) |
2012-04-01 – 2015-03-31
|
| Keywords | 病理学 / 動脈硬化 / アポトーシス |
|---|
| 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.
|
| Free Research Field |
病理学
|
