2015 Fiscal Year Final Research Report
Neurokinin receptor signaling in Asthma
| Project/Area Number |
25463203
|
|---|
| Research Category |
Grant-in-Aid for Scientific Research (C)
|
| Allocation Type | Multi-year Fund |
|---|
| Section | 一般 |
|---|
| Research Field |
Orthodontics/Pediatric dentistry
|
|---|
| Research Institution | Tsurumi University |
|---|
Principal Investigator |
|
|---|
| Co-Investigator(Renkei-kenkyūsha) |
ENDO Yasuo 東北大学, 歯学研究科, 大学院非常勤講師 (50005039)
WAKITA Ryo 東京医科歯科大学, 医歯学総合研究科(歯), 准教授 (60376712)
|
|---|
| Project Period (FY) |
2013-04-01 – 2016-03-31
|
| Keywords | Neurokinin receptor / 気管支喘息 / 気管支平滑筋 / 細胞増殖 |
|---|
| Outline of Final Research Achievements |
Asthma is a chronic obstructive pulmonary disease characterized by inflammation, airway hyperresponsiveness, and smooth muscle remodeling. Molecular pathways regulating airway smooth muscle (ASM) proliferation could serve as potential therapeutic targets to reduce asthma-related airway narrowing. G-protein coupled receptors (GPCRs) have been found to promote ASM proliferation through signaling that involves phosphorylation of Akt. Tachykinin neurokinin-1 (NK1) receptor is known to be pro-contractile in the airway. Since NK1 activation in various tumor models enhances mitogenesis, we originally hypothesized that NK1 receptor activation would promote pathogenic ASM proliferation. But the activation of NK1 receptors by NK1 receptor agonist, SM-SubP inhibited growth factor-induced cell proliferation and Akt phosphorylation in human ASM-NK1 cells. The NK1 GPCR may be a unique anti-proliferation target in ASM cells to mitigate ASM remodeling in asthma.
|
| Free Research Field |
炎症免疫
|
