| Project/Area Number |
16K19058
|
|---|
| Research Category |
Grant-in-Aid for Young Scientists (B)
|
| Allocation Type | Multi-year Fund |
|---|
| Research Field |
Pathological medical chemistry
|
|---|
| Research Institution | Nara Medical University |
|---|
Principal Investigator |
Kyotani Yoji 奈良県立医科大学, 医学部, 助教 (10706534)
|
|---|
| Project Period (FY) |
2016-04-01 – 2019-03-31
|
| Project Status |
Completed (Fiscal Year 2018)
|
| Budget Amount *help |
¥4,030,000 (Direct Cost: ¥3,100,000、Indirect Cost: ¥930,000)
Fiscal Year 2017: ¥2,860,000 (Direct Cost: ¥2,200,000、Indirect Cost: ¥660,000)
Fiscal Year 2016: ¥1,170,000 (Direct Cost: ¥900,000、Indirect Cost: ¥270,000)
|
|---|
| Keywords | 間歇的低酸素 / エピレグリン / インターロイキン-6 / Intermittent hypoxia / Epiregulin / シクロオキシゲナーゼ / 睡眠時無呼吸 |
|---|
| Outline of Final Research Achievements |
Obstructive sleep apnea (OSA) is characterized by intermittent hypoxia (IH) and a risk factor in the progression of cardiovascular diseases. In this study, we found that IH induced pro-inflammatory cytokine interleukin (IL)-6, resulting in an increase of epiregulin (ER) which is involved in vascular wall thickness. It was recently reported that ER was a crucial factor in an inflammation amplifier which was induced by IL-6. It is therefore thought that IH-induced increases of ER and IL-6 are involved in the development and the progression of several diseases as well as cardiovascular diseases. Further investigation of intracellular mechanisms for IH will establish the therapeutic strategy and prophylaxis against several diseases in patients with OSA.
|
| Academic Significance and Societal Importance of the Research Achievements |
間歇的低酸素 (IH) によるエピレグリン (ER) 発現増加にインターロイキン (IL)-6が関与することが明らかとなった。IL-6はその増幅回路により慢性炎症性疾患に関わっており、ERはその増幅回路の因子の1つである。これにより、OSAが慢性炎症性疾患の発症・進展に関与する可能性が示唆された。
IHによるER増加メカニズムに関して、我々は転写因子やマイクロRNAの関与に否定的なデータを得ており、のこるERの発現制御メカニズムは限られてきている。
本研究は、IHによるER発現増加メカニズムの解明の足がかりとなると共に、その解明が慢性炎症性疾患等の治療および予防戦略へと繋がることを示した。
|
