| Project/Area Number |
16590658
|
|---|
| Research Category |
Grant-in-Aid for Scientific Research (C)
|
| Allocation Type | Single-year Grants |
|---|
| Section | 一般 |
|---|
| Research Field |
Circulatory organs internal medicine
|
|---|
| Research Institution | Gunma University |
|---|
Principal Investigator |
YOKOYAMA Tomoyuki GUNMA UNIVERSITY, Laboratory Science, professor, 医学部, 教授 (70312890)
|
|---|
| Co-Investigator(Kenkyū-buntansha) |
ARAI Masashi , 医学部, 講師 (60270857)
KURABAYASHI Masahiko GUNMA UNIVERSITY, Medicine and Biological Science, professor, 医学研究科, 教授 (00215047)
|
|---|
| Project Period (FY) |
2004 – 2005
|
| Project Status |
Completed (Fiscal Year 2005)
|
| Budget Amount *help |
¥3,100,000 (Direct Cost: ¥3,100,000)
Fiscal Year 2005: ¥800,000 (Direct Cost: ¥800,000)
Fiscal Year 2004: ¥2,300,000 (Direct Cost: ¥2,300,000)
|
|---|
| Keywords | leptin / leptin receptor / ischemia / reperfusion / hypertrophy / pressure overload |
|---|
| Research Abstract |
(1)Ischemia/reperfusion in rat heart induces leptin and leptin receptor gene expression.
We examined the expression of leptin (ob) and leptin receptor (ob-R) genes in the rat heart following ischemia/reperfusion. Ischemia/reperfusion was induced by coronary artery ligation, and mRNA was obtained from hearts 0.5 to 36 h after initiating reperfusion. Expressions of ob and ob-R mRNA were examined by Real-time quantitative RT-PCR and immunohistochemistry. The ob and ob-Ra mRNAs and proteins significantly exceeded amounts in control hearts after 8 h of reperfusion, and they were present at ischemic wound sites locally. To determine the functional effects of leptin in ischemic heart, rats were treated with anti-leptin antibodies prior to ischemia/reperfusion. This treatment partially prevented elevation of the mRNA expression levels of inflammatory markers such as TNF-α and IL-1β in ischemic hearts.
(2)Hypertensive stress directly up-regulates expression of leptin and the long form of the lept
… More
in receptor (ob-Rb) in rat cardiac myocytes
Pressure overload was produced by ligation of the abdominal aorta. Using expression of the real-time polymerase chain reaction (PCR), leptin and the long form of the leptin receptor (ob-Rb) gene were significantly increased at 2 and 4 weeks, but expression of the short form of the leptin receptor (ob-Ra) was unchanged after banding. When we examined protein expression of ob-Rb, ob-Rb protein was detected by immunohistochemistry in hypertrophied cardiomyocytes. Plasma leptin concentrations were not different between the control and banding groups. To clarify which hypertension-related stimuli induces ob and ob-Rb expression in the heart, we examined ob and ob-Rb mRNA expression in neonatal rat cardiac myocytes treated with angiotensin II (ANGII), endothelin-1 (ET-1), or cyclic mechanical stretch. ANGII and ET-1 increased only ob mRNA expression. However, mechanical stretch activated both ob and ob-Rb expression in a time-dependent manner, but ob-Ra was unaffected by any stress. Less
|
