Mechanisms of leptin receptor isoforms expression in heart diseases
Mechanisms of leptin receptor isoforms expression in heart diseases
批准号:
16590658
负责人:
YOKOYAMA Tomoyuki
金额:
$1.98万
依托单位:
依托单位国家:
日本
项目类别:
Grant-in-Aid for Scientific Research (C)
财政年份:
2004
资助国家:
日本
项目状态:
已结题
起止时间:
2004 至 2005
中文摘要
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英文摘要
(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 myocytesPressure 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
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Carvedilol effectively blocks oxidative stress-mediated down regulation of sarcoplasmic reticulum Ca(2+)一ATPase 2 gene transcription through modification of Sp1 binding.
卡维地洛通过修饰 Sp1 结合,有效阻断氧化应激介导的肌浆网 Ca(2+)-ATPase 2 基因转录下调。
DOI:
--
发表时间:
2005
期刊:
Biochem Biophys Res Common. 328(1)
影响因子:
--
作者:
[Koitabashi M, Arai M, Yokoyama T他]
通讯作者:
Yokoyama T他
DOI:
10.1016/j.bbrc.2004.12.139
发表时间:
2005-03-04
期刊:
BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS
影响因子:
3.1
作者:
[Koitabashi, N, Arai, M, Kurabayashi, M]
通讯作者:
Kurabayashi, M
DOI:
10.5694/j.1326-5377.2006.tb00116.x
发表时间:
2006-01-16
期刊:
MEDICAL JOURNAL OF AUSTRALIA
影响因子:
11.4
作者:
[Motooka, M, Koike, H, Kennedy, NL]
通讯作者:
Kennedy, NL
Usefulness of fasting 18F-FDG PET in identification of cardiac sarcoldosis.
空腹 18F-FDG PET 在鉴别心脏结节病中的作用。
DOI:
--
发表时间:
2004
期刊:
J Nuci Med. 45(12)
影响因子:
--
作者:
[Okumura W, Iwasaki T, Yokoyama T 他]
通讯作者:
Yokoyama T 他
Mechanisms of cardiac dysfunction in metabolic syndrome
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批准号:18590761
-
项目类别:Grant-in-Aid for Scientific Research (C)
-
资助金额:$2.39万
-
财政年份:2006
-
负责人:YOKOYAMA Tomoyuki
-
依托单位:
Regulation of the tumor necrosis factor-α promoter in the development of heart failure
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批准号:14570636
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项目类别:Grant-in-Aid for Scientific Research (C)
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资助金额:$2.56万
-
财政年份:2002
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负责人:YOKOYAMA Tomoyuki
-
依托单位:
Mechanism of tumor necrosis factor gene expression in the development of heart failure and cardiac hypertrophy
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批准号:12835001
-
项目类别:Grant-in-Aid for Scientific Research (C)
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资助金额:$2.69万
-
财政年份:2000
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负责人:YOKOYAMA Tomoyuki
-
依托单位:
国内基金
海外基金
Leptin receptor阳性细胞通过分泌Hedgehog蛋白调控椎间盘退变及修复的谱系研究
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批准号:--
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项目类别:面上项目
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资助金额:52万元
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批准年份:2022
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负责人:傅强
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依托单位:
Leptin Receptor负向调控应力刺激诱导的后纵韧带骨化的分子机制及转化研究
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批准号:81401821
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项目类别:青年科学基金项目
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资助金额:23.0万元
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批准年份:2014
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负责人:陈剑
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依托单位: