相关实验视频

Updated: Jan 10, 2026

Receptor Autoradiography Protocol for the Localized Visualization of Angiotensin II Receptors

Receptor Autoradiography Protocol for the Localized Visualization of Angiotensin II Receptors

Published on: June 7, 2016

血管素II,miR-34a和AGTRAP在动脉光滑肌肉细胞中的交叉交叉

Maria Cristina Florio¹, Sara Sileno², Liqun Jiang¹

¹Laboratory of Cardiovascular Science, National Institute On Aging, National Institutes of Health, Baltimore, MD, USA.

|November 25, 2025

概括

动脉衰老涉及增加的血管素II (Ang II) 信号传递和microRNA-34a (miR-34a). 这项研究揭示了miR-34a针对ATRAP,增强Ang II在血管细胞中的促炎作用,从而导致血管衰老.

科学领域:

心血管生物学心血管生物学
分子生物学分子生物学
衰老研究研究衰老研究

背景情况:

动脉衰老与通过Ang II型1受体 (AT1R) 和增加microRNA-34a (miR-34a) 表达的增加的血管素II (Ang II) 信号传递有关.
与AT1R相关的蛋白质 (ATRAP) 通过结合和促进AT1R内部化来抑制Ang II信号传递.

研究的目的:

调查miR-34a是否针对ATRAP,并通过AT1R在血管光滑肌细胞 (VSMC) 中加剧Ang II促炎信号传递.

主要方法:

在灵长类动物和动物动脉和VSMC中分析了miR-34a和AGTRAP表达的年龄相关变化.
在人类大动脉光滑肌细胞 (HASMC) 中评估了Ang II和miR-34a对AGTRAP,SIRT1和亲炎性基因表达的影响.
证实了miR-34a对AGTRAP的直接向,并评估了AGTRAP调节对miR-34a和SIRT1的影响.

主要成果:

动脉中的miR-34a表达随着年龄的增长而增加,而AGTRAP蛋白减少.
在VSMC中,Ang II提高了miR-34a,并降低了AGTRAP和SIRT1.
miR-34a直接针对AGTRAP,这种相互作用增强了miR-34a的表达并降低了SIRT1.
格II和miR-34a诱导了促炎基因 (IL-6,COX2,MCP-1,MFGE8),这种效应被AGTRAP过度表达所阻断.

结论:

格II上调 miR-34a,创建一个反循环,下调 ATRAP,从而放大格II信号.
与年龄相关的ATRAP下降有助于血管衰老,可能通过miR-34a/AGTRAP通路.

关键词:

在 AGTRAP 公司.衰老的衰老衰老的衰老动脉衰老是动脉的衰老.在MFGE8中,MFGE8是什么?这是一架米R-34a.一个SIRT1系统.

更多相关视频

Subcutaneous Angiotensin II Infusion using Osmotic Pumps Induces Aortic Aneurysms in Mice

Subcutaneous Angiotensin II Infusion using Osmotic Pumps Induces Aortic Aneurysms in Mice

Published on: September 28, 2015

Live Cell Imaging and 3D Analysis of Angiotensin Receptor Type 1a Trafficking in Transfected Human Embryonic Kidney Cells Using Confocal Microscopy

Live Cell Imaging and 3D Analysis of Angiotensin Receptor Type 1a Trafficking in Transfected Human Embryonic Kidney Cells Using Confocal Microscopy

Published on: March 27, 2017

相关概念视频

Antihypertensive Drugs: Angiotensin II Receptor Blockers

Antihypertensive Drugs: Angiotensin II Receptor Blockers

In the renin-angiotensin-aldosterone system, a hormone called angiotensin II plays a crucial role. It binds to the AT1 receptors in vascular smooth muscles coupled with Gq proteins. The activation of these receptors activates an enzyme called phospholipase C, which releases two molecules: inositol trisphosphate and diacylglycerol. These molecules cause a chain reaction that leads to the phosphorylation of myosin light chains and promotes interaction between actin and myosin, leading to smooth...

Antihypertensive Drugs: Angiotensin-Converting Enzyme Inhibitors

Antihypertensive Drugs: Angiotensin-Converting Enzyme Inhibitors

Angiotensin-converting enzyme (ACE), a vital component of the renin-angiotensin-aldosterone system, is abundant in lung endothelial cells. ACE converts the inactive decapeptide, angiotensin I, into the active octapeptide, angiotensin II. This potent vasoconstrictor narrows blood vessels, increasing resistance to blood flow and elevating blood pressure. Angiotensin II also stimulates aldosterone production, encouraging kidney cells to reabsorb more sodium and water from urine, thereby increasing...

Antihypertensive Drugs: Direct Renin Inhibitors

Antihypertensive Drugs: Direct Renin Inhibitors

The renin-angiotensin-aldosterone system (RAAS) is an intricate physiological pathway involving numerous enzymes and hormones, including renin, angiotensin-converting enzyme (ACE), angiotensin I and II, and aldosterone. Imbalances within this system increase the production of angiotensin II and aldosterone. Increased angiotensin II levels promote vasoconstriction and blood pressure elevation. Concurrently, higher aldosterone levels stimulate sodium and water reabsorption in the kidneys,...

Heart Failure Drugs: Inhibitors of Renin-Angiotensin System

Heart Failure Drugs: Inhibitors of Renin-Angiotensin System

The activation of the sympathetic nervous system and the renin-angiotensin-aldosterone system (RAAS) contributes to cardiac remodeling, and inhibiting the RAAS is a pharmacological target in heart failure management. As a result, neurohumoral modulation is a crucial treatment principle for managing heart failure. This approach involves using medications like ACE inhibitors (ACEIs), angiotensin receptor blockers (ARBs), β-blockers, mineralocorticoid receptor antagonists (MRAs), and neutral...

Adrenergic Receptors: ɑ Subtype

Adrenergic Receptors: ɑ Subtype

Adrenoceptors are classified into α and ꞵ classes based on their potencies to catecholamine agonists. α-adrenoceptors show the following order of catecholamine potency:
Adrenaline ≥ Noradrenaline >> Isoprenaline
α-adrenoceptors are further divided into α1 and α2-adrenoceptors.
α1-Adrenoceptors: These receptors are located postsynaptically on the effector organs and cause constriction of smooth muscle mediated by activation of phospholipase...

Antihypertensive Drugs: Action of β1 Blockers

Antihypertensive Drugs: Action of β₁ Blockers

β1-receptors are primarily located in the heart and kidneys. In cardiac myocytes, these receptors interact with neurotransmitters released by the sympathetic nervous system during heightened activity or danger. As a result, β1-receptors get activated, initiating a series of biochemical processes. Excessive activation of beta receptors due to chronic stress can abnormally increase heart rate and contractility, resulting in high blood pressure or hypertension. To counteract this,...