相关实验视频

Updated: Jul 29, 2026

Intracoronary Acetylcholine Provocation Testing for Assessment of Coronary Vasomotor Disorders

Intracoronary Acetylcholine Provocation Testing for Assessment of Coronary Vasomotor Disorders

Published on: August 18, 2016

历史胺诱导组织因子表达:对急性冠状动脉综合征的影响

Jan Steffel¹, Alexander Akhmedov, Helen Greutert

¹Cardiovascular Research, Physiology Institute, University of Zurich, Winterthurerstrasse 190, CH-8057 Zürich, Switzerland.

|July 13, 2005

概括

组胺通过H1受体和MAP激酶触发血管细胞中的组织因子 (TF) 表达,可能影响变异性心痛和急性冠状动脉综合征.

科学领域:

心血管生物学心血管生物学
分子医学是分子医学.
细胞信号传递细胞信号传递

背景情况:

已知胺会引起冠状动脉,导致变异性胸痛和心肌梗塞.
基因组胺在血栓形成中的特定作用尚不清楚.
这项研究调查了组胺在血管细胞中诱导组织因子 (TF) 表达的潜力.

研究的目的:

为了确定基因组胺是否诱导人体大动脉内皮和血管光滑肌细胞中的组织因子 (TF) 表达.
为了阐明受体通路和细胞内信号级联涉及组胺诱导的TF表达.
探索对诸如变异性心痛和急性冠状动脉综合征等疾病的影响.

主要方法:

人类大动脉内皮和血管光滑肌细胞被用组胺治疗.
组织因子 (TF) 和TF途径抑制剂表达被评估使用RT-PCR和北方斑点.
研究了MAP激酶 (p38,ERK,JNK) 和酸丁醇3-激酶 (PI3K) 信号通路.
使用了受体对抗性 (H1和H2) 和特定酶抑制.

主要成果:

组胺通过H1受体,而不是H2受体,以度依赖的方式诱导TF表达.
组胺刺激了TF mRNA和蛋白质的表达,增加了表面活性.
这种效应是由p38,ERK和JNK MAP激酶的激活介导的.
抑制PI3K增强了基因组胺诱导的TF表达,而抑制Rho-酶没有影响.

结论:

组胺通过H1受体激活,诱导血管细胞中的TF表达.
这种信号通路涉及p38,ERK和JNK MAP激酶.
这些发现表明一种新的机制将组胺胺与血栓形成联系起来,并为心血管事件提供潜在的治疗点.

更多相关视频

Extracellular Vesicle Tissue Factor Activity Assay

Extracellular Vesicle Tissue Factor Activity Assay

Published on: December 29, 2023

Flow Cytometry Analysis of Tissue Factor Expression in Human Platelets

Flow Cytometry Analysis of Tissue Factor Expression in Human Platelets

Published on: November 22, 2024

相关概念视频

Myocarditis I: Introduction

Myocarditis I: Introduction

Myocarditis is inflammation of the myocardium, which is the muscular layer of the heart.EtiologyMyocarditis has a diverse etiology, including a wide range of infectious and non-infectious causes:Infectious CausesViral: Common viruses include Coxsackie A and B, adenovirus, parvovirus B19, enteroviruses, and influenza A.Bacterial: Examples include infections caused by Streptococcus, Staphylococcus, and Mycoplasma species.Rickettsial: Infections like Rocky Mountain spotted fever can result in...

Acute Coronary Syndrome I: Introduction

Acute Coronary Syndrome I: Introduction

Acute Coronary Syndrome (ACS) encompasses a spectrum of heart conditions caused by sudden obstruction of coronary arteries, typically resulting from the rupture of an atherosclerotic plaque and subsequent thrombus (blood clot) formation. This obstruction can lead to partial or complete blockage of blood flow, causing varying degrees of myocardial ischemia or infarction.ACS includes the following clinical entities:Unstable Angina (UA)Non-ST-Elevation Myocardial Infarction (NSTEMI)ST-Elevation...

Acute Coronary Syndrome II: Pathophysiology and Clinical Manifestations

Acute Coronary Syndrome II: Pathophysiology and Clinical Manifestations

The pathophysiology of Acute Coronary Syndrome [ACD] involves several key processes:The main underlying cause of ACD is atherosclerosis, a chronic inflammatory disease characterized by the buildup of lipid-laden plaques within the coronary arteries.As the atherosclerotic plaque grows in the coronary artery, it may become unstable due to the formation of a lipid-rich core and a thin fibrous cap. Inflammatory cells within the plaque, such as macrophages, secrete enzymes that degrade the...

Acute Coronary Syndrome III: Diagnostic Studies

Acute Coronary Syndrome III: Diagnostic Studies

Diagnosing acute coronary syndrome or ACS begins with a thorough patient history. Notable symptoms include central, crushing chest pain radiating to the left arm, neck, jaw, or back, along with shortness of breath, sweating (diaphoresis), nausea, vomiting, dizziness, and palpitations.It is crucial to note any history of cardiac illnesses and assess risk factors, including age, gender, smoking, hypertension, diabetes, hyperlipidemia, and a sedentary lifestyle.During physical examination, vital...

Acute Inflammation I: Inflammatory Response

Acute Inflammation I: Inflammatory Response

Acute inflammation is a rapid, short-lived physiological response to tissue injury or infection, designed to eliminate harmful agents and initiate repair. This tightly regulated process typically lasts from minutes to several days and is triggered by factors such as microbial invasion, physical trauma, or chemical injury.Recognition and Mediator ReleaseThe inflammatory response begins when resident immune cells—such as mast cells, macrophages, and dendritic cells—detect damage-associated...

Acute Inflammation III: Local and Systemic Effects

Acute Inflammation III: Local and Systemic Effects

Acute inflammation produces a coordinated set of local and systemic changes that limit injury, eliminate pathogens, and initiate repair. These responses arise within minutes of infection, trauma, or chemical insult and are driven by vascular alterations and leukocyte-derived mediators. When the stimulus resolves, the reaction typically abates within days.Local EffectsAt the site of injury, arteriolar vasodilation increases blood flow, resulting in redness and warmth. Simultaneously, increased...