相关实验视频

Updated: Sep 13, 2025

A Model of Experimental Steatosis In Vitro: Hepatocyte Cell Culture in Lipid Overload-Conditioned Medium

A Model of Experimental Steatosis In Vitro: Hepatocyte Cell Culture in Lipid Overload-Conditioned Medium

Published on: May 18, 2021

由FOS降低调节的FABP4通过非激活ERK/STAT-1信号通路缓解棕酸诱导的内皮细胞功能障碍

Mengting Ruan¹, Jin Zhang²

¹Department of Obstetrics, Zhuji People's Hospital of Zhejiang Province, Zhuji, Zhejiang, P.R. China.

Cell biochemistry and biophysics

|July 28, 2025

概括

脂肪酸结合蛋白4 (FABP4) 在孕前症 (PE) 中升高. 通过抑制ERK/STAT-1通路,FABP4干扰可以防止棕酸诱导的内皮细胞功能障碍,这种干扰可能由FOS介导.

科学领域:

生殖生物学生殖生物学
分子医学是分子医学.
细胞生物学细胞生物学

背景情况:

孕前 (PE) 是一种严重的妊娠并发症,其特点是高血压和器官损伤.
对于PE病原体的潜在机制的理解尚不完全,因此需要对关键分子参与者的进一步研究.
脂肪酸结合蛋白4 (FABP4) 已与代谢障碍有关,但其在PE中的具体作用尚不清楚.

研究的目的:

阐明FABP4在产前 (PE) 病变发生过程中的作用.
调查FABP4在PE中影响内皮细胞功能的潜在分子机制.
探索FOS蛋白在调节FABP4活动及其下游信号传递中的潜在参与.

主要方法:

使用RT-qPCR对PE患者和对照者的血液和胎盘组织中FABP4表达的量化.
在体外研究中,使用人静脉内皮细胞 (HUVEC),用棕酸 (PA) 处理以模仿PE条件.
通过转染 (sh-FABP4,sh-FOS,Ov-FOS) 来操纵FABP4和FOS表达,并评估细胞活力,细胞亡 (TUNEL试验),迁移,入侵 (伤口愈合,Transwell试验) 和血管生成 (管形成试验).
分析与亡相关的蛋白质和ERK/STAT-1信号通路.
路西法酶记者和ChIP测试以确定FABP4促进剂活性和FOS与FABP4结合的FOS.

主要成果:

在PE患者的血液和胎盘组织以及PA治疗的HUVEC中,FABP4表达显著增加.
干扰FABP4表达减少了细胞亡,并通过不激活ERK/STAT-1信号通路,增强了PA诱导的HUVEC中的迁移,入侵和血管生成.
发现FOS降低了FABP4活性,并抑制了FABP4/ERK/STAT-1信号通路,这表明它具有保护作用.

结论:

通过促进内皮细胞功能障碍,FABP4在孕前的发病过程中发挥着至关重要的作用.
通过激活ERK/STAT-1信号通路,FABP4会加剧PA诱导的内皮细胞损伤.
FOS可以通过抑制FABP4/ERK/STAT-1通路来保护PA诱导的内皮细胞功能障碍,突出显示PE的潜在治疗标.

关键词:

在 ERK/STAT-1 中.内皮细胞功能障碍内皮细胞功能障碍在FABP4中,FABP4是指FABP4.这就是FOSOS.棕酸是一种棕酸.孕前症孕前症

更多相关视频

Methods to Study Mrp4-containing Macromolecular Complexes in the Regulation of Fibroblast Migration

Methods to Study Mrp4-containing Macromolecular Complexes in the Regulation of Fibroblast Migration

Published on: May 19, 2016

Network Pharmacology Prediction and Metabolomics Validation of the Mechanism of Fructus Phyllanthi against Hyperlipidemia

Network Pharmacology Prediction and Metabolomics Validation of the Mechanism of Fructus Phyllanthi against Hyperlipidemia

Published on: April 7, 2023

相关概念视频

NF-κB-dependent Signaling Pathway

NF-κB-dependent Signaling Pathway

The transcription factor NF-κB was discovered in 1986 in the lab of Nobel laureate Professor David Baltimore, for its interaction with the immunoglobulin light chain enhancer in B-cells. After more than three decades of study, it is now evident that NF-κB regulates the expression of over 100 genes. Most of these genes play an essential role in the innate and adaptive immune responses as well as the inflammatory responses of animals.
NF-κB-dependent Signaling Mechanism
The...

cAMP-dependent Protein Kinase Pathways

cAMP-dependent Protein Kinase Pathways

Cyclic Adenosine Monophosphate (cAMP) is an essential second messenger that activates protein kinase A (PKA) and regulates various biological processes. A single epinephrine molecule binds to GPCR and activates several heterotrimeric G proteins, each stimulating multiple adenylyl cyclase, amplifying the signal, and synthesizing large numbers of cAMP molecules. Small changes in cAMP concentration affect PKA activity. The binding of four cAMP molecules induces a conformational change in PKA,...

Peripheral Artery Disease I: Introduction

Peripheral Artery Disease I: Introduction

Peripheral artery disease (PAD) predominantly results from atherosclerosis, which involves the accumulation of fatty deposits, or plaques, within the walls of arteries. This causes them to narrow and harden, significantly reducing blood flow. PAD predominantly affects the legs, particularly the arteries supplying the thighs and calves. In rare cases, it may involve other arteries, including those in the arms.Etiology of PAD:The principal cause of PAD is atherosclerosis, which results from fatty...