Related Experiment Video
Updated: Apr 3, 2026
Subcutaneous Angiotensin II Infusion using Osmotic Pumps Induces Aortic Aneurysms in Mice
Published on: September 28, 2015
Apolipoprotein-J prevents angiotensin II-induced apoptosis in neonatal rat ventricular cells
Yanzhuo Ma1, Lingfeng Kong2, Kai Nan3
1Department of Cardiology, Bethune International Peace Hospital, Shijiazhuang, Hebei, China. 297400148@qq.com.
Insights
Apolipoprotein-J (ApoJ) protects heart cells from damage caused by angiotensin II (AngII). This study shows ApoJ reduces cell injury and inflammation via specific molecular pathways, highlighting its potential therapeutic role in cardiovascular diseases.
Area of Science:
- Cardiovascular Biology
- Cellular Signaling
- Molecular Medicine
Background:
- Angiotensin II (AngII) up-regulation is implicated in various cardiac diseases.
- Apolipoprotein-J (ApoJ) elevation is observed in cardiovascular disease, suggesting a protective role.
- Neonatal rat ventricular cells (NRVCs) are used to study cardiac cell responses.
Purpose of the Study:
- To investigate the protective effects of ApoJ against AngII-induced cytotoxicity in NRVCs.
- To elucidate the molecular mechanisms underlying ApoJ's protective action.
Main Methods:
- NRVCs were exposed to AngII, with and without ApoJ overexpression via adenovirus.
- Key signaling pathways including PI3K-Akt, ROS, MAPK, and NF-κB were analyzed.
- Specific inhibitors (LY294002, SB203580, PDTC) and ROS scavengers (Mn(III)TBAP) were used.
Main Results:
- ApoJ overexpression significantly reduced AngII-induced NRVC injury and Nox2/gp91(phox) expression.
- ApoJ increased Akt phosphorylation, and PI3K inhibition abolished its protective effects.
- ApoJ inhibited AngII-induced p38 MAPK and NF-κB p65 activation.
- ROS scavenging and inhibition of p38 MAPK/NF-κB mimicked ApoJ's protective effects.
Conclusions:
- ApoJ acts as a cytoprotective protein in NRVCs against AngII toxicity.
- The protective mechanism involves modulation of the PI3K-Akt-ROS and MAPK/NF-κB signaling pathways.
- ApoJ demonstrates potential as a therapeutic agent for AngII-related cardiovascular conditions.
Background:
Up-regulation of angiotensin II (AngII) occurs in cardiac diseases, such as congestive heart failure, cardiac hypertrophy, myocardial ischemia and atrial fibrillation, which represent major health problems. Evidence from in vivo studies suggests that the level of Apolipoprotein-J (ApoJ) is also elevated but plays a protective role in cardiovascular disease. This study aimed to evaluate the protective effects of ApoJ against cytotoxicity of AngII in neonatal rat ventricular cells (NRVCs).
Methods And Results:
In culture, NRVCs were damaged by exposure to AngII, and ApoJ overexpression using an adenovirus vector significantly reduced the AngII-induced cell injury. ApoJ also prevented AngII from augmenting Nox2/gp91(phox) expression. The reactive oxygen species (ROS) scavenger, Mn(III)TBAP, showed similar results of attenuating AngII-induced cell damage. Furthermore, ApoJ overexpression increased phosphorylation of Akt, and the phosphatidylinositol 3-kinase (PI3K) inhibitor LY294002 diminished the antioxidant effects of ApoJ, and prevented the protective effect of ApoJ against the cytotoxicity of AngII. Moreover, upregulation of nuclear factor κB (NF-κB) p65 expression and phosphorylation of p38 mitogen-activated protein kinase (MAPK) mediated by AngII in cultured NRVCs were significantly inhibited by overexpression of ApoJ. The p38 MAPK inhibitor SB203580 and the NF-κB inhibitor PDTC protected NRVCs from injury caused by AngII.
Conclusions:
ApoJ serves as a cytoprotective protein in NRVCs against cytotoxicity of AngII through the PI3K-Akt-ROS and MAPK/ NF-κB pathways.
More Related Videos
Related Concept Videos
01:30Antihypertensive Drugs: Angiotensin-Converting Enzyme Inhibitors
01:26Heart Failure Drugs: Inhibitors of Renin-Angiotensin System
01:25Antihypertensive Drugs: Direct Renin Inhibitors