Abstract
BackgroundOxidized low-density lipoprotein (ox-LDL) is crucial in cardiac injury. Apolipoprotein-J (ApoJ) contributes to antiapoptotic effects in the heart. We aimed to evaluate the protective effects of ApoJ against ox-LDL cytotoxicity in Neonatal rat ventricular cells (NRVCs).Methods and resultsNRVCs were damaged by exposure to ox-LDL, as shown by increased caspase-3/7 activity, enhanced caspase-3 expression, and decreased cell viability. ApoJ overexpression, using an adenovirus vector, significantly reduced ox-LDL-induced cell injury. ApoJ also prevented ox-LDL from augmenting reactive oxygen species (ROS) production, as demonstrated by elevated Nox2/gp91phox and P47 expression. Furthermore, ApoJ overexpression reduced CaMKIIδ expression elicited by ox-LDL in cultured NRVCs. Upregulating CaMKIIδ activity, mediated by ox-LDL, was significantly inhibited by ApoJ overexpression. A CaMKIIδ inhibitor, KN93, prevented ApoJ’s protective effect against ox-LDL cytotoxicity. A ROS scavenger, Mn (III)meso-tetrakis (4-benzoic acid) porphyrin (Mn (III)TBAP), also attenuated CaMKIIδ’s increased expression and activity, induced by ox-LDL, and showed similar results to ApoJ by attenuating ox-LDL-induced cell damage, as ApoJ did.ConclusionsApoJ confers cytoprotection to NRVCs against ox-LDL cytotoxicity through the ROS-CaMKII pathways.
Highlights
Oxidized low-density lipoprotein is crucial in cardiac injury
ApoJ overexpression prevented cell injury induced by oxLDL To determine whether ApoJ attenuated cell injury induced by Oxidized low-density lipoprotein (ox-LDL), the Neonatal rat ventricular cells (NRVCs) were infected with recombinant adenovirus with and without ApoJ
Ox-LDL was added into the NRVCs 36 h after adenovirus infection
Summary
Apolipoprotein-J (ApoJ) contributes to antiapoptotic effects in the heart. We aimed to evaluate the protective effects of ApoJ against oxLDL cytotoxicity in Neonatal rat ventricular cells (NRVCs). Apolipoprotein-J (ApoJ) is a multifunctional glycoprotein widely present in tissues and body fluids. ApoJ expression is upregulated in acute myocardial infarction, atherosclerosis, myocarditis, oxidative stress, inflammation, and after injury in general [1]. Blocking secreted ApoJ leads to increased apoptosis of neuroblastoma cells induced by the chemotherapeutic drug doxorubicin [4]. ApoJ produces cardioprotective effects on ischemically challenged H9C2 cells and isolated adult ventricular rat cardiomyocytes after ischemia-induced death [5]. ApoJ-deficient mice show more impaired cardiac function and worse myocardial scarring compared to wild-type mice. ApoJ may play a critical role in reducing injury to both normal and diseased cells
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