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Lipids Health Dis. 2019 May 22;18(1):117. doi: 10.1186/s12944-019-1066-8.

Apolipoprotein-J blocks increased cell injury elicited by ox-LDL via inhibiting ROS-CaMKII pathway.

Author information

1
Department of Cardiology, Bethune International Peace Hospital, 398, Zhongshan Road, Shijiazhuang, 050082, Hebei, China.
2
Health and Medical Development Research Center of Hebei Province, Shijiazhuang, Hebei, China.
3
Department of Cardiology, Bethune International Peace Hospital, 398, Zhongshan Road, Shijiazhuang, 050082, Hebei, China. muyeqiufeng2008@163.com.

Abstract

BACKGROUND:

Oxidized 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 RESULTS:

NRVCs 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.

CONCLUSIONS:

ApoJ confers cytoprotection to NRVCs against ox-LDL cytotoxicity through the ROS-CaMKII pathways.

KEYWORDS:

Apolipoprotein-J; Apoptosis; Neonatal rat ventricular cells; Ox-LDL

PMID:
31113434
PMCID:
PMC6530009
DOI:
10.1186/s12944-019-1066-8
[Indexed for MEDLINE]
Free PMC Article

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