Literature DB >> 25277999

Activation of liver-X-receptor α but not liver-X-receptor β protects against myocardial ischemia/reperfusion injury.

Qing He1, Jun Pu2, Ancai Yuan1, Wayne Bond Lau1, Erhe Gao1, Walter J Koch1, Xin-Liang Ma2, Ben He2.   

Abstract

BACKGROUND: Liver-X-receptors, LXRα (NR1H3) and LXRβ (NR1H2), encode 2 different but highly homologous isoforms of transcription factors belonging to the nuclear receptor superfamily. Whether LXRα and LXRβ subtypes have discrete roles in the regulation of cardiac physiology/pathology is unknown. We determine the role of each LXR subtype in myocardial ischemia/reperfusion (MI/R) injury. METHODS AND
RESULTS: Mice (wild type; those genetically depleted of LXRα, LXRβ, or both; and those overexpressing LXRα or LXRβ by in vivo intramyocardial adenoviral vector) were subjected to MI/R injury. Both LXRα and LXRβ were detected in wild-type mouse heart. LXRα, but not LXRβ, was significantly upregulated after MI/R. Dual activation of LXRα and LXRβ by natural and synthetic agonists reduced myocardial infarction and improved contractile function after MI/R. Mechanistically, LXR activation inhibited MI/R-induced oxidative stress and nitrative stress, attenuated endoplasmic reticulum stress and mitochondrial dysfunction, and reduced cardiomyocyte apoptosis in ischemic/reperfused myocardium. The aforementioned cardioprotective effects of LXR agonists were impaired in the setting of cardiac-specific gene silencing of LXRα, but not LXRβ subtype. Moreover, LXRα/β double-knockout and LXRα-knockout mice, but not LXRβ-knockout mice, increased MI/R injury, exacerbated MI/R-induced oxidative/nitrative stress, and aggravated endoplasmic reticulum stress and mitochondrial dysfunction. Furthermore, cardiac LXRα, not LXRβ, overexpression via adenoviral transfection suppressed MI/R injury.
CONCLUSIONS: Our study provides the first direct evidence that the LXRα, but not LXRβ, subtype is a novel endogenous cardiac protective receptor against MI/R injury. Drug development strategies specifically targeting LXRα may be beneficial in treating ischemic heart disease.
© 2014 American Heart Association, Inc.

Entities:  

Keywords:  apoptosis; myocardium; receptors, cytoplasmic and nuclear; reperfusion injury

Mesh:

Substances:

Year:  2014        PMID: 25277999      PMCID: PMC4527689          DOI: 10.1161/CIRCHEARTFAILURE.114.001260

Source DB:  PubMed          Journal:  Circ Heart Fail        ISSN: 1941-3289            Impact factor:   8.790


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