The macrophage LBP gene is an LXR target that promotes macrophage survival and atherosclerosis

Sallam, Tamer; Ito, Ayaka; Rong, Xianglu; Kim, Jason; Stijn, Caroline van; Chamberlain, Brian T.; Jung, Michael E.; Chao, Lily C.; Jones, Michael Owen; Gilliland, Thomas; Wu, Xiaohui; Su, Grace L.; Tangirala, Rajendra K.; Tontonoz, Peter; Hong, Cynthia

doi:10.1194/jlr.m047548

Cited by 24 publications

(22 citation statements)

References 76 publications

(82 reference statements)

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“…Compared to mice housed at T a of 22°C, thermoneutral housing of Apoe −− mice increased atherosclerotic lesion area by ~94% (Figure 4A). The increase in lesion area in thermoneutral mice was most apparent in the descending aorta (~3-fold increase), which develops atherosclerosis later in the course of the disease than the arch in en face analysis (Figure 4B, C) (Hong et al, 2012; Sallam et al, 2014). Staining of representative aortic root sections revealed that chow or WD-fed Apoe −− mice housed at T a of 30°C had larger lesions, which were enriched in neutral lipids (Oil Red O), macrophages (CD68) and smooth muscle cells (SMA) (Figure 4D).…”

Section: Resultsmentioning

confidence: 99%

Thermoneutral Housing Accelerates Metabolic Inflammation to Potentiate Atherosclerosis but Not Insulin Resistance

et al. 2016

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SUMMARY Chronic, low-grade inflammation triggered by excess intake of dietary lipids has been proposed to contribute to the pathogenesis of metabolic disorders, such as obesity, insulin resistance, type 2 diabetes, and atherosclerosis. Although considerable evidence supports a causal association between inflammation and metabolic diseases, most tests of this link have been performed in cold-stressed mice that are housed below their thermoneutral zone. We report here that thermoneutral housing of mice has a profound effect on the development of metabolic inflammation, insulin resistance, and atherosclerosis. Mice housed at thermoneutrality develop metabolic inflammation in adipose tissue and in the vasculature at an accelerated rate. Unexpectedly, this increased inflammatory response contributes to the progression of atherosclerosis but not insulin resistance. These findings not only suggest that metabolic inflammation can be uncoupled from obesity-associated insulin resistance, but also point to how thermal stress might limit our ability to faithfully model human diseases in mice.

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Section: Resultsmentioning

confidence: 99%

Thermoneutral Housing Accelerates Metabolic Inflammation to Potentiate Atherosclerosis but Not Insulin Resistance

et al. 2016

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“…An additional interesting effect that has been ascribed to sidechain-oxysterols and triggered through the LXR-RXR pathway is the stimulation of an anti-inflammatory phenotype in macrophages, i.e. an important process in the modulation of inflammatory and immunologic events (Töröcsik et al, 2009), which can lead to the survival not only of immune cells (Joseph et al, 2004) but also of foam cells (Sallam et al, 2014) and tumor cells (York and Bensinger, 2013). Still, the overall effect of oxysterols, usually present in mixture within human tissues and biological fluids, on the modulation of inflammation and immunity is far from being fully elucidated.…”

Section: Oxysterol-mediated Activation Of Transcription Factorsmentioning

confidence: 99%

Oxysterols and mechanisms of survival signaling

Vurusaner

Leonarduzzi

Gamba

et al. 2016

Molecular Aspects of Medicine

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“…In advanced lesions LXR activation induces the expression of genes that increase cholesterol efflux, reduce inflammation, stabilize the fibrous cap, induce macrophage egress from the lesion, repress apoptosis, and improve the clearance of apoptotic debris. 36-40, 46-49, 52-54, 67, 73-78, 80, 148-150 …”

Section: Highlightsmentioning

confidence: 99%

“…LPS binding protein (LBP) is an other LXR target linked to the control of apoptosis 49 . LBP is a member of a family of lipid transfer proteins, which includes PLTP and CETP.…”

Section: Introductionmentioning

confidence: 99%