2012
DOI: 10.1016/j.lfs.2012.04.003
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Sphingomyelin synthase 2 over-expression induces expression of aortic inflammatory biomarkers and decreases circulating EPCs in ApoE KO mice

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Cited by 24 publications
(12 citation statements)
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“…SMases may hydrolyze LDL-sphingomyelin in the arterial wall increasing LDL-ceramide and aggregation of lipoproteins leading to initiation and progression of atherosclerosis 49 . Over expression of SMS2 in mice exaggerates atherosclerotic inflammation 50 , whereas inhibition of sphingolipid synthesis by myriocin reduces atherosclerosis 51 . Further, LDL receptor knockout mice transplanted with bone marrow cells derived from Sms2 − / − mice show decreased atherosclerotic lesions 52 .…”
Section: Cardiovascular Diseasesmentioning
confidence: 99%
“…SMases may hydrolyze LDL-sphingomyelin in the arterial wall increasing LDL-ceramide and aggregation of lipoproteins leading to initiation and progression of atherosclerosis 49 . Over expression of SMS2 in mice exaggerates atherosclerotic inflammation 50 , whereas inhibition of sphingolipid synthesis by myriocin reduces atherosclerosis 51 . Further, LDL receptor knockout mice transplanted with bone marrow cells derived from Sms2 − / − mice show decreased atherosclerotic lesions 52 .…”
Section: Cardiovascular Diseasesmentioning
confidence: 99%
“…Consistently, LDL from SMS2 transgenic mice exhibit proatherogenic properties with increased in vitro aggregation upon SMase treatment [ 35 ]. Also, SMS2 overexpression in mice with adenovirus exaggerated atherosclerotic inflammation with elevations in cyclooxygenase-2 (COX-2) and matrix metalloproteinase-2 (MMP-2) in aorta [ 91 ]. Myriocin treatment decreased sphingomyelin and ceramide levels in plasma and consequently resulted in less atherosclerotic lesions in aorta from HFD-fed Apo-E deficient mice [ 87 , 92 , 93 ].…”
Section: Sphingolipids In Hfd-induced Pathobiologymentioning
confidence: 99%
“…Inhibition of SMS in EC was reported to attenuate lipopolysaccaride (LPS)-induced lung injury in animals through enhancement of the EC barrier by reducing loss of SM from lipid rafts in the cell membrane 27 . Elevated plasma SM levels are a prognostic marker in acute coronary syndrome 28 , and overexpression of SMS is suggested to be related to EC dysfunction, a decrease of CD34/KDR-positive endothelial progenitor cells, and development of atherosclerosis in ApoE knock-out mice 29 . Thus, plasmalogens and SM play an important role in EC function and their plasma levels reflect various disease states.…”
Section: Introductionmentioning
confidence: 99%