Key result
Oncostatin M activates LDL-receptor transcription independent of intracellular cholesterol levels and reduces circulating cholesterol in hyperlipidemic animals.
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Oncostatin M activates LDL-receptor transcription through a sterol-independent pathway, offering a potential novel therapeutic target for hyperlipidemia.
Reduction in blood levels of low-density lipoprotein (LDL) cholesterol lowers the risk of coronary heart disease. The elucidation of cellular pathways that control LDL-receptor expression through a cholesterol-mediated negative feedback mechanism has provided a crucial molecular basis for the development and clinical applications of statins in the treatment of hypercholesterolemia. The characterization of signaling transduction pathways elicited by cytokine oncostatin M (OM) in liver cells has revealed a novel cellular pathway that activates LDL-receptor transcription independent of intracellular levels of cholesterol and sterol-regulatory element binding proteins. This transcriptional activation is achieved through interactions of the sterol-independent regulatory element of LDL-receptor promoter and transcription factors Egr1 and c/EBPbeta, and is dependent upon the activation of the extracellular signal-regulated kinase signaling cascade by OM. In vivo OM administration in hyperlipidemic animals reduces circulating cholesterol and prevents lipid accumulation in the liver. Exploring this sterol-independent cellular pathway may lead to new therapeutic advances.
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Liu et al. (2006) conducted a review in Hypercholesterolemia. Oncostatin M (OM) was evaluated on LDL-receptor transcription and circulating cholesterol. Oncostatin M activates LDL-receptor transcription independent of intracellular cholesterol levels and reduces circulating cholesterol in hyperlipidemic animals.
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