A novel posttranscriptional mechanism for dietary cholesterol-mediated suppression of liver LDL receptor expression[S]

It is well-established that over-accumulation of dietary cholesterol in the liver inhibits sterol-regulatory element binding protein (SREBP)-mediated LDL receptor (LDLR) gene transcription leading to a reduced hepatic LDLR mRNA level in hypercholesterolemic animals. However, it is unknown whether el...

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Published inJournal of lipid research Vol. 55; no. 7; pp. 1397 - 1407
Main Authors Singh, Amar Bahadur, Kan, Chin Fung Kelvin, Shende, Vikram, Dong, Bin, Liu, Jingwen
Format Journal Article
LanguageEnglish
Published United States Elsevier Inc 01.07.2014
The American Society for Biochemistry and Molecular Biology
Elsevier
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Abstract It is well-established that over-accumulation of dietary cholesterol in the liver inhibits sterol-regulatory element binding protein (SREBP)-mediated LDL receptor (LDLR) gene transcription leading to a reduced hepatic LDLR mRNA level in hypercholesterolemic animals. However, it is unknown whether elevated cholesterol levels can elicit a cellular response to increase LDLR mRNA turnover to further repress LDLR expression in liver tissue. In the current study, we examined the effect of a high cholesterol diet on the hepatic expression of LDLR mRNA binding proteins in three different animal models and in cultured hepatic cells. Our results demonstrate that high cholesterol feeding specifically elevates the hepatic expression of LDLR mRNA decay promoting factor heterogeneous nuclear ribonucleoprotein (HNRNP)D without affecting expressions of other LDLR mRNA binding proteins in vivo and in vitro. Employing the approach of adenovirus-mediated gene knockdown, we further show that depletion of HNRNPD in the liver results in a marked reduction of serum LDL-cholesterol and a substantial increase in liver LDLR expression in hyperlipidemic mice. Additional studies of gene knockdown in albumin-luciferase-untranslated region (UTR) transgenic mice provide strong evidence supporting the essential role of 3′UTR in HNRNPD-mediated LDLR mRNA degradation in liver tissue. Altogether, this work identifies a novel posttranscriptional regulatory mechanism by which dietary cholesterol inhibits liver LDLR expression via inducing HNRNPD to accelerate LDLR mRNA degradation.
AbstractList It is well-established that over-accumulation of dietary cholesterol in the liver inhibits sterol-regulatory element binding protein (SREBP)-mediated LDL receptor (LDLR) gene transcription leading to a reduced hepatic LDLR mRNA level in hypercholesterolemic animals. However, it is unknown whether elevated cholesterol levels can elicit a cellular response to increase LDLR mRNA turnover to further repress LDLR expression in liver tissue. In the current study, we examined the effect of a high cholesterol diet on the hepatic expression of LDLR mRNA binding proteins in three different animal models and in cultured hepatic cells. Our results demonstrate that high cholesterol feeding specifically elevates the hepatic expression of LDLR mRNA decay promoting factor heterogeneous nuclear ribonucleoprotein (HNRNP)D without affecting expressions of other LDLR mRNA binding proteins in vivo and in vitro. Employing the approach of adenovirus-mediated gene knockdown, we further show that depletion of HNRNPD in the liver results in a marked reduction of serum LDL-cholesterol and a substantial increase in liver LDLR expression in hyperlipidemic mice. Additional studies of gene knockdown in albumin-luciferase-untranslated region (UTR) transgenic mice provide strong evidence supporting the essential role of 3′UTR in HNRNPD-mediated LDLR mRNA degradation in liver tissue. Altogether, this work identifies a novel posttranscriptional regulatory mechanism by which dietary cholesterol inhibits liver LDLR expression via inducing HNRNPD to accelerate LDLR mRNA degradation.
Author Liu, Jingwen
Kan, Chin Fung Kelvin
Singh, Amar Bahadur
Shende, Vikram
Dong, Bin
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Issue 7
Keywords posttranscriptional regulation
adenylate-uridylate-rich element-binding proteins
low density lipoprotein
heterogeneous nuclear ribonucleoprotein D
messenger ribonucleic acid stability
hypercholesterolemia
Language English
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Elsevier
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Snippet It is well-established that over-accumulation of dietary cholesterol in the liver inhibits sterol-regulatory element binding protein (SREBP)-mediated LDL...
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SubjectTerms 3' Untranslated Regions
adenylate-uridylate-rich element-binding proteins
Animals
Cholesterol, Dietary - pharmacology
Gene Expression Regulation - drug effects
heterogeneous nuclear ribonucleoprotein D
Heterogeneous-Nuclear Ribonucleoprotein D - genetics
Heterogeneous-Nuclear Ribonucleoprotein D - metabolism
hypercholesterolemia
Liver - metabolism
low density lipoprotein
Male
messenger ribonucleic acid stability
Mice
Mice, Transgenic
posttranscriptional regulation
Receptors, LDL - biosynthesis
Receptors, LDL - genetics
RNA Stability - drug effects
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Title A novel posttranscriptional mechanism for dietary cholesterol-mediated suppression of liver LDL receptor expression[S]
URI https://dx.doi.org/10.1194/jlr.M049429
https://www.ncbi.nlm.nih.gov/pubmed/24792925
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