High density lipoprotein metabolism in low density lipoprotein receptor-deficient mice
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High density lipoprotein metabolism in low density lipoprotein receptor-deficient mice. / Rinninger, Franz; Heine, Markus; Singaraja, Roshni; Hayden, Michael; Brundert, May; Ramakrishnan, Rajasekhar; Heeren, Joerg.
In: J LIPID RES, Vol. 55, No. 9, 01.09.2014, p. 1914-1924.Research output: SCORING: Contribution to journal › SCORING: Journal article › Research › peer-review
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TY - JOUR
T1 - High density lipoprotein metabolism in low density lipoprotein receptor-deficient mice
AU - Rinninger, Franz
AU - Heine, Markus
AU - Singaraja, Roshni
AU - Hayden, Michael
AU - Brundert, May
AU - Ramakrishnan, Rajasekhar
AU - Heeren, Joerg
N1 - Copyright © 2014 by the American Society for Biochemistry and Molecular Biology, Inc.
PY - 2014/9/1
Y1 - 2014/9/1
N2 - The LDL receptor (LDLR) and scavenger receptor class B type I (SR-BI) play physiological roles in LDL and HDL metabolism in vivo. In this study, we explored HDL metabolism in LDLR-deficient mice in comparison with WT littermates. Murine HDL was radiolabeled in the protein ((125)I) and in the cholesteryl ester (CE) moiety ([(3)H]). The metabolism of (125)I-/[(3)H]HDL was investigated in plasma and in tissues of mice and in murine hepatocytes. In WT mice, liver and adrenals selectively take up HDL-associated CE ([(3)H]). In contrast, in LDLR(-/-) mice, selective HDL CE uptake is significantly reduced in liver and adrenals. In hepatocytes isolated from LDLR(-/-) mice, selective HDL CE uptake is substantially diminished compared with WT liver cells. Hepatic and adrenal protein expression of lipoprotein receptors SR-BI, cluster of differentiation 36 (CD36), and LDL receptor-related protein 1 (LRP1) was analyzed by immunoblots. The respective protein levels were identical both in hepatic and adrenal membranes prepared from WT or from LDLR(-/-) mice. In summary, an LDLR deficiency substantially decreases selective HDL CE uptake by liver and adrenals. This decrease is independent from regulation of receptor proteins like SR-BI, CD36, and LRP1. Thus, LDLR expression has a substantial impact on both HDL and LDL metabolism in mice.
AB - The LDL receptor (LDLR) and scavenger receptor class B type I (SR-BI) play physiological roles in LDL and HDL metabolism in vivo. In this study, we explored HDL metabolism in LDLR-deficient mice in comparison with WT littermates. Murine HDL was radiolabeled in the protein ((125)I) and in the cholesteryl ester (CE) moiety ([(3)H]). The metabolism of (125)I-/[(3)H]HDL was investigated in plasma and in tissues of mice and in murine hepatocytes. In WT mice, liver and adrenals selectively take up HDL-associated CE ([(3)H]). In contrast, in LDLR(-/-) mice, selective HDL CE uptake is significantly reduced in liver and adrenals. In hepatocytes isolated from LDLR(-/-) mice, selective HDL CE uptake is substantially diminished compared with WT liver cells. Hepatic and adrenal protein expression of lipoprotein receptors SR-BI, cluster of differentiation 36 (CD36), and LDL receptor-related protein 1 (LRP1) was analyzed by immunoblots. The respective protein levels were identical both in hepatic and adrenal membranes prepared from WT or from LDLR(-/-) mice. In summary, an LDLR deficiency substantially decreases selective HDL CE uptake by liver and adrenals. This decrease is independent from regulation of receptor proteins like SR-BI, CD36, and LRP1. Thus, LDLR expression has a substantial impact on both HDL and LDL metabolism in mice.
U2 - 10.1194/jlr.M048819
DO - 10.1194/jlr.M048819
M3 - SCORING: Journal article
C2 - 24954421
VL - 55
SP - 1914
EP - 1924
JO - J LIPID RES
JF - J LIPID RES
SN - 0022-2275
IS - 9
ER -
