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Overexpression of low density lipoprotein receptor eliminates apolipoprotein B100-containing lipoproteins from circulation and markedly prevents early atherogenesis in apolipoprotein E-deficient mice.
Atherosclerosis. 2000 Dec; 153(2):295-302.A

Abstract

Apolipoprotein E (ApoE) plays a pivotal role in the metabolism of apolipoprotein B (apoB)-containing lipoproteins. The defective apoE gene in humans can cause elevated plasma levels of apoB-containing lipoproteins such as chylomicron remnant and intermediate density lipoprotein (IDL). In this study, we examined whether liver-selective high-level expression of low-density lipoprotein receptor (LDLR) could affect the lipoprotein profile and atherogenesis in apoE-deficient (apoE-/-) mice. ApoE knockout mice expressing LDLR transgene in liver [apoE-/-;Tg(LDLR+/-)] were prepared after mating apoE-/- mice with the human LDLR transgenic mice. The apoE-/-;Tg(LDLR+/-) and littermate apoE-/- mice were fed a normal diet and sacrificed at 18 weeks of age. (1) The plasma levels of cholesterol and triglyceride in apoE-/-;Tg(LDLR+/-) mice were 51 and 33% lower than those of apoE-/- mice, respectively. (2) In the plasma of apoE-/-;Tg(LDLR+/-) mice, the levels of apoB-containing lipoprotein were reduced and apoB100-containg particles were totally eliminated. (3) By histochemical analysis, apoE-/-;Tg(LDLR+/-) mice showed drastic suppression of early atherogenesis; the lesion area of these mice was 1/70 of that in the littermate apoE-/- mice. These results indicate that, even in apoE-defective subjects, induction of hepatic LDLR expression could protect from early atherogenesis.

Authors+Show Affiliations

Department of Geriatric Medicine, Graduate School of Medicine, Kyoto University, Japan.No affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

11164418

Citation

Murayama, T, et al. "Overexpression of Low Density Lipoprotein Receptor Eliminates Apolipoprotein B100-containing Lipoproteins From Circulation and Markedly Prevents Early Atherogenesis in Apolipoprotein E-deficient Mice." Atherosclerosis, vol. 153, no. 2, 2000, pp. 295-302.
Murayama T, Yokode M, Horiuchi H, et al. Overexpression of low density lipoprotein receptor eliminates apolipoprotein B100-containing lipoproteins from circulation and markedly prevents early atherogenesis in apolipoprotein E-deficient mice. Atherosclerosis. 2000;153(2):295-302.
Murayama, T., Yokode, M., Horiuchi, H., Yoshida, H., Sano, H., & Kita, T. (2000). Overexpression of low density lipoprotein receptor eliminates apolipoprotein B100-containing lipoproteins from circulation and markedly prevents early atherogenesis in apolipoprotein E-deficient mice. Atherosclerosis, 153(2), 295-302.
Murayama T, et al. Overexpression of Low Density Lipoprotein Receptor Eliminates Apolipoprotein B100-containing Lipoproteins From Circulation and Markedly Prevents Early Atherogenesis in Apolipoprotein E-deficient Mice. Atherosclerosis. 2000;153(2):295-302. PubMed PMID: 11164418.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Overexpression of low density lipoprotein receptor eliminates apolipoprotein B100-containing lipoproteins from circulation and markedly prevents early atherogenesis in apolipoprotein E-deficient mice. AU - Murayama,T, AU - Yokode,M, AU - Horiuchi,H, AU - Yoshida,H, AU - Sano,H, AU - Kita,T, PY - 2001/2/13/pubmed PY - 2001/4/21/medline PY - 2001/2/13/entrez SP - 295 EP - 302 JF - Atherosclerosis JO - Atherosclerosis VL - 153 IS - 2 N2 - Apolipoprotein E (ApoE) plays a pivotal role in the metabolism of apolipoprotein B (apoB)-containing lipoproteins. The defective apoE gene in humans can cause elevated plasma levels of apoB-containing lipoproteins such as chylomicron remnant and intermediate density lipoprotein (IDL). In this study, we examined whether liver-selective high-level expression of low-density lipoprotein receptor (LDLR) could affect the lipoprotein profile and atherogenesis in apoE-deficient (apoE-/-) mice. ApoE knockout mice expressing LDLR transgene in liver [apoE-/-;Tg(LDLR+/-)] were prepared after mating apoE-/- mice with the human LDLR transgenic mice. The apoE-/-;Tg(LDLR+/-) and littermate apoE-/- mice were fed a normal diet and sacrificed at 18 weeks of age. (1) The plasma levels of cholesterol and triglyceride in apoE-/-;Tg(LDLR+/-) mice were 51 and 33% lower than those of apoE-/- mice, respectively. (2) In the plasma of apoE-/-;Tg(LDLR+/-) mice, the levels of apoB-containing lipoprotein were reduced and apoB100-containg particles were totally eliminated. (3) By histochemical analysis, apoE-/-;Tg(LDLR+/-) mice showed drastic suppression of early atherogenesis; the lesion area of these mice was 1/70 of that in the littermate apoE-/- mice. These results indicate that, even in apoE-defective subjects, induction of hepatic LDLR expression could protect from early atherogenesis. SN - 0021-9150 UR - https://www.unboundmedicine.com/medline/citation/11164418/Overexpression_of_low_density_lipoprotein_receptor_eliminates_apolipoprotein_B100_containing_lipoproteins_from_circulation_and_markedly_prevents_early_atherogenesis_in_apolipoprotein_E_deficient_mice_ L2 - https://linkinghub.elsevier.com/retrieve/pii/S0021-9150(00)00414-7 DB - PRIME DP - Unbound Medicine ER -