Lipid Accumulation and Foam Cell Formation in Chinese Hamster Ovary Cells Overexpressing Very Low Density Lipoprotein Receptor

Suzuki, Jinya; Takahashi, Sadao; Oida, Koji; Shimada, Akihiko; Kohno, Mitsuyuki; Tamai, Toshitaka; Miyabo, Susumu; Yamamoto, Tokuo; Nakai, Tsuguhiko

doi:10.1006/bbrc.1995.1119

Cited by 43 publications

(27 citation statements)

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“…For example, transplantation of VLDLR-expressing macrophages into VLDLR-deficient mice accelerated the development of atherosclerotic lesions (29). Overexpression of VLDLR increased ␤-VLDL-induced lipid accumulation (30). In contrast, it has been shown that treatment of VLDLR-and apoER2-overexpressing macrophages with apoE down-regulated proinflammatory gene and up-regulated anti-inflammatory gene expression in these macrophages (31).…”

Section: Discussionmentioning

confidence: 97%

Up-regulation of ATP Binding Cassette Transporter A1 Expression by Very Low Density Lipoprotein Receptor and Apolipoprotein E Receptor 2

Chen

Guo

Okoro

et al. 2012

Journal of Biological Chemistry

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Background: VLDLR and apoER2 are receptors for reelin and apoE. Results: Reelin or apoE3 induced macrophage ABCA1 expression and increased cholesterol efflux. Down-regulation of VLDLR, apoER2, or inhibition of Dab1, PI3K, PKC and Sp1 attenuated reelin-or apoE3-induced ABCA1 expression. Conclusion: Activation of VLDLR-and apoER2-mediated signaling up-regulates ABCA1 expression. Significance: Up-regulation of ABCA1 expression is a novel function of VLDLR and apoER2.

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Section: Discussionmentioning

confidence: 97%

Up-regulation of ATP Binding Cassette Transporter A1 Expression by Very Low Density Lipoprotein Receptor and Apolipoprotein E Receptor 2

Chen

Guo

Okoro

et al. 2012

Journal of Biological Chemistry

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“…This difference underlies the fact that VLDLR mediates the uptake of only IDL but not LDL, whereas LDLR mediates the uptake of both IDL and LDL. 19 We used low-dose HD-Ad-LDLR therapy to treat LDLR À/À mice at an early age and followed the animals the duration of their lives. With this strategy, HD-Ad-LDLR therapy might have prolonged the lifespan of these mice, as 2 years after treatment the only surviving mice were those that had received the HD-Ad-LDLR.…”

Section: Discussionmentioning

confidence: 99%

Low-density lipoprotein receptor gene therapy using helper-dependent adenovirus produces long-term protection against atherosclerosis in a mouse model of familial hypercholesterolemia

et al. 2004

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We tested the efficacy of low-density lipoprotein receptor (LDLR) therapy using helper-dependent adenovirus (HD-Ad), comparing it with that of very low-density lipoprotein receptor (VLDLR), an LDLR homolog. We treated high cholesterol diet fed LDLR À/À mice with a single intravenous injection of HD-Ad expressing monkey LDLR (1.5 Â 10 13 or 5 Â 10 12 VP/kg) or VLDLR. Throughout the 24-week experiment, plasma cholesterol of LDLR-treated mice was lower than that of VLDLR-treated mice, which was in turn lower than that of PBS-treated mice. Anti-LDLR antibodies developed in 2/10 mice treated with high-dose HD-Ad-LDLR but in none (0/14) of the other treatment groups. HD-Ad-treated mice displayed significant retardation of atherosclerotic lesion progression. We next tested the long-term efficacy of low-dose HD-Ad-LDLR injected into 12-week-old LDLR À/À mice. After 60 weeks, atherosclerosis lesions covered B50% of the surface of aortas of control mice, whereas aortas of treated mice were essentially lesion-free. The lipid lowering effect of HD-Ad-LDLR lasted at least 108 weeks (42 years) when all control mice had died. In addition to retarding lesion progression, treatment caused lesion remodeling from a vulnerablelooking to a more stable-appearing phenotype. In conclusion, HD-Ad-mediated LDLR gene therapy is effective in conferring long-term protection against atherosclerosis in a mouse model of familial hypercholesterolemia.

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“…Plasmids encoding the human VLDL receptor (ph-VLR2) or pSV2-neo, which contains the neomycin resistance gene, were transfected to ldlA-7 cells (mutant Chinese hamster ovary cells that lack LDL receptors) which was kindly provided by Dr. Monty Krieger (Department of Biology, Massachusetts Institute of Technology, Cambridge, MA) using lipofectin as described previously [1][2][3]9,12]. Positive cell clones for the human VLDL receptor were designated VLDL-R cells.…”

Section: Isolation Of Transfected Cellsmentioning

confidence: 99%

Very low density lipoprotein receptor binds apolipoprotein E2/2 as well as apolipoprotein E3/3

et al. 1996

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Lipid Accumulation and Foam Cell Formation in Chinese Hamster Ovary Cells Overexpressing Very Low Density Lipoprotein Receptor

Cited by 43 publications

References 0 publications

Up-regulation of ATP Binding Cassette Transporter A1 Expression by Very Low Density Lipoprotein Receptor and Apolipoprotein E Receptor 2

Up-regulation of ATP Binding Cassette Transporter A1 Expression by Very Low Density Lipoprotein Receptor and Apolipoprotein E Receptor 2

Low-density lipoprotein receptor gene therapy using helper-dependent adenovirus produces long-term protection against atherosclerosis in a mouse model of familial hypercholesterolemia

Very low density lipoprotein receptor binds apolipoprotein E2/2 as well as apolipoprotein E3/3

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