Atherogenesis in transgenic mice with human apolipoprotein B and lipoprotein (a).

Callow, Matthew J.; Verstuyft, Judy G.; Tangirala, Rajendra K.; Palinski, Wulf; Rubin, Edward M.

doi:10.1172/jci118203

Cited by 85 publications

(52 citation statements)

References 36 publications

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“…85,86 Atherosclerosis was studied in STZ-induced diabetic human apoB expressing transgenic mice. 87,88 Diabetes led to minor changes in plasma lipoproteins and atherosclerosis was unchanged.…”

Section: The Apob Transgenics Do Not Normally Develop Diabetes-inducementioning

confidence: 99%

Diabetic Vascular Disease

Goldberg

Dansky

2006

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Abstract-It is well known that humans with diabetes have more atherosclerosis and its complications. The causes of this relationship are, however, unclear. Although recent data show that improved glycemic control reduces arterial disease in type 1 diabetes, other studies have shown that subjects with "prediabetes" have more cardiovascular disease before the development of hyperglycemia. Thus, either hyperglycemia and/or lack of insulin actions are toxic to arteries, or metabolic derangements exclusive of hyperglycemia are atherogenic. For Ͼ50 years animal models of diabetes and atherosclerosis have been used to uncover potential mechanisms underlying diabetes associated cardiovascular disease. Surprisingly, diabetes alone increases vascular disease in only a few select animal models. Increased atherosclerosis has been found in several animals and lines of genetically modified mice; however, diabetes often also leads to greater hyperlipidemia. This makes it difficult to separate the toxic effects of insulin lack and/or hyperglycemia from those caused by the lipids. These studies are reviewed, as well as more recent investigations using new methods to create diabetic-atherosclerotic models.

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Section: The Apob Transgenics Do Not Normally Develop Diabetes-inducementioning

confidence: 99%

Diabetic Vascular Disease

Goldberg

Dansky

2006

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“…Introduction of the apo(a) transgene into human apoB-100 transgenic mice did not significantly potentiate the development of aortic fatty lesions in the absence or presence of the LDL receptor. 5,6,12 Probably the atherogenic effects of apoB-100 may have overwhelmed the subtle effects of apo(a) and masked the difference.…”

Section: See Page 88mentioning

confidence: 99%

Lipoprotein(a) and Atherosclerosis

Ishibashi

2001

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“…11,12 Atherogenic potential of free apo(a) was demonstrated in transgenic mice expressing human apo(a). These mice developed atherosclerosis due to focal apo(a) accumulation in the vessel wall leading to inhibition of transforming growth factor-␤ (TGF-␤) activity, activation of smooth muscle cells, and subsequent accumulation of lipids in the vessel wall.…”

Section: Introductionmentioning

confidence: 99%

“…11,13,14 Additionally, the atherogenic potential of Lp(a) was demonstrated in double transgenic mice expressing both human apo(a) and human apoB-100. 12 Due to its great atherogenicity, many attempts were made in the past to medicate individuals with increased Lp(a) levels with drugs or diets. None of those proved to be of value, as almost all drugs such as statins or bile acid sequestrants, which lower plasma LDL by increasing specific receptors in the liver, have very inconsistent effects and sometimes even cause an increase of Lp(a) concentrations.…”

Section: Introductionmentioning

confidence: 99%

Adenovirus-mediated apo(a)-antisense-RNA expression efficiently inhibits apo(a) synthesis in vitro and in vivo

et al. 2001

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Apo(a) is a very atherogenic plasma protein without apparent function, which is highly expressed in humans. The variation in plasma Lp(a) concentration among individuals is considerable. Approximately 10-15% of the white population exhibit plasma Lp(a) concentrations above the atherogenic cut-off value of approximately 30 mg/dl. Since there is currently no safe way of treating those patients with drugs, we have tested the possibility of interfering with apo(a) biosynthesis by adenovirus-mediated expression of antisense apo(a) mRNA comprising the 5Ј UTR, the signal sequence and the first three kringles of native apo(a). Transduction of rat hepatoma McA RH 7777 cells which stably expressed apo(a) with 18 kringle IV (KIV) domains with apo(a)-antisense adenovirus (AS-Ad) at multiplicity of infection (MOI) of 30 reduced

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Atherogenesis in transgenic mice with human apolipoprotein B and lipoprotein (a).

Cited by 85 publications

References 36 publications

Diabetic Vascular Disease

Diabetic Vascular Disease

Lipoprotein(a) and Atherosclerosis

Adenovirus-mediated apo(a)-antisense-RNA expression efficiently inhibits apo(a) synthesis in vitro and in vivo

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