B-lipoproteins

All. Alessi, M. C., Parra, H. J., Joly, P., Vu-Dac, N., Bard, J. M., Fruchart, J. C., and Juhan-Vague, I., The increased plasma Lp(a) B-lipoprotein particle concentration in angina pectoris is not associated with hypofibrinolysis. Clin. Chim. Acta 188, 119-128 (1990). 

Fig. 13. Lipoprotein size as a function of apoB size. (A) Lipoprotein radius, in A units, is plotted as a function of the length of the apoB polypeptide, in centile units. These data, taken from Table VI, were obtained from the spectra of different sizes of lipoproteins and apoBs secreted by pulse-labeled HepG2 cells after puromycin treatment and analyzed as shown in the previous figure. The straight line through the points has an intercept of 18.8 A and a slope of 0.946 A/centile. (B) Lipoprotein core circumference, in A units, is plotted as a function of the molecular weight of the C-terminally truncated apoB polypeptide. These are the same data as plotted in A, lipoprotein core circumference was calculated as 2tr(A - /), where R is lipoprotein radius, and I = 20.2 A, the thickness of the shell.

Part of the CE formed in HDL is transferred to apo B lipoproteins, particularly VLDL and LDL, by a CE transfer protein (CETP), prior to removal of these lipoproteins by the liver. Another part of the CE in HDL is selectively internalized by the liver and by tissues synthesizing steroid hormones, by a scavenger receptor protein (SR-BI) (Chapter 20). Finally some CE is internalized as part of intact HDL by hepatic HDL receptors/binding proteins. 

Gordon, D.A., Jamil, H., Gregg, R.E., Olofsson, S-O. Boren, J. (19%) J. Biol Chem., 271, 33047-33053. Inhibition of the microsomal triglyceride transfer protein blocks the first step of apolipoprotein B lipoprotein assembly but not the addition of bulk core lipids in the second step. 

Fig. 5A -D. Spectra of lipoproteins from hemolymph and ovary of crabs. A Lipoprotein from ovary of crab Cancer pagurus) in 0.2 M phosphate buffer, pH 7. (Zagalsky et al. 1967) B Lipoprotein II (female-specific lipoprotein) isolated from hemolymph of vitellogenic blue crab Callinectes sapidus). Lipoprotein was in 0.05 M TRIS buffer (pH 8.0). (Lee and Puppione 1988). C Ovorverdin from Homarus gammarus in 0.5 M NaCl — 5 mm EDTA (pH 5). (Zagalsky 1985). D Lipoproteins from ovary of scallop, Pecten maximus, in 0.2 M phosphate buffer (pH 7). Free carotenoids were released from the lipoproteins by extraction with acetone. (Zagalsky et al. 1967)...

Fig. 1. Sequential immunoprecipitation of lipoproteins (VLDL, LDLi, and LDL2). P, precipitate S, soluble fraction. The purpose of the first stage of the isolation procedure is to establish small quantities of apolipoproteins C-I, C-II, C-III, and E not bound to Apo B (LP-C-I, LP-C-II, LP-C-in, and LP-E) The second stage is concerned with the separation of Apo B lipoproteins which contain Apo E (LP-B C-I C-II C-III E, LP-B E), Apo B lipoproteins which only contain Apo C (LP-B C-I C-II C-III), Apo B lipoproteins which may only contain Apo C-I or Apo C-II (LP-B C-I, LP-B C-II), and lipoproteins which only contain Apo B (LP-B). Major lipoprotein particles are underlined. The same fractionation procedure can be carried out by the use of immunosorbers...

To evaluate the potential correlation between specific epitopes on B lipoprotein subpopulations and predisposition to coronary artery disease, recently we have quantitated lipoprotein particles recognized by three well-characterized monoclonal antibodies in normal and CAD patients. 

The processing of apo B in the liver plays a central role in controlling apo B lipoprotein secretion (Ganji et al. 2003). This is regulated by (Davis 1999 Ginsberg 1995) ... 

LCAT deficiency in LDLr-/- mice and Apo E -/- mice fed an atherogenic diet, resulted in aortic cholesterol deposition likely caused by a reduction in plasma HDL, increased saturation of CE in apo B lipoproteins, and in the Apo E -/- background, increased plasma Apo B lipoprotein concentration (470). LCAT-deficient mice are associated with an increase in oxidative stress that is paradoxically reversed in a hyperlipidemic background possibly caused by the redistribution of paraoxonase (PON) to the non-HDL fraction. This may in part contribute to the reduced atherosclerosis seen in Apo E -/- xLCAT -/- mice (this could explain the surprising finding that LCAT-deficient subjects have severe hypoalphalipoproteinemia yet are not prone to premature CHD) (477). 

Smith, E. B. Lipoprotein patterns in myocardial infarction. Relationship between the components identified by paper electrophoresis and in the ultracentrifuge. Lancet 1967/11, 910. 

Number of animals Number of EC counted Pinches Number of animals Infiltration of B-lipoprotein... 

Camejo G, Hurt-Camejo E, Wiklund O and Bondjers G. Association of apo B lipoproteins with arterial proteoglycans, pathological significance and molecular basis. Atherosclerosis 139 205-22, 1998. 

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