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Human and mouse apoAI differ substantially in primary structure and form nascent HDL particle populations significantly divergent in size distribution (38, 54).
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However, mouse apoAI nascent HDL synthesized by BHK-ABCA1 cells segregated into a larger and smaller species, just as human apoAI nascent HDL particles did (Fig. 10 A).
Furthermore, when mouse apoAI is overexpressed using adeno-associated virus vectors in apoAI-null mice, it drives production of HDL with a more complex size distribution reminiscent of human HDL (58).
Thus, mouse apoAI exhibits a greater tendency than human apoAI to form larger nascent HDL particles, but possesses the ability to produce two different size HDL species in proportion to the available cell lipid:apoAI ratio.
Furthermore, the available cell lipid:apoAI ratio also affected the size distribution of nascent mouse apoAI HDL particles (Fig. 10 B).
Nonetheless, the large/small particle ratios for the mouse nascent HDL increased with the transition from the low to high available cell lipid:apoAI ratio (Fig. 10 B), indicating that structural features responsible for the genesis of nascent HDL particle heterogeneity are conserved to some degree between human and mouse apoAI.
Mouse apoAI, in contrast, drives production of more homogenous mature HDL particles comprising a single size species in vivo (55, 57), which would suggest, if the nascent-mature HDL correspondence were to hold, that it also generates a single species of nascent HDL in vitro.
Why do these mouse models differ?
Mouse strains differ in their susceptibility to stroke-induced immunosuppression.
Morphology of adipocytes in adipose tissue from eNOS knockout mice and DDAH mice did not differ.
Sunderkotter, C. et al. Subpopulations of mouse blood monocytes differ in maturation stage and inflammatory response.
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