| First Author | Wang Y | Year | 2011 |
| Journal | J Lipid Res | Volume | 52 |
| Issue | 8 | Pages | 1461-70 |
| PubMed ID | 21622630 | Mgi Jnum | J:174979 |
| Mgi Id | MGI:5141582 | Doi | 10.1194/jlr.M013235 |
| Citation | Wang Y, et al. (2011) ApoA-I deficiency in mice is associated with redistribution of apoA-II and aggravated AApoAII amyloidosis. J Lipid Res 52(8):1461-1470 |
| abstractText | Apolipoprotein A-II (apoA-II) is the second major apolipoprotein following apolipoprotein A-I (apoA-I) in HDL. ApoA-II has multiple physiological functions and can form senile amyloid fibrils (AApoAII) in mice. Most circulating apoA-II is present in lipoprotein A-I/A-II. To study the influence of apoA-I on apoA-II and AApoAII amyloidosis, apoA-I-deficient (C57BL/6J.Apoa1(-/-)) mice were used. Apoa1(-/-) mice showed the expected significant reduction in total cholesterol (TC), HDL cholesterol (HDL-C), and triglyceride (TG) plasma levels. Unexpectedly, we found that apoA-I deficiency led to redistribution of apoA-II in HDL and an age-related increase in apoA-II levels, accompanied by larger HDL particle size and an age-related increase in TC, HDL-C, and TG. Aggravated AApoAII amyloidosis was induced in Apoa1(-/-) mice systemically, especially in the heart. These results indicate that apoA-I plays key roles in maintaining apoA-II distribution and HDL particle size. Furthermore, apoA-II redistribution may be the main reason for aggravated AApoAII amyloidosis in Apoa1(-/-) mice. These results may shed new light on the relationship between apoA-I and apoA-II as well as provide new information concerning amyloidosis mechanism and therapy. |
