ApoA-I deficiency in mice is associated with redistribution of apoA-II and aggravated AApoAII amyloidosis[S]

• Published in: Journal of lipid research Vol. 52; no. 8; pp. 1461 - 1470
• Main Authors: Wang, Yaoyong, Sawashita, Jinko, Qian, Jinze, Zhang, Beiru, Fu, Xiaoying, Tian, Geng, Chen, Lei, Mori, Masayuki, Higuchi, Keiichi
• Format: Journal Article
• Language: English
• Published: United States Elsevier Inc 01.08.2011; The American Society for Biochemistry and Molecular Biology; Elsevier
• Subjects: age; Aging; Amyloid - biosynthesis; amyloid heart disease; Amyloidosis - metabolism; Amyloidosis - pathology; Amyloidosis - physiopathology; Animals; Apolipoprotein A-I - deficiency; Apolipoprotein A-I - genetics; Apolipoprotein A-II - blood; Apolipoprotein A-II - genetics; apolipoproteins; cholesterol; Cholesterol, HDL - blood; distribution; Female; Gene Deletion; lipids; Liver - chemistry; Liver - metabolism; Mice; Mice, Inbred C57BL; Mice, Knockout; Myocardium - chemistry; Myocardium - metabolism; Particle Size; RNA, Messenger - analysis; RNA, Messenger - biosynthesis; Triglycerides - blood; cholesterol; apolipoproteins; lipids; amyloid heart disease; distribution; age

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 ap...