FUNCTION OF SERUM AMYLOID A PROTEIN (SAA)

血清淀粉样蛋白 A (SAA) 的功能

• 批准号: 2080013
• 负责人: FREDERICK C. DE BEER
• 金额: $ 17.98万
• 依托单位: UNIVERSITY OF KENTUCKY
• 依托单位国家: 美国
• 财政年份: 1992
• 资助国家: 美国
• 起止时间: 1992-08-01 至 1996-07-31
• 项目状态: 已结题
• 来源: https://reporter.nih.gov/project-details/2080013
• 关键词: amyloidosis; apolipoproteins; cardiovascular disorder; disease /disorder proneness /risk; endopeptidases; enzyme induction /repression; family genetics; high density lipoproteins; human subject; inflammation; isoelectric point; lipid transport; molecular pathology; northern blottings; protein sequence; protein transport; restriction fragment length polymorphism; rheumatoid arthritis

During the acute phase response, serum amyloid A protein apolipoprotein, increases 1,000 fold, and becomes a major component of HDL. In spite of intense modern interest in the HDL particle, the teleological role of this alteration of HDL by SAA in acute inflammation is unknown. We propose that a major role may be facilitation of delivery by HDL of needed phospholipid in peripheral sites of inflammation, where consumption of phospholipid in cell membrane destruction, prostonoid synthesis and the phosphatidyl inositol cell activation pathway is considerable. Chronic persistence of A-SAA render HDL less capable of mediating reverse cholesterol transport and provides a molecular explanation for the increased mortality of patients with chronic active rheumatoid arthritis from particularly cardiovascular disease. In addition to acute phase SAA (A-SAA), we have characterized a new SAA subfamily constitutive on normal HDL (C-SAA). This establishes the existence of a SAA superfamily with two distinct subfamilies. We propose that the C-SAA subfamily play a role in the normal biological function of HDL in that it promotes reverse cholesterol transport by causing the degradation of apo-AII. We will investigate whether during inflammation, aberrant induction of C-SAA might cause pathological neutral protease release with destructive potential. The studies proposed will extend our understanding of the physiologic role of the SAA's in inflammation and may help explain the propensity to advanced atherosclerosis in patients with chronic inflammatory rheumatic diseases.

在急性反应期，血清淀粉样蛋白A载脂蛋白，

项目成果

Serum amyloid A (SAA): influence on HDL-mediated cellular cholesterol efflux.

• 发表时间: 1995-05
• 期刊: Journal of lipid research
• 影响因子: 6.5
• 作者: C. Banka;T. Yuan;M. Beer;M. Kindy;L. Curtiss;F. D. Beer

Structural prerequisites for serum amyloid A fibril formation.

血清淀粉样蛋白 A 原纤维形成的结构先决条件。

• 发表时间: 1993
• 期刊: The Journal of biological chemistry
• 作者: deBeer,MC;deBeer,FC;McCubbin,WD;Kay,CM;Kindy,MS
• 通讯作者: Kindy,MS

Mouse serum amyloid A protein (SAA5) structure and expression.

小鼠血清淀粉样蛋白 A 蛋白 (SAA5) 结构和表达。

• 发表时间: 1994
• 期刊: The Journal of biological chemistry
• 作者: deBeer,MC;Kindy,MS;Lane,WS;deBeer,FC
• 通讯作者: deBeer,FC

Serum amyloid A protein enhances the activity of secretory non-pancreatic phospholipase A2.

血清淀粉样蛋白 A 增强分泌型非胰腺磷脂酶 A2 的活性。

• DOI: 10.1042/bj3090461
• 发表时间: 1995
• 期刊: The Biochemical journal
• 作者: Pruzanski,W;deBeer,FC;deBeer,MC;Stefanski,E;Vadas,P
• 通讯作者: Vadas,P