Amyloid A in Preeclamptic Toxemia

Abstract

Acute-phase serum amyloid A proteins are secreted as a response to the acute inflammatory trigger. These proteins have various functions, involving the transportation of cholesterol to the liver to be secreted within the bile, the employment of immune cells to inflammatory zones, and the activation of enzymes that cause degradation of extracellular matrix. Acute-phase serum amyloid A are involved in numerous chronic inflammatory disorders, e.g. amyloidosis, atherosclerosis, and rheumatoid arthritis. Three Acute-phase serum amyloid A proteins genes have been revealed and displayed in humans, although the third gene, SAA3, is believed to be a pseudogene that does not form messenger RNA or subsequent protein synthesis. Molecular weights of the human proteins are estimated at 11.7 kDa for serum amyloid A type 1 and 12.8 kDa for serum amyloid A type 4 (Webb et al., 2015). Preeclampsia is a common complication of gestation and remains a chief cause of maternal and fetal mortality. The clinical symptoms of preeclampsia are caused by widespread endothelial dysfunction proposed to be a part of an exaggerated maternal inflammatory response to