Abstract
AbstractAlbumin has been implicated in Alzheimer's disease since it can bind to and transport amyloid beta, the causative agent; albumin is also a potent inhibitor of amyloid beta polymerization. In a pilot phase study of Human Brain Proteome Project, we found evidence that albumin may be synthesized in immortalized human microglial cells, human primary microglial cells, and human fetal and adult brain tissues. We also found the synthesis and secretion is enhanced upon microglial activation by Amyloid [beta]~1-42~, lipopolysaccharide treatment or human Alzheimer's brain.
Highlights
Albumin is the most abundant plasma protein with multifunctional properties such as ligand-binding and transport, maintaining the colloid osmotic pressure of plasma, and regulating neutrophil function [1]
We used immunostaining for albumin and microglial markers in human cells and brain tissues to confirm that albumin is expressed in microglial cells both in vitro and in vivo
In immunocytochemistry (ICC), all HMO6 cells were double-positive for microglial markers (CD11b [19] and Iba1 [20]) and albumin (Fig. 1a); human primary microglial cells staining positive for Iba1 coexpressed albumin (Fig. 1b)
Summary
Albumin is the most abundant plasma protein with multifunctional properties such as ligand-binding and transport, maintaining the colloid osmotic pressure of plasma, and regulating neutrophil function [1]. Despite the evidence of non-hepatic transcription of albumin in many tissues, non-hepatic synthesis of albumin at the protein level has been rarely confirmed. Yamaguchi et al [18] provided convincing evidence of albumin synthesis in bone tissues cultured in serum-, albumin-free medium.
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