SAA3Serum Amyloid A3 Protein
Copyright 1988-2018, All rights reserved.
References in periodicals archive ?
(v) Genes of potentially secreted proteins were identified of which some may serve as markers in blood for analysis of degree of protection (Cxcl9, Gp2, and Pla2g2d), intensity of infection (Retnla, Saa3, Il6, and Illb), or adaptive recall responses (Ighg, C1qb).
Supporting the overall assertion that dietary TCDF exposure leads to a broad inflammatory response in mice is the significant elevation of fecal IgA, fecal LCN-2, serum LPS, and mRNA expression of intestinal innate immune factors including Il-1[beta], Il-10, Tnf-[alpha], Saa1, and Saa3 reported here.
(A) qPCR analysis of inflammatory cytokine (IL-1[beta], TNF-[alpha], IL-10, Saa1, and Saa3) mRNA expression in the ileum of [Ahr.sup.+/+] mice.
In Salles et al.'s study [15], after a 2-week high fat diet (HFD), TNF-[alpha]-knockout (TNF-[alpha]-KO) mice presented twofold more adipose fat pad mass than control mice, while interestingly TNF-[alpha]-KO mice showed lower hepatic TG and ceramide accumulation in liver, with significantly declined adipose inflammatory markers, including resistin, monocyte chemotactic protein-1 (MCP-1), SAA3, and F4/80, implying decreased levels of inflammatory cytokines in adipose tissue might improve fat storage capacity of adipose tissue to prevent abnormal lipid deposition in nonadipose tissues.
DAVID analysis for cluster 5 (see Supplemental Material, Excel Tabic IE) identified one functional category (secretion; p < 0.03) for three of these genes (Saa3, Cxcl5, and Timp 1).
In the present review we will describe the information available on the role of adipokines in RA pathogenesis, focusing on the role of adiponectin, leptin, chemerin, visfatin, resistin, lipocalin 2, SAA3,and a few others, inlight of their possible consideration as new potential circulating biomarkers of disease activity and therapeutic response.
The serum amyloid A3 (SAA3) belongs to the family of acute phase serum amyloid A proteins produced by hepatocytes [138] and other cell types, including adipocytes [139, 140].
In a rabbit Ag-induced arthritis model, upregulation of SAA3 transcripts was detected in cells infiltrating into the inflamed joint, in the area where pannus formation starts and, most notably, also in chondrocytes.
Microarray and pathway analyses identified significant differences in inflammatory mediator expression between [Il10.sup.+/+] and [Il10.sup.-/-] mice in response to [O.sub.3] and suggested novel genetic targets [e.g., cathepsin E (Ctse) and serum amyloid A3 (Saa3)] affiliated with Il10 expression and response to environmental oxidant exposure.
Genes > 2-fold higher in [Il10.sup.-/-] mice than in [Il10.sup.+/+] mice included those encoding CTSE, WDFY1 (WD repeat and FYVE domain containing 1), IL-1[beta], SAA3, nicotinamide nucleotide transhydrogenase (NNT), and peptidylglycine [alpha]-amidating monooxygenase (PAM).
Conversely, betaine homocysteine methyltransferase (BHMT, 60% of control), serum amyloid 3 (Saa3, 30% of control), and sulfotransferase-related protein 2 (SULT-X2, 1% of control) were decreased.