scholarly journals Acute Serum Amyloid A Induces Migration, Angiogenesis, and Inflammation in Synovial Cells In Vitro and in a Human Rheumatoid Arthritis/SCID Mouse Chimera Model

2010 ◽  
Vol 184 (11) ◽  
pp. 6427-6437 ◽  
Author(s):  
Mary Connolly ◽  
Alessandra Marrelli ◽  
Mark Blades ◽  
Jennifer McCormick ◽  
Paola Maderna ◽  
...  
Keyword(s):  
Rheumatoid Arthritis ◽  
Scid Mouse ◽  
Serum Amyloid A ◽  
Serum Amyloid ◽  
Human Rheumatoid Arthritis ◽  
Synovial Cells ◽  
Amyloid A

Abstract 226: Serum Amyloid A Isoforms and the Capacity to Mediate Cholesterol Efflux

2014 ◽  
Vol 34 (suppl_1) ◽  
Author(s):  
Hussein Yassine ◽  
Olgica Trenchevska ◽  
Chad Borges ◽  
Dobrin Nedelkov ◽  
Randall W Nelson ◽  
...  
Keyword(s):  
Cholesterol Efflux ◽  
Serum Amyloid A ◽  
Hdl Cholesterol ◽  
Acute Phase Reactant ◽  
Serum Amyloid ◽  
Amyloid A ◽  
Cholesterol Levels ◽  
Acute Phase Reactant Protein

Serum Amyloid A (SAA) is an acute phase reactant protein that exists in multiple isoforms, can form HDL, and participates in cholesterol efflux. In vitro studies suggest that the SAA 2.1 isoform has an increased capacity to mediate cholesterol efflux compared to the other isoforms. We examined SAA isoforms using a novel mass spectrometric immunoassay (MSIA) and HDL’s cholesterol efflux capacity (via ABCA-1 and SR-BI) in samples from 59 subjects with (n=33) and without type 2 diabetes (n=26). SAA 1.1 levels were detectable in 58, SAA 2.1 in 14 and SAA 2.2 in 36 of the 59 subjects. SAA 2.1 levels significantly correlated with SR-BI cholesterol efflux (r=0.71, p=0.01, n=14), but not ABCA-1 mediated efflux (r=0.1, P=0.1). This correlation was not explained by changes in HDL phospholipids, Apo A-I or HDL cholesterol levels. In contrast, SAA 2.2 or 1.1 levels did not correlate with changes in SR-BI or ABCA-1 mediated efflux. Although the SAA 2.1 isoform is less frequently detected in plasma, our data confirm that it is closely linked with HDL mediated cholesterol efflux, particularly that is SR-BI mediated.

An involvement of SR-B1 mediated p38 MAPK signaling pathway in serum amyloid A-induced angiogenesis in rheumatoid arthritis

2015 ◽  
Vol 66 (2) ◽  
pp. 340-345 ◽  
Author(s):  
Chengcheng Hong ◽  
Chen Shen ◽  
Hongmei Ding ◽  
Shanshan Huang ◽  
Yun Mu ◽  
...  
Keyword(s):  
Rheumatoid Arthritis ◽  
Signaling Pathway ◽  
P38 Mapk ◽  
Serum Amyloid A ◽  
Mapk Signaling ◽  
Mapk Signaling Pathway ◽  
Serum Amyloid ◽  
Amyloid A

Synovial Fluid from Rheumatoid Arthritis Patients Contains Sufficient Levels of IL-1β and IL-6 to Promote Production of Serum Amyloid A By HEP3B Cells

Cytokine ◽  
1995 ◽  
Vol 7 (2) ◽  
pp. 209-219 ◽  
Author(s):  
Patricia A. McNiff ◽  
Caroline Stewart ◽  
James Sullivan ◽  
Henry J. Showell ◽  
Christopher A. Gabel
Keyword(s):  
Rheumatoid Arthritis ◽  
Synovial Fluid ◽  
Serum Amyloid A ◽  
Serum Amyloid ◽  
Amyloid A ◽  
Hep3b Cells

scholarly journals Ex Vivo and In Vitro Effect of Serum Amyloid A in the Induction of Macrophage M2 Markers and Efferocytosis of Apoptotic Neutrophils

2015 ◽  
Vol 194 (10) ◽  
pp. 4891-4900 ◽  
Author(s):  
Lei Sun ◽  
Huibin Zhou ◽  
Ziyan Zhu ◽  
Qian Yan ◽  
Lili Wang ◽  
...  
Keyword(s):  
Serum Amyloid A ◽  
Ex Vivo ◽  
Serum Amyloid ◽  
Amyloid A ◽  
Vitro Effect

Serum amyloid A stimulates lipoprotein-associated phospholipase A2 expression in vitro and in vivo

2013 ◽  
Vol 228 (2) ◽  
pp. 370-379 ◽  
Author(s):  
Bo Li ◽  
Zhe Dong ◽  
Hui Liu ◽  
Yan-fei Xia ◽  
Xiao-man Liu ◽  
...  
Keyword(s):  
Phospholipase A2 ◽  
Serum Amyloid A ◽  
Serum Amyloid ◽  
Amyloid A

scholarly journals Serum amyloid A induces G-CSF expression and neutrophilia via Toll-like receptor 2

Blood ◽  
2009 ◽  
Vol 113 (2) ◽  
pp. 429-437 ◽  
Author(s):  
Rong L. He ◽  
Jian Zhou ◽  
Crystal Z. Hanson ◽  
Jia Chen ◽  
Ni Cheng ◽  
...  
Keyword(s):  
Serum Amyloid A ◽  
Inflammatory Diseases ◽  
Serum Amyloid ◽  
Proteinase K ◽  
In Vivo Studies ◽  
Toll Like Receptor ◽  
Amyloid A ◽  
Toll Like Receptor 2

Abstract The acute-phase protein serum amyloid A (SAA) is commonly considered a marker for inflammatory diseases; however, its precise role in inflammation and infection, which often result in neutrophilia, remains ambiguous. In this study, we demonstrate that SAA is a potent endogenous stimulator of granulocyte colony-stimulated factor (G-CSF), a principal cytokine-regulating granulocytosis. This effect of SAA is dependent on Toll-like receptor 2 (TLR2). Our data demonstrate that, in mouse macrophages, both G-CSF mRNA and protein were significantly increased after SAA stimulation. The induction of G-CSF was blocked by an anti-TLR2 antibody and markedly decreased in the TLR2-deficient macrophages. SAA stimulation results in the activation of nuclear factor–κB and binding activity to the CK-1 element of the G-CSF promoter region. In vitro reconstitution experiments also support that TLR2 mediates SAA-induced G-CSF expression. In addition, SAA-induced secretion of G-CSF was sensitive to heat and proteinase K treatment, yet insensitive to polymyxin B treatment, indicating that the induction is a direct effect of SAA. Finally, our in vivo studies confirmed that SAA treatment results in a significant increase in plasma G-CSF and neutrophilia, whereas these responses are ablated in G-CSF– or TLR2-deficient mice.

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