Interaction between serum amyloid A and leukocytes—A possible role in the progression of vascular complications in diabetes

Hatanaka, Elaine; Monteagudo, Patrícia Teófilo; Marrocos, Mauro Sergio Martins; Čampa, Ana

doi:10.1016/j.imlet.2006.12.005

Cited by 42 publications

(41 citation statements)

References 48 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…p-values: p < 0.05 was set as the signifi cance level in the comparison between the subjects with glucose levels of < and ≥ 6.1 mmol/L (t-tests). (7)(8)(9), and in fact, the present study demonstrated a higher SAA level in the hyperglycemic population than in the counterpart population, in line with the prior studies (11,12). This inflammatory condition creates sympathetic activation, leading to increased HRs (4,6).…”

Section: Resultssupporting

confidence: 91%

See 1 more Smart Citation

Possible relationship between the heart rates and serum amyloid A in a hyperglycemic population

Kotani

Uurtuya

Taniguchi

et al. 2015

BST

View full text Add to dashboard Cite

Section: Resultssupporting

confidence: 91%

“…The SAA level is sometimes increased in hyperglycemic subjects (11,12). Several prior studies have indicated a positive correlation between the HRs and C-reactive protein (CRP), another inflammatory marker (13,14).…”

Section: Introductionmentioning

confidence: 99%

Possible relationship between the heart rates and serum amyloid A in a hyperglycemic population

Kotani

Uurtuya

Taniguchi

et al. 2015

BST

View full text Add to dashboard Cite

“…Also, the fact that neutrophils and monocytes of diabetic patients are more responsive to SAA regarding cytokine production and cell migration [37] further strengthens the need to study the potential effect of SAA in obesity and insulin resistance. Increased levels of SAA may contribute to a sustained accumulation and activation of inflammatory cells, as well as to the vascular complications observed in diabetic patients [37].…”

Section: Discussionmentioning

confidence: 99%

“…Increased levels of SAA may contribute to a sustained accumulation and activation of inflammatory cells, as well as to the vascular complications observed in diabetic patients [37]. Immunofluorescence for perilipin (red), F4/80 (green) and nuclear staining with DAPI (blue) (middle column) and SAA (red) immunostaining (right column).…”

Section: Discussionmentioning

confidence: 99%

Serum amyloid A links endotoxaemia to weight gain and insulin resistance in mice

et al. 2016

Self Cite

View full text Add to dashboard Cite

Aims/hypothesis Pre-adipocytes and adipocytes are responsive to the acute phase protein serum amyloid A (SAA). The combined effects triggered by SAA encompass an increase in preadipocyte proliferation, an induction of TNF-α and IL-6 release and a decrease in glucose uptake in mature adipocytes, strongly supporting a role for SAA in obesity and related comorbidities. This study addressed whether SAA depletion modulates weight gain and insulin resistance induced by a high-fat diet (HFD). Methods Male Swiss Webster mice were fed an HFD for 10 weeks under an SAA-targeted antisense oligonucleotide (ASO SAA ) treatment in order to evaluate the role of SAA in weight gain. Results With ASO SAA treatment, mice receiving an HFD did not differ in energy intake when compared with their controls, but were prevented from gaining weight and developing insulin resistance. The phenotype was characterised by a lack of adipose tissue expansion, with low accumulation of epididymal, retroperitoneal and subcutaneous fat content and decreased inflammatory markers, such as SAA3 and toll-like receptor (TLR)-4 expression, as well as macrophage infiltration into the adipose tissue. Furthermore, a metabolic status similar to chow-fed mice counterparts could be observed, with equivalent levels of leptin, adiponectin, IGF-I, SAA, fasting glucose and insulin, and remarkable improvement in glucose and insulin tolerance test profiles. Surprisingly, the expected HFD-induced metabolic endotoxaemia was also prevented by the ASO SAA treatment. Conclusions/interpretationThis study provides further evidence of the role of SAA in weight gain and insulin resistance. Moreover, we also suggest that beyond its proliferative and inflammatory effects, SAA is part of the lipopolysaccharide signalling pathway that links inflammation to obesity and insulin resistance.

show abstract

“…A-SAA, a rapid response acute-phase protein circulates at very high levels in RA (23) and has been reported in cardiovascular disease (24) and diabetes (25). In chronic inflammation, it may induce amyloidosis and organ failure (26).…”

Section: Discussionmentioning

confidence: 99%

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

Connolly

Marrelli

Blades

et al. 2010

The Journal of Immunology

107

View full text Add to dashboard Cite

Serum amyloid A (A-SAA), an acute-phase protein with cytokine-like properties, is expressed at sites of inflammation. This study investigated the effects of A-SAA on chemokine-regulated migration and angiogenesis using rheumatoid arthritis (RA) cells and whole-tissue explants in vitro, ex vivo, and in vivo. A-SAA levels were measured by real-time PCR and ELISA. IL-8 and MCP-1 expression was examined in RA synovial fibroblasts, human microvascular endothelial cells, and RA synovial explants by ELISA. Neutrophil transendothelial cell migration, cell adhesion, invasion, and migration were examined using transwell leukocyte/monocyte migration assays, invasion assays, and adhesion assays with or without anti–MCP-1/anti–IL-8. NF-κB was examined using a specific inhibitor and Western blotting. An RA synovial/SCID mouse chimera model was used to examine the effects of A-SAA on cell migration, proliferation, and angiogenesis in vivo. High expression of A-SAA was demonstrated in RA patients (p < 0.05). A-SAA induced chemokine expression in a time- and dose-dependent manner (p < 0.05). Blockade with anti-scavenger receptor class B member 1 and lipoxin A4 (A-SAA receptors) significantly reduced chemokine expression in RA synovial tissue explants (p < 0.05). A-SAA induced cell invasion, neutrophil–transendothelial cell migration, monocyte migration, and adhesion (all p < 0.05), effects that were blocked by anti–IL-8 or anti–MCP-1. A-SAA–induced chemokine expression was mediated through NF-κB in RA explants (p < 0.05). Finally, in the RA synovial/SCID mouse chimera model, we demonstrated for the first time in vivo that A-SAA directly induces monocyte migration from the murine circulation into RA synovial grafts, synovial cell proliferation, and angiogenesis (p < 0.05). A-SAA promotes cell migrational mechanisms and angiogenesis critical to RA pathogenesis.

show abstract

Interaction between serum amyloid A and leukocytes—A possible role in the progression of vascular complications in diabetes

Cited by 42 publications

References 48 publications

Possible relationship between the heart rates and serum amyloid A in a hyperglycemic population

Possible relationship between the heart rates and serum amyloid A in a hyperglycemic population

Serum amyloid A links endotoxaemia to weight gain and insulin resistance in mice

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

Contact Info

Product

Resources

About