Serum amyloid A enrichment impairs the anti-inflammatory ability of HDL from diabetic nephropathy patients

Mao, Jing; Sun, Jia; Yang, Ke; Shen, Wei Feng; Lü, Lin; Zhang, Rui Yan; Tong, Xuemei; Liu, Yan

doi:10.1016/j.jdiacomp.2017.07.005

Cited by 17 publications

(12 citation statements)

References 36 publications

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“…Previous studies identified that ABCA1 plays a major role in high-density lipoprotein formation (Feingold and Grunfeld, 2000 ; Rosenson et al, 2016 ). As high-density lipoproteins were considered to have anti-inflammatory and other beneficial effects (Murphy et al, 2012 ; Mao et al, 2017 ), ABCA1 was implicated in macrophage-associated inflammatory diseases. Microglia are specialized resident macrophages in the neural retina, and they are normally located in the nerve fiber layer, ganglion cell layer, inner plexiform layer, and outer plexiform layer (Chinnery et al, 2017 ).…”

Section: Discussionmentioning

confidence: 99%

Reduced Annexin A1 Secretion by ABCA1 Causes Retinal Inflammation and Ganglion Cell Apoptosis in a Murine Glaucoma Model

Chen

et al. 2018

Front. Cell. Neurosci.

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Variants near the ATP-binding cassette transporter A1 (ABCA1) gene are associated with elevated intraocular pressure and newly discovered risk factors for glaucoma. Previous studies have shown an association between ABCA1 deficiency and retinal inflammation. Using a mouse model of ischemia-reperfusion (IR) induced by acute intraocular pressure elevation, we found that the retinal expression of ABCA1 protein was decreased. An induction of ABCA1 expression by liver X receptor agonist TO901317 reduced retinal ganglion cell (RGC) apoptosis after IR and promoted membrane translocation and secretion of the anti-inflammatory factor annexin A1 (ANXA1). Moreover, ABCA1 and ANXA1 co-localized in cell membranes, and the interaction domain is amino acid 196 to 274 of ANXA1 fragment. TO901317 also reduced microglia migration and activation and decreased the expression of pro-inflammatory cytokines interleukin (IL)-17A and IL-1β, which could be reversed by the ANXA1 receptor blocker Boc2. Overexpression of TANK-binding kinase 1 (TBK1) increased ABCA1 degradation, which was reversed by the proteasome inhibitor carbobenzoxy-L-leucyl-L-leucyl-L-leucinal (MG132). Silencing Tbk1 with siRNA increased ABCA1 expression and promoted ANXA1 membrane translocation. These results indicate a novel IR mechanism, that leads via TBK1 activation to ABCA1 ubiquitination. This degradation decreases ANXA1 secretion, thus facilitating retinal inflammation and RGC apoptosis. Our findings suggest a potential treatment strategy to prevent RGC apoptosis in retinal ischemia and glaucoma.

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Section: Discussionmentioning

confidence: 99%

Reduced Annexin A1 Secretion by ABCA1 Causes Retinal Inflammation and Ganglion Cell Apoptosis in a Murine Glaucoma Model

Chen

et al. 2018

Front. Cell. Neurosci.

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“…Binding of SAA to HDL can displace other apolipoproteins, particularly ApoA-I, thus diminishing HDL's participation in anti-atherogenic lipid metabolism and transport pathways and, consequently, promoting increased endothelial proteoglycan expression, an early event in the pathogenesis of atherosclerosis [17,18]. SAA enrichment can impair anti-inflammatory properties of HDL as shown in patients with diabetic nephropathy [19] and may interfere with HDL's modulation of pro-atherogenic modifications to low-density lipoprotein (LDL), endothelial cell adhesion molecules i.e., intracellular adhesion molecule/vascular cell adhesion molecule (ICAM/VCAM) expression and monocyte infiltration into the artery wall [20,21]. HDL also inhibits SAA-mediated reactive oxygen species generation and Nod-like receptor protein 3 (NLRP3) inflammasome activation [22].…”

Section: Introductionmentioning

confidence: 99%

High-Density Lipoprotein (HDL) Inhibits Serum Amyloid A (SAA)-Induced Vascular and Renal Dysfunctions in Apolipoprotein E-Deficient Mice

Cai

Ahmad

Hossain

et al. 2020

IJMS

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Serum amyloid A (SAA) promotes endothelial inflammation and dysfunction that is associated with cardiovascular disease and renal pathologies. SAA is an apoprotein for high-density lipoprotein (HDL) and its sequestration to HDL diminishes SAA bioactivity. Herein we investigated the effect of co-supplementing HDL on SAA-mediated changes to vascular and renal function in apolipoprotein E-deficient (ApoE−/−) mice in the absence of a high-fat diet. Male ApoE−/− mice received recombinant human SAA or vehicle (control) by intraperitoneal (i.p.) injection every three days for two weeks with or without freshly isolated human HDL supplemented by intravenous (i.v.) injection in the two weeks preceding SAA stimulation. Aorta and kidney were harvested 4 or 18 weeks after commencement of treatment. At 4 weeks after commencement of treatment, SAA increased aortic vascular cell adhesion molecule (VCAM)-1 expression and F2-isoprostane level and decreased cyclic guanosine monophosphate (cGMP), consistent with SAA stimulating endothelial dysfunction and promoting atherosclerosis. SAA also stimulated renal injury and inflammation that manifested as increased urinary protein, kidney injury molecule (KIM)-1, and renal tissue cytokine/chemokine levels as well as increased protein tyrosine chlorination and P38 MAPkinase activation and decreased in Bowman’s space, confirming that SAA elicited a pro-inflammatory phenotype in the kidney. At 18 weeks, vascular lesions increased significantly in the cohort of ApoE−/− mice treated with SAA alone. By contrast, pretreatment of mice with HDL decreased SAA pro-inflammatory activity, inhibited SAA enhancement of aortic lesion size and renal function, and prevented changes to glomerular Bowman’s space. Taken together, these data indicate that supplemented HDL reduces SAA-mediated endothelial and renal dysfunction in an atherosclerosis-prone mouse model.

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“…There is a large amount of SAA-mRNA expression in liver fat cells of obese patients, and its expression is related to BMI [25]. In type 2 diabetes, the level of SAA is significantly higher than normal, which is mainly related to the fact that SAA can cause insulin resistance, affect the reverse transport of cholesterol, and stimulate mononuclear macrophages to damage vascular endothelium [26][27][28][29][30]. As we all know, atherosclerosis, obesity, and type 2 diabetes are all risk factors for VAD.…”

Section: Discussionmentioning

confidence: 99%

The Relationship between Serum Amyloid A Level and Cognitive Dysfunction in Patients with Vascular Dementia: Preliminary Findings

Huang

2021

BioMed Research International

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Objective. This study was aimed at investigating the relationship between serum amyloid A (SAA) levels and cognitive dysfunction in patients with vascular dementia (VAD). Methods. Using cross-sectional research methods, 146 patients with VAD were selected as the VAD group and 70 normal people were selected as the NC group. Upon admission, the clinical and biochemical characteristics of the two groups of study subjects were collected, and the MMSE scale was used to assess cognitive function. A sandwich enzyme-linked immunosorbent assay was used to detect SAA levels. Results. There was no significant difference in clinical data and biochemical characteristics in the VAD group ( p > 0.05 ). Compared with the VAD group, the NC group has a higher level of education ( p < 0.05 ). The SAA level of the VAD group was higher than that of the NC group, and there was a significant difference ( p < 0.05 ). Spearman correlation analysis showed that SAA and MMSE in the VAD group were negatively correlated. Further multiple regression analysis showed that the serum amyloid A level is an independent risk factor for cognitive dysfunction in VAD patients. Conclusion. The level of SAA in VAD patients is significantly increased, which can be used as a potential peripheral blood marker to predict cognitive impairment in VAD patients.

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Serum amyloid A enrichment impairs the anti-inflammatory ability of HDL from diabetic nephropathy patients

Cited by 17 publications

References 36 publications

Reduced Annexin A1 Secretion by ABCA1 Causes Retinal Inflammation and Ganglion Cell Apoptosis in a Murine Glaucoma Model

Reduced Annexin A1 Secretion by ABCA1 Causes Retinal Inflammation and Ganglion Cell Apoptosis in a Murine Glaucoma Model

High-Density Lipoprotein (HDL) Inhibits Serum Amyloid A (SAA)-Induced Vascular and Renal Dysfunctions in Apolipoprotein E-Deficient Mice

The Relationship between Serum Amyloid A Level and Cognitive Dysfunction in Patients with Vascular Dementia: Preliminary Findings

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