Effects of scavenger receptors-1 class A stimulation on macrophage morphology and highly modified advanced glycation end product-protein phagocytosis

Hamasaki, Shuichi; Kobori, Takuro; Yamazaki, Yui; Kitaura, Atsuhiro; Niwa, Akira; Nishinaka, Takashi; Nishibori, Masahiro; Mori, Shuji; Nakao, Shinichi; Takahashi, Hideo

doi:10.1038/s41598-018-24325-y

Cited by 31 publications

(32 citation statements)

References 52 publications

(46 reference statements)

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“…The direct role of AGE in stimulating the expression of scavenger receptors and promoting phagocytosis has been revealed in a recent study [44]. In this study, AGE-modified bovine serum albumin induced morphological changes in cultured murine macrophages, increasing their phagocytic activity.…”

Section: The Role Of Hyperglycemia and Advanced Glycation End-productmentioning

confidence: 57%

The Diabetes Mellitus–Atherosclerosis Connection: The Role of Lipid and Glucose Metabolism and Chronic Inflammation

Poznyak

Grechko

Poggio

et al. 2020

IJMS

692

359

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Diabetes mellitus comprises a group of carbohydrate metabolism disorders that share a common main feature of chronic hyperglycemia that results from defects of insulin secretion, insulin action, or both. Insulin is an important anabolic hormone, and its deficiency leads to various metabolic abnormalities in proteins, lipids, and carbohydrates. Atherosclerosis develops as a result of a multistep process ultimately leading to cardiovascular disease associated with high morbidity and mortality. Alteration of lipid metabolism is a risk factor and characteristic feature of atherosclerosis. Possible links between the two chronic disorders depending on altered metabolic pathways have been investigated in numerous studies. It was shown that both types of diabetes mellitus can actually induce atherosclerosis development or further accelerate its progression. Elevated glucose level, dyslipidemia, and other metabolic alterations that accompany the disease development are tightly involved in the pathogenesis of atherosclerosis at almost every step of the atherogenic process. Chronic inflammation is currently considered as one of the key factors in atherosclerosis development and is present starting from the earliest stages of the pathology initiation. It may also be regarded as one of the possible links between atherosclerosis and diabetes mellitus. However, the data available so far do not allow for developing effective anti-inflammatory therapeutic strategies that would stop atherosclerotic lesion progression or induce lesion reduction. In this review, we summarize the main aspects of diabetes mellitus that possibly affect the atherogenic process and its relationship with chronic inflammation. We also discuss the established pathophysiological features that link atherosclerosis and diabetes mellitus, such as oxidative stress, altered protein kinase signaling, and the role of certain miRNA and epigenetic modifications.

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Section: The Role Of Hyperglycemia and Advanced Glycation End-productmentioning

confidence: 57%

The Diabetes Mellitus–Atherosclerosis Connection: The Role of Lipid and Glucose Metabolism and Chronic Inflammation

Poznyak

Grechko

Poggio

et al. 2020

IJMS

692

359

View full text Add to dashboard Cite

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“…Advanced glycation end-products (AGE) that derived from prolonged exposure of proteins to sugars is another kinds ligand of the SR-A. On account of the affinity to SR-A, fucoidan may be potential candidates for inhibitors of toxic AGE uptake, so the toxicity of AGE endocytosis can be attenuated by fucoidan ( Figure 2 ) [ 22 ].…”

Section: Molecular Targets Of Fucoidanmentioning

confidence: 99%

Molecular Targets and Related Biologic Activities of Fucoidan: A Review

et al. 2020

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Fucoidan—a marine natural active polysaccharide derived from brown algae with a variety of medicinal activities and low toxicity—has been used as clinical drug for renal diseases for nearly 20 years. The pharmacological mechanism of fucoidan has been well-investigated, based on target molecules and downstream signaling pathways. This review summarizes some important molecular targets of fucoidan and its related biologic activities, including scavenger receptor (SR), Toll-like receptors (TLRs), C-type lectin (CLEC) and some newly found target molecules, which may be beneficial for further understanding the pharmacological mechanism of fucoidan and discovering its new functions, as well as developing related clinical or adjuvant drugs and functional preparations.

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“…AGEs interact with two types of cell surface AGE receptors expressed on macrophages [ 14 ]. A scavenger receptor, scavenger receptor-1 class A (SR-A)/CD204, was involved in AGEs uptake by a mouse macrophage cell line, RAW264.7 cells, despite its physiological role remain unclear [ 15 ]. Among constitute other types of AGE receptors, receptor for AGE (RAGE) and TLR4 initiate specific cellular signalling events.…”

Section: Introductionmentioning

confidence: 99%

Advanced glycation end-products reduce lipopolysaccharide uptake by macrophages

et al. 2021

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Hyperglycaemia provides a suitable environment for infections and the mechanisms of glucose toxicity include the formation of advanced glycation end-products (AGEs), which comprise non-enzymatically glycosylated proteins, lipids, and nucleic acid amino groups. Among AGE-associated phenotypes, glycolaldehyde-derived toxic AGE (AGE-3) is involved in the pathogenesis of diabetic complications. Internalisation of endotoxin by various cell types contributes to innate immune responses against bacterial infection. An endotoxin derived from Gram-negative bacteria, lipopolysaccharide (LPS), was reported to enhance its own uptake by RAW264.7 mouse macrophage-like cells, and an LPS binding protein, CD14, was involved in the LPS uptake. The LPS uptake induced the activation of RAW264.7 leading to the production of chemokine CXC motif ligand (CXCL) 10, which promotes T helper cell type 1 responses. Previously, we reported that AGE-3 was internalised into RAW264.7 cells through scavenger receptor-1 Class A. We hypothesized that AGEs uptake interrupt LPS uptake and impair innate immune response to LPS in RAW264.7 cells. In the present study, we found that AGE-3 attenuated CD14 expression, LPS uptake, and CXCL10 production, which was concentration-dependent, whereas LPS did not affect AGE uptake. AGEs were reported to stimulate the receptor for AGEs and Toll-like receptor 4, which cause inflammatory reactions. We found that inhibitors for RAGE, but not Toll-like receptor 4, restored the AGE-induced suppression of CD14 expression, LPS uptake, and CXCL10 production. These results indicate that the receptor for the AGE-initiated pathway partially impairs the immune response in diabetes patients.

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Effects of scavenger receptors-1 class A stimulation on macrophage morphology and highly modified advanced glycation end product-protein phagocytosis

Cited by 31 publications

References 52 publications

The Diabetes Mellitus–Atherosclerosis Connection: The Role of Lipid and Glucose Metabolism and Chronic Inflammation

The Diabetes Mellitus–Atherosclerosis Connection: The Role of Lipid and Glucose Metabolism and Chronic Inflammation

Molecular Targets and Related Biologic Activities of Fucoidan: A Review

Advanced glycation end-products reduce lipopolysaccharide uptake by macrophages

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