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Advanced glycation endproduct (AGE) receptor 1 is a negative regulator of the inflammatory response to AGE in mesangial cells
Open accessAbstract
Advanced glycation endproducts (AGE) contribute to kidney disease due to diabetes or aging by means of mesangial cell (MC) receptors, such as the receptor for AGE (RAGE), which promote oxidant-stress-dependent NF-kappaB activation and inflammatory gene expression. MC also express scavenger receptors SR-I and SR-II and AGE receptors 1, 2, and 3 (AGE-R1, -R2, and -R3), some of which are linked to AGE turnover. Because AGE-R1 expression is found suppressed in severe diabetic kidney disease, as other receptors increase, we investigated whether his molecule has a protective role against AGE-induced MC injury. A stable murine MC line overexpressing AGE-R1 (R1-MC) was generated, exhibiting a 1.8- to 2.7-fold increase in (125)I-AGE-specific binding, uptake, and degradation, compared with mock-MC. However, AGE-stimulated NF-kappaB activity and mitogen-activated protein kinase (MAPK) (p44/42) phosphorylation were found markedly suppressed in R1-MC. Additionally, AGE-stimulated macrophage chemotaxis protein 1 and RAGE overexpression were abolished in R1-MC. The effect of R1 on RAGE signaling was investigated after overexpressing RAGE in Chinese hamster ovary cells, which lack RAGE. AGE stimulation elicited NF-kappaB and MAPK activities in RAGE-Chinese hamster ovary cells; however, after cotransfection with R1, these responses were suppressed. Also, after silencing endogenous R1 in wild-type MC by R1 small interfering RNA, AGE-mediated MAPK/p44/42 activation exceeded by >2-fold that of mock-MC, consistent with loss of the activation-inhibitory properties of native AGE-R1. AGE-R1, although enhancing AGE removal, is also a distinct receptor in that it suppresses AGE-mediated MC inflammatory injury through negative regulation of RAGE, a previously uncharacterized pathway that may protect renal and other tissue injury due to diabetes and aging.
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“The concentration of linoleic acid in blood lipids (578,579) or granulocytes (374) was not associated with CRP or IL-6 concentration”
From Dietary factors and low-grade inflammation in relation to overweight and obesity (2011) · cites this paper as [578]
In the citing paper
“Data from an Italian study showed no association between a-linolenic acid in plasma fatty acids and several cytokines including IL-6 and TNF-a, but there was an inverse association with CRP (578)”
From Dietary factors and low-grade inflammation in relation to overweight and obesity (2011) · cites this paper as [578]
In the citing paper
“Data from an Italian study showed no association between a-linolenic acid in plasma fatty acids and several cytokines including IL-6 and TNF-a, but there was an inverse association with CRP (578)”
From Dietary factors and low-grade inflammation in relation to overweight and obesity (2011) · cites this paper as [578]
In the citing paper
“Ferrucci et al. (578) reported no association between arachidonic acid in plasma and CRP, TNF-a, IL-1b, IL-10 and sIL-6R concentrations, while there was an inverse association with IL-6 and IL-1ra concentrations and a positive association with TGF-b”
From Dietary factors and low-grade inflammation in relation to overweight and obesity (2011) · cites this paper as [578]
In the citing paper
“In an elderly Italian population, plasma EPA was inversely associated with IL-6 concentration and positively associated with the concentrations of the anti-inflammatory cytokines IL-10 and TGFb (578) .”
From Dietary factors and low-grade inflammation in relation to overweight and obesity (2011) · cites this paper as [578]
In the citing paper
“The concentration of a-linolenic acid in blood lipids (578,579,582) or granulocytes (374) was not associated with CRP or IL-6 concentration.”
From Dietary factors and low-grade inflammation in relation to overweight and obesity (2011) · cites this paper as [578]
In the citing paper
“Ferrucci et al. (578) reported no association between arachidonic acid in plasma and CRP, TNF-a, IL-1b, IL-10 and sIL-6R concentrations, while there was an inverse association with IL-6 and IL-1ra concentrations and a positive association with TGF-b”
From Dietary factors and low-grade inflammation in relation to overweight and obesity (2011) · cites this paper as [578]
In the citing paper
“Furthermore, plasma DHA was inversely associated with IL-6 and TNF-a concentrations and was also positively associated with the concentrations of IL-10 and TGF-b (578) .”
From Dietary factors and low-grade inflammation in relation to overweight and obesity (2011) · cites this paper as [578]
In the citing paper
“Ferrucci et al. (578) reported no association between arachidonic acid in plasma and CRP, TNF-a, IL-1b, IL-10 and sIL-6R concentrations, while there was an inverse association with IL-6 and IL-1ra concentrations and a positive association with TGF-b”
From Dietary factors and low-grade inflammation in relation to overweight and obesity (2011) · cites this paper as [578]
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Self-citation
Metadata
- Authors
- Lu, C., He, J. C., Cai, W., Liu, H., Zhu, L., & Vlassara, H.
- Affiliations
- Mount Sinai Health System (US)
- Department of Geriatrics and Adult Development, Division of Experimental Diabetes and Aging, and Department of Medicine, Division of Nephrology, Mount Sinai School of Medicine, New York, NY 10029
- Corresponding author
- Vlassara, Helen
- ORCID
- Liu, Huixian
- Venue
- Proceedings of the National Academy of Sciences
- Publisher
- National Academy of Sciences
- Published
- 2004-08-02
- Volume
- 101
- Issue
- 32
- Pages
- 11767-11772
- ISSN
- 0027-8424 (ISSN-L)
- 1091-6490
- PMC
- PMC511050
- OpenAlex
- W2030022427
- Cited by
- 228
- References
- 48
- Citations by year
- 2026: 3 · 2025: 5 · 2024: 8 · 2023: 6 · 2022: 7 · 2021: 13 · 2020: 11 · 2019: 8 · 2018: 9 · 2017: 15 · 2016: 13 · 2015: 15 · 2014: 8 · 2013: 13 · 2012: 16
- FWCI
- 7.46
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- Proceedings of the National Academy of Sciences (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- Funders
- National Institutes of Health
- National Institute of Diabetes and Digestive and Kidney Diseases (R01DK054788, DK54788)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Clinical Biochemistry › Advanced Glycation End Products research
- Health Sciences › Medicine › Nephrology › Chronic Kidney Disease and Diabetes
- Health Sciences › Medicine › Nephrology › Dialysis and Renal Disease Management
- Keywords
- advanced glycation end products, receptor for advanced glycation end products, mesangial cells, diabetic nephropathy, inflammation, NF-κB signaling, kidney injury
- MeSH terms
- Receptor for Advanced Glycation End Products, Animals, Cell Line, Gene Expression Regulation, Glomerular Mesangium, Humans, Inflammation, Phosphorylation, Receptors, Immunologic, Transfection, Signal Transduction, NF-kappa B, Glycation End Products, Advanced, Chemokine CCL2, COS Cells, Mitogen-Activated Protein Kinase 1, Mitogen-Activated Protein Kinases, Mitogen-Activated Protein Kinase 3, Mice
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