In Vitro Methodologies to Study the Role of Advanced Glycation End Products (AGEs) in Neurodegeneration
Abstract
:1. Introduction
2. AGEs and Neurodegeneration
2.1. Evidence Associating AGEs with Neurodegeneration
2.2. Concepts in AGE-Mediated Neurodegeneration
3. In Vitro Models to Study the Effect of AGEs on the Neuro-Immune Axis
3.1. Monocultures
3.1.1. Models of Brain Inflammation
Microglial Cell Models
- Immortalised microglial cell lines
- Animal-derived microglia cell lines
- Human derived microglial cell lines
- Human and animal-derived primary microglial cells
3.1.2. Other Inflammation Models
- Monocytes Cell Models
Immortalised Monocyte Cell Lines
- Human derived monocytic lines
- Human and animal-derived primary monocytes
3.1.3. Neuronal Cell Lines
- Animal neuronal cell lines
- Human neuronal cell lines
- Primary neuronal cells
3.1.4. Brain Endothelial Cells
- Animal-derived immortalised cell lines
- Human derived immortalised cell lines
- Primary endothelial cells
3.2. Reporter Cell Lines
3.3. iPSCs
3.4. Two-Dimensional Co-Cultures
3.5. Three-Dimensional Models and Microfluidics
4. Advisable In Vitro Models for AGE-Related Research
Advisable Model per Endpoint | Advantages | Disadvantages | References | |
---|---|---|---|---|
Neuroinflammation | HMC3 microglial line | Human line, RAGE expression, M1 and M2 phenotype, existing literature on AGEs effects | No aggregate formation | [128,129,132,133,310] |
Co-culture of neurons with microglia in transwell | Well-established models, they give insights into how AGE indirectly affects neuron viability by activating microglia, easy to establish and interpret, comparative studies on the responses, i.e., SH-SY5Y/HMC3 | No aggregate formation | [285,286,287,288,290,309] | |
iPSC-derived microglia | Patient-derived cells with diseased genotypic background, formation of aggregates | Non-high throughput, expensive, laborious procedure, low efficiency of differentiated cells | [263,264] | |
NF-κΒ reporter cell lines | Very informative to understand AGE signalling | Most of the available lines are no brain-related lines | [154,159,244,246,247,254] | |
Neurotoxicity | SH-SY5Y | Human line, extensively used in AGE-studies, RAGE expression, intracellular formation of AGEs, differentiated to dopaminergic neurons, Lewy body formation observed | Multiple differentiation protocols exist, possible unstable genome due to cancerous origin | [100,170,171,188,189,192,195,197,200,205] |
iPSC derived neurons | Patient-derived cells with diseased genotypic background, formation of aggregates | Non-high throughput, expensive, laborious, low efficiency | [258,265] | |
Nrf-2 reporter cell lines | Very informative to understand AGE signalling and the potential protective effects of AGE inhibitors | No brain-related lines are available | [249,252] | |
BBB | hCMEC/D3 | Human line, expression of endothelial junctional markers and transporters, RAGE expression, applied in AGE and ND research, widely used and characterised BBB model | Exhibit lower TEER than primary endothelial cells | [311] |
iPSC derived brain endothelial cells | Patient-derived cells with diseased genotypic background, formation of aggregates, high TEER values | Non-high-throughput, expensive, laborious, low efficiency, reproducibility not confirmed | [267,272] | |
Co-cultures of brain endothelial cells with microglia in transwells | Well-established models, paracrine communication between cell types, more representative of BBB physiology, easy to establish and interpret | No aggregate formation, complicated | [57,226,273,292,293,294] | |
BBB-on-a-chip | 3D, fluid shear stress, ECM, paracrine and juxtacrine signalling, combination of cell types | Complex | [304,305] |
5. Conclusions and Main Challenges in AGE In Vitro Research
Author Contributions
Funding
Institutional Review Board Statement
Informed Consent Statement
Data Availability Statement
Acknowledgments
Conflicts of Interest
References
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Relevant Endpoint | Cell Type | Line Name | Origin | Exposed to | Outcome | Reference |
---|---|---|---|---|---|---|
Neuroinflammation/inflammation | Microglia | BV2 | mouse | MGO-BSA | ↑ •NO, ROS, NLRP3, NF-κΒ, TNF-α, IL-6, MAPKs, RAGE, COX-2 | [89] |
N11 | mouse | Glu-BSA | Microglial activation, ↑ •NO, IL-6, MCP-1, TNF-α | [119,120,242] | ||
Glu-CEA | ↑ •NO, iNOS, TNF-α, IL_6 | [114,118] | ||||
HMC3 | Human | Glu-HSA | ↑ •NO, apoptosis Anti-RAGE prevented cell death | [133] | ||
Glu-BSA | Activated microglia (↑ Glu-5, CR3/43), ↑ RAGE, TNF-α Anti-RAGE decreased TNF-α | [132] | ||||
HMO6 | Human | Aβ peptide | ↑ RAGE, synthesis of AGE-albumin | [96,98,122] | ||
Monocytes/macrophages | THP-1 | Human | Glu-BSA | ↑ VEGF, IL-6, TNF-α, iNOS, RAGE, promoted M1 phenotype | [92,151,160] | |
MG-H1 | ↑ Adhesion to HUVECs | [243] | ||||
S100b | ↑ RAGE, MCP-1, IP-10, COX-2, NOX2, O2•, NF-κB activation. LR90 blocked the expression of pro-inflammatory cytokines, NF-κΒ and decreased the adhesion of THP-1 to endothelial cells. | [154] | ||||
Hypoxia | ↑ AGEs, MCP-1, RAGE, NF-κΒ, Μ1 phenotype | [153,155,156] | ||||
MGO | ↑ secretion of AGEs, glycation of cell surface proteins, unchanged ROS and RAGE, ↑ IL-1β, IL-8, TNF-α ↑ migration, Impaired chemotaxis | [157,158] | ||||
MGO-BSA | ↑ COX2, TNF-α, M-CSF | [152,159,160] | ||||
Neurodegeneration/neurotoxicity | Neuronal | PC12 | Rat | Ribosylated-BSA | ↑ apoptosis, iNOS, COX2, pp38 | [177,178,179] |
Glu-BSA | ↑ apoptosis, RAGE, NF-κΒ | |||||
Glu + MGO | ↑ protein carbonyls, ROS, RAGE, NF-κΒ | |||||
Neuro2A | mouse | MGO | ↑ ROS, apoptosis, intracellular CML | [181,182] | ||
SH-SY5Y | human | AGE-BSA | ↑ RAGE, ROS, apoptosis, NF-κB, AMPK | [195] | ||
MGO | ↑ apoptosis, ROS, MDA, mitochondrial damage ↓SOD, CAT, GSH | [170] | ||||
Ribosylated α-synuclein | ↑ ROS | [200] | ||||
GA | ↑ AGE accumulation intracellularly, apoptosis, VEGF, TGF-β, phosphorylated tau ↓GAPDH activity | [100,171] | ||||
LUHMES | Human | AGE-BSA | ↑ RAGE, MAPKs, Bax | [122] | ||
BBB | Endothelial | bEnd.3 | Mouse | MGO-BSA | ↑ monolayer permeability, ROS ↓SOD2 activity, impaired respiratory metabolism | [59] |
BMECs | Human or animal | AGE-BSA | ↓claudin-5, TEER, Unchanged occludin-1 and ZO-1, ↑ monolayer permeability due to ↑ VEGF, MMP-2 leading to thickening of the basement membrane and barrier disruption | [58] | ||
HUVECs | human | Glu-BSA MGO-BSA MGO-OvA, CML-BSA | ↓GSH activity ↑ GPx activity | [167] | ||
Glycated insulin | ↓viability, Bcl-2 ↑ Bax, ROS, permeability | [57] | ||||
MGO | ↑ ROS, apoptosis, Bax, MAPKs ↓Bcl-2, GLO-1, unchanged Nrf2 ↑ monolayer permeability, actin stress fibers ↓ZO-1, Cx43, GJIC | [237,240,241] |
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Chrysanthou, M.; Miro Estruch, I.; Rietjens, I.M.C.M.; Wichers, H.J.; Hoppenbrouwers, T. In Vitro Methodologies to Study the Role of Advanced Glycation End Products (AGEs) in Neurodegeneration. Nutrients 2022, 14, 363. https://doi.org/10.3390/nu14020363
Chrysanthou M, Miro Estruch I, Rietjens IMCM, Wichers HJ, Hoppenbrouwers T. In Vitro Methodologies to Study the Role of Advanced Glycation End Products (AGEs) in Neurodegeneration. Nutrients. 2022; 14(2):363. https://doi.org/10.3390/nu14020363
Chicago/Turabian StyleChrysanthou, Marialena, Ignacio Miro Estruch, Ivonne M. C. M. Rietjens, Harry J. Wichers, and Tamara Hoppenbrouwers. 2022. "In Vitro Methodologies to Study the Role of Advanced Glycation End Products (AGEs) in Neurodegeneration" Nutrients 14, no. 2: 363. https://doi.org/10.3390/nu14020363
APA StyleChrysanthou, M., Miro Estruch, I., Rietjens, I. M. C. M., Wichers, H. J., & Hoppenbrouwers, T. (2022). In Vitro Methodologies to Study the Role of Advanced Glycation End Products (AGEs) in Neurodegeneration. Nutrients, 14(2), 363. https://doi.org/10.3390/nu14020363