Activation of toll-like receptor, RAGE and HMGB1 signalling in malformations of cortical development
Abstract
Recent evidence in experimental models of seizures and in temporal lobe epilepsy support an important role of high-mobility group box 1 and toll-like receptor 4 signalling in the mechanisms of hyperexcitability leading to the development and perpetuation of seizures. In this study, we investigated the expression and cellular distribution of toll-like receptors 2 and 4, and of the receptor for advanced glycation end products, and their endogenous ligand high-mobility group box 1, in epilepsy associated with focal malformations of cortical development. Immunohistochemistry showed increased expression of toll-like receptors 2 and 4 and receptor for advanced glycation end products in reactive glial cells in focal cortical dysplasia, cortical tubers from patients with the tuberous sclerosis complex and in gangliogliomas. Toll-like receptor 2 was predominantly detected in cells of the microglia/macrophage lineage and in balloon cells in focal cortical dysplasia, and giant cells in tuberous sclerosis complex. The toll-like receptor 4 and receptor for advanced glycation end products were expressed in astrocytes, as well as in dysplastic neurons. Real-time quantitative polymerase chain reaction confirmed the increased receptors messenger RNA level in all pathological series. These receptors were not detected in control cortex specimens. In control cortex, high-mobility group box 1 was ubiquitously detected in nuclei of glial and neuronal cells. In pathological specimens, protein stain…
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Gangliogliomas and focal cortical dysplasia type IIb are characterized by prominent activation of various inflammatory pathways, including the TIR signaling pathway.
“GG and FCD type IIb represent a major cause of drug-resistant epilepsy [23], [25] and are characterized by a prominent activation of various inflammatory pathways, including the TIR signaling pathway [9], [40]–[43].”
From MicroRNA-146a: A Key Regulator of Astrocyte-Mediated Inflammatory Response (2012) · cites this paper as [9]
Astrocytes are a major source and/or targets of pro-epileptogenic inflammatory signaling such as IL-1, HMGB1, and TLR pathways.
“In particular, both in vitro and in vivo data, point to the role of astrocytes as a major source and/or targets of pro-epileptogenic inflammatory signaling, such as the interleukin(IL)-1, High Mobility Group Box 1 (HMGB1) and Toll-like receptor (TLR) signaling pathways [1], [3], [6]–[9].”
From MicroRNA-146a: A Key Regulator of Astrocyte-Mediated Inflammatory Response (2012) · cites this paper as [9]
Cites
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Self-citationAstrocytes in the initiation and progression of epilepsy
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Self-citationToll-like receptor signaling in amyotrophic lateral sclerosis spinal cord tissue
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Self-citationInterweaving epilepsy and neurodegeneration: Vitamin E as a treatment approach
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Self-citation
- Authors
- Zurolo, E., Iyer, A., Maroso, M., Carbonell, C., Anink, J. J., Ravizza, T., Fluiter, K., Spliet, W. G. M., van Rijen, P. C., Vezzani, A., & Aronica, E.
- Venue
- Brain
- Publisher
- Oxford University Press (OUP)
- Published
- 2011-03-16
- Volume
- 134
- Issue
- 4
- Pages
- 1015-1032
- ISSN
- 0006-8950
- 1460-2156
- Cited by
- 184
- References
- 4
- Language
- en
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