Gene Expression Analysis of Tuberous Sclerosis Complex Cortical Tubers Reveals Increased Expression of Adhesion and Inflammatory Factors
Open accessAbstract
Cortical tubers in patients with tuberous sclerosis complex are associated with disabling neurological manifestations, including intractable epilepsy. While these malformations are believed to result from the effects of TSC1 or TSC2 gene mutations, the molecular mechanisms leading to tuber formation, as well as the onset of seizures, remain largely unknown. We used the Affymetrix Gene Chip platform to provide the first genome‐wide investigation of gene expression in surgically resected tubers, compared with histological normal perituberal tissue from the same patients or autopsy control tissue. We identified 2501 differentially expressed genes in cortical tubers compared with autopsy controls. Expression of genes associated with cell adhesion, for example,VCAM1,integrins and CD44, or with the inflammatory response, including complement factors,serpinA3,CCL2 and several cytokines, was increased in cortical tubers, whereas genes related to synaptic transmission, for example, the glial glutamate transporter GLT‐1, and voltage‐gated channel activity, exhibited lower expression. Gene expression in perituberal cortex was distinct from autopsy control cortex suggesting that even in the absence of tissue pathology the transcriptome is altered in TSC. Changes in gene expression yield insights into new candidate genes that may contribute to tuber formation or seizure onset, representing new targets for potential therapeutic development.
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Gene-expression analysis of tuber tissue has revealed increased expression of astrocyte-enriched genes and prominent neuroinflammation.
“Indeed, gene-expression analysis of tuber tissue has revealed increased expression of astrocyte-enriched genes and prominent neuroinflammation14,15.”
From mTORC1 drives cell-autonomous astrocyte reactivity in tuberous sclerosis (2026) · cites this paper as [15]
The Results (Gene ontology, pathway, and expression analysis; page not provided) report increased expression of immune and inflammatory-response genes in cortical tubers, supporting the neuroinflammation portion of the claim. The passages do not establish increased expression of astrocyte-enriched genes; the reported glial glutamate transporter SLC1A2 was instead lower in tubers. (LLM, conf=0.86)
Experimental — accuracy not yet measuredBoth the innate and the adaptive immune responses are activated in epilepsy-associated lesions.
“Both the innate and the adaptive immune responses are activated in these lesions ([5]; reviewed in [3]).”
From MicroRNA-146a: A Key Regulator of Astrocyte-Mediated Inflammatory Response (2012) · cites this paper as [5]
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Arai, Y., Takashima, S., & Becker, L. E. (2000) · Pathobiology · doi:10.1159/000028118 · Cited by 17 · see citing works
Gene Profiling in Temporal Lobe Epilepsy Tissue and Dysplastic Lesions
Crino, P. B., & Becker, A. J. (2006) · Epilepsia · doi:10.1111/j.1528-1167.2006.00712.x · Cited by 12 · see citing works
Self-citation
Flagged first, then by citations
Research works printed but not linked: 2
- [27]Gomez M Sampson J Whittemore V The Tuberous Sclerosis Complex 1999 Oxford Oxford University Press
- [79]van Vliet EA da Costa Araújo S Redeker S van Schaik R Aronica E Gorter JA Long-lasting increased permeability of the blood-brain barrier may contribute to seizure progression in temporal lobe epilepsy Brain 2007 130 2 521 534 17124188
Cited by
Sorted by citations
The role of inflammation in epilepsy
Vezzani, A., French, J., Bartfai, T., & Baram, T. Z. (2011) · Nature Reviews Neurology · doi:10.1038/nrneurol.2010.178 · Cited by 1,876 · see citing works
MicroRNA-146a: A Key Regulator of Astrocyte-Mediated Inflammatory Response
Iyer, A., Zurolo, E., Prabowo, A., Fluiter, K., Spliet, W. G. M., van Rijen, P. C., Gorter, J. A., & Aronica, E. (2012) · PLoS ONE · doi:10.1371/journal.pone.0044789 · Cited by 330 · see citing works
Self-citationZimmer, T. S., Broekaart, D. W. M., Gruber, V.-E., van Vliet, E. A., Mühlebner, A., & Aronica, E. (2020) · Frontiers in Neurology · doi:10.3389/fneur.2020.01028 · Cited by 48 · see citing works
Self-citationmTORC1 drives cell-autonomous astrocyte reactivity in tuberous sclerosis
Li, T. L., Blair, J. D., Yoo, T., Grant, G. A., Hockemeyer, D., Porter, B. E., & Bateup, H. S. (2026) · Nature · doi:10.1038/s41586-026-11054-w · Cited by 1 · see citing works
- Authors
- Boer, K., Crino, P. B., Gorter, J. A., Nellist, M., Jansen, F. E., Spliet, W. G. M., Van Rijen, P. C., Wittink, F. R. A., Breit, T. M., Troost, D., Wadman, W. J., & Aronica, E.
- Affiliations
- Amsterdam UMC Location University of Amsterdam (NL)
- University of Pennsylvania Health System (US)
- Stichting Epilepsie Instellingen Nederland (NL)
- Erasmus MC (NL)
- University Medical Center Utrecht (NL)
- University of Amsterdam (NL)
- ORCID
- Venue
- Brain Pathology
- Publisher
- Wiley
- Published
- 2010-06-07
- Volume
- 20
- Issue
- 4
- Pages
- 704-719
- ISSN
- 1015-6305 (ISSN-L)
- 1750-3639
- PMC
- PMC2888867
- OpenAlex
- W2159452633
- Cited by
- 148
- References
- 87
- Citations by year
- 2026: 4 · 2025: 5 · 2024: 11 · 2023: 13 · 2022: 6 · 2021: 9 · 2020: 13 · 2019: 6 · 2018: 6 · 2017: 13 · 2016: 13 · 2015: 6 · 2014: 11 · 2013: 11 · 2012: 8
- FWCI
- 4.59
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- Brain Pathology (publishedVersion)
- Europe PMC (PubMed Central) (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- Pure Amsterdam UMC (publishedVersion)
- Data Archiving and Networked Services (DANS) (submittedVersion)
- EUR Research Repository (Erasmus University Rotterdam) (submittedVersion)
- RePub (Erasmus University Rotterdam) (submittedVersion, other-oa)
- UvA-DARE (University of Amsterdam) (submittedVersion)
- RePub (Erasmus University Rotterdam) (submittedVersion)
- Funders
- U.S. Department of Defense
- National Institute of Neurological Disorders and Stroke (NS045021, R01NS045021)
- Topics
- Health Sciences › Medicine › Physiology › Tuberous Sclerosis Complex Research
- Health Sciences › Medicine › Psychiatry and Mental health › Epilepsy research and treatment
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › PI3K/AKT/mTOR signaling in cancer
- Keywords
- tuberous sclerosis complex, cortical tubers, gene expression profiling, drug-resistant epilepsy, cell adhesion genes, inflammatory response genes, TSC1, TSC2, differentially expressed genes, synaptic transmission, glutamate transporter GLT-1, voltage-gated ion channels, complement proteins, cytokines, integrins, CD44, VCAM-1, alpha-1-antichymotrypsin, MCP-1
- MeSH terms
- Adolescent, Adult, Aged, Cell Adhesion, Cerebral Cortex, Child, Child, Preschool, Female, Humans, Immunohistochemistry, Infant, Inflammation, Male, Middle Aged, Tuberous Sclerosis, Biomarkers, Gene Expression, Reverse Transcriptase Polymerase Chain Reaction, Genome-Wide Association Study
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
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