Subcellular reorganization and altered phosphorylation of the astrocytic gap junction protein connexin43 in human and experimental temporal lobe epilepsy
Abstract
Dysfunctional astrocytes are increasingly recognized as key players in the development and progression of mesial temporal lobe epilepsy (MTLE). One of the dramatic changes astrocytes undergo in MTLE with hippocampal sclerosis (HS) is loss of gap junction coupling. To further elucidate molecular mechanism(s) underlying this alteration, we assessed expression, cellular localization and phosphorylation status of astrocytic gap junction proteins in human and experimental MTLE-HS. In addition to conventional confocal analysis of immunohistochemical staining we employed expansion microscopy, which allowed visualization of blood-brain-barrier (BBB) associated cellular elements at a sub-µm scale. Western Blot analysis showed that plasma membrane expression of connexin43 (Cx43) and Cx30 were not significantly different in hippocampal specimens with and without sclerosis. However, we observed a pronounced subcellular redistribution of Cx43 toward perivascular endfeet in HS, an effect that was accompanied by increased plaque size. Furthermore, in HS Cx43 was characterized by enhanced C-terminal phosphorylation of sites affecting channel permeability. Prominent albumin immunoreactivity was found in the perivascular space of HS tissue, indicating that BBB damage and consequential albumin extravasation was involved in Cx43 dysregulation. Together, our results suggest that subcellular reorganization and/or abnormal posttranslational processing rather than transcriptional downregulation of a…
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In temporal lobe epilepsy, increased microvascular density, loss of tight junctions, and IgG leakage are observed in hippocampal resections from humans and in rodent epileptic models.
“Increased microvascular density, loss of tight junctions, and IgG leakage are observed in hippocampal resections from humans with temporal lobe epilepsy (499), and are also observed in rodent epileptic models (145, 499).”
From Blood-Brain Barrier: From Physiology to Disease and Back (2019) · cites this paper as [145]
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- Authors
- Deshpande, T., Li, T., Herde, M. K., Becker, A., Vatter, H., Schwarz, M. K., Henneberger, C., Steinhäuser, C., & Bedner, P.
- Affiliations
- University of Bonn (DE)
- Corresponding author
- Steinhäuser, Christian
- ORCID
- Venue
- Glia
- Publisher
- Wiley
- Published
- 2017-08-10
- Volume
- 65
- Issue
- 11
- Pages
- 1809-1820
- ISSN
- 0894-1491 (ISSN-L)
- OpenAlex
- W2743770531
- Cited by
- 87
- References
- 41
- Citations by year
- 2026: 5 · 2025: 5 · 2024: 9 · 2023: 10 · 2022: 13 · 2021: 18 · 2020: 10 · 2019: 6 · 2018: 9 · 2017: 1 · 2016: 1
- FWCI
- 2.91
- Type
- journal article
- Language
- en
- Open access
- closed
- Licence
- Locations
- Glia (publishedVersion)
- PubMed (publishedVersion)
- DZNE Pub (submittedVersion)
- Funders
- NRW-Rückkehrerprogramm
- German Research Foundation (SFB1089 B03, SPP1757 HE6949/1, HE6949/3, STE552/3)
- SPP1757 young investigator
- European Union (ERA-NET NEURON project “BrIE”)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Connexins and lens biology
- Health Sciences › Medicine › Psychiatry and Mental health › Epilepsy research and treatment
- Life Sciences › Neuroscience › Neurology › Barrier Structure and Function Studies
- Keywords
- connexin 43, connexin 30, astrocytes, mesial temporal lobe epilepsy, hippocampal sclerosis, electrical coupling, subcellular redistribution, C-terminal phosphorylation, blood-brain barrier disruption, albumin extravasation, expansion microscopy
- MeSH terms
- Connexin 30, Chondroitin Sulfate Proteoglycan 4, Animals, Antigens, Astrocytes, Cell Membrane, Disease Models, Animal, Epilepsy, Temporal Lobe, Female, Glial Fibrillary Acidic Protein, Hippocampus, Humans, Kainic Acid, Male, Mice, Transgenic, Proteoglycans, Subcellular Fractions, Up-Regulation, Connexin 43, Excitatory Amino Acid Agonists, Platelet Endothelial Cell Adhesion Molecule-1, Mice, S100 Calcium Binding Protein beta Subunit
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