Losartan prevents acquired epilepsy via TGF‐β signaling suppression
Open accessAbstract
Objective: Acquired epilepsy is frequently associated with structural lesions after trauma, stroke, and infections. Although seizures are often difficult to treat, there is no clinically applicable strategy to prevent the development of epilepsy in patients at risk. We have recently shown that vascular injury is associated with activation of albumin‐mediated transforming growth factor β (TGF‐β) signaling, and followed by local inflammatory response and epileptiform activity ex vivo. Here we investigated albumin‐mediated TGF‐β signaling and tested the efficacy of blocking the TGF‐β pathway in preventing epilepsy. Methods: We addressed the role of TGF‐β signaling in epileptogenesis in 2 different rat models of vascular injury, combining in vitro and in vivo biochemical assays, gene expression, and magnetic resonance and direct optical imaging for blood–brain barrier permeability and vascular reactivity. Long‐term electrocorticographic recordings were acquired in freely behaving animals. Results: We demonstrate that serum‐derived albumin preferentially induces activation of the activin receptor‐like kinase 5 pathway of TGF‐β receptor I in astrocytes. We further show that the angiotensin II type 1 receptor antagonist, losartan, previously identified as a blocker of peripheral TGF‐β signaling, effectively blocks albumin‐induced TGF‐β activation in the brain. Most importantly, losartan prevents the development of delayed recurrent spontaneous seizures, an effect that persists weeks after drug withdrawal. Interpretation: TGF‐β signaling, activated in astrocytes by serum‐derived albumin, is involved in epileptogenesis. We propose losartan, a drug approved by the US Food and Drug Administration, as an efficient antiepileptogenic therapy for epilepsy associated with vascular injury. Ann Neurol 2014;75:864–875
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In vivo pharmacological blockade of TGFβRI/II using SB431542 and losartan decreases Smad2/3 signaling in the peri-infarct tissue during the period of GDF activity after stroke.
“Furthermore, in vivo pharmacological blockade of TGFβRI/II using SB431542 and losartan19,20 decreases Smad2/3 signaling in the peri-infarct tissue (Supplementary Fig. 5) during the period of GDF activity after stroke.”
From GDF10 is a signal for axonal sprouting and functional recovery after stroke (2015) · cites this paper as [19]
The Results section on local losartan application reports that losartan significantly blocked an albumin-induced increase in cortical p-Smad2/3 in vivo. The Results section on Smad phosphorylation reports an effect of SB431542 only in cultured astrocytes. This paper does not establish that either drug reduced Smad2/3 signaling in peri-infarct tissue during GDF activity after stroke; the citing sentence points to its own Supplementary Fig. 5 for that observation. (LLM, conf=0.87)
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- Authors
- Bar‐Klein, G., Cacheaux, L. P., Kamintsky, L., Prager, O., Weissberg, I., Schoknecht, K., Cheng, P., Kim, S. Y., Wood, L., Heinemann, U., Kaufer, D., & Friedman, A.
- Affiliations
- Ben-Gurion University of the Negev (IL)
- University of California, Berkeley (US)
- Departments of Physiology and Cell Biology Cognitive and Brain Sciences, Zlotowski Center for Neuroscience, Ben‐Gurion University of the Negev Beer‐Sheva Israel
- Charité – Universitätsmedizin Berlin (DE)
- Helen Wills Neuroscience Institute and Department of Integrative Biology University of California, Berkeley Berkeley CA
- Corresponding author
- Friedman, Alon
- ORCID
- Venue
- Annals of Neurology
- Publisher
- Wiley
- Published
- 2014-05-28
- Volume
- 75
- Issue
- 6
- Pages
- 864-875
- ISSN
- 0364-5134 (ISSN-L)
- 1531-8249
- PMC
- PMC4077937
- OpenAlex
- W1746603715
- Cited by
- 270
- References
- 63
- Citations by year
- 2026: 18 · 2025: 11 · 2024: 28 · 2023: 24 · 2022: 23 · 2021: 26 · 2020: 29 · 2019: 30 · 2018: 15 · 2017: 26 · 2016: 17 · 2015: 13 · 2014: 10
- FWCI
- 16.78
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- Annals of Neurology (publishedVersion)
- PubMed (publishedVersion)
- PubMed Central (acceptedVersion)
- Funders
- National Institutes of Health (RO1/NINDS NS066005)
- United States - Israel Binational Science Foundation (2007185)
- Israel Science Foundation (713/11)
- The European Unions Seventh Framework Program (FP7/2007-2013), EPITARGET (602102)
- Topics
- Health Sciences › Medicine › Psychiatry and Mental health › Epilepsy research and treatment
- Health Sciences › Medicine › Neurology › Traumatic Brain Injury and Neurovascular Disturbances
- Life Sciences › Neuroscience › Neurology › Barrier Structure and Function Studies
- Keywords
- losartan, acquired epilepsy, epileptogenesis, TGF-beta signaling, serum albumin, vascular injury, angiotensin II type 1 receptor, ALK5, astrocytes, blood-brain barrier permeability, vascular reactivity, antiepileptogenic therapy, spontaneous seizures, electrocorticography
- MeSH terms
- Animals, Animals, Newborn, Anticonvulsants, Astrocytes, Benzamides, Blood-Brain Barrier, Cells, Cultured, Cerebral Cortex, Dioxoles, Disease Models, Animal, Embryo, Mammalian, Endocytosis, Epilepsy, Male, Neurons, Phosphopyruvate Hydratase, Signal Transduction, Transforming Growth Factor beta, Rats, Wistar, Losartan, Rats
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