ArticleTranslational stroke research2019
The Contractile Apparatus Is Essential for the Integrity of the Blood-Brain Barrier After Experimental Subarachnoid Hemorrhage.
Article in Translational stroke research, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.
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Who cites it
29 citing papers in PubMed, 38 citations in OpenAlex.
- Blood‑brain barrier dysfunction in epilepsy: Mechanisms, therapeutic strategies and future orientation (Review).International journal of molecular medicine · 2025Review
- Mechanisms and potential therapeutic molecular targets in blood-brain barrier disruption following subarachnoid hemorrhage: a review of early brain injury.Frontiers in neurology · 2025Review
- TREM-1 as a potential gatekeeper of neuroinflammatory responses: therapeutic validation and mechanistic insights in experimental traumatic brain injury.Frontiers in immunology · 2025Article
- The sentinel against brain injury post-subarachnoid hemorrhage: efferocytosis of erythrocytes by leptomeningeal lymphatic endothelial cells.Theranostics · 2025Article
- Incidence and Factors in Delayed Neurological Deficits after Subarachnoid Hemorrhage in Mice.Brain hemorrhages · 2024Article
- Endothelial TREM-1 receptor regulates the blood-brain barrier integrity after intracerebral hemorrhage in mice via SYK/β-catenin signaling.CNS neuroscience & therapeutics · 2023Article
- Endogenous FGF21 attenuates blood-brain barrier disruption in penumbra after delayed recanalization in MCAO rats through FGFR1/PI3K/Akt pathway.Zhong nan da xue xue bao. Yi xue ban = Journal of Central South University. Medical sciences · 2023Article
- CCL5/CCR5-mediated peripheral inflammation exacerbates blood‒brain barrier disruption after intracerebral hemorrhage in mice.Journal of translational medicine · 2023Article
- Hemorrhagic Cerebral Insults and Secondary Takotsubo Syndrome: Findings in a Novel In Vitro Model Using Human Blood Samples.International journal of molecular sciences · 2022Article
- Confirming Subarachnoid Hemorrhage Induction in the Endovascular Puncture Mouse Model.Brain hemorrhages · 2022Article
- The blood-brain barrier and the neurovascular unit in subarachnoid hemorrhage: molecular events and potential treatments.Fluids and barriers of the CNS · 2022Review
- Met-RANTES preserves the blood-brain barrier through inhibiting CCR1/SRC/Rac1 pathway after intracerebral hemorrhage in mice.Fluids and barriers of the CNS · 2022Article
- Article
- MFGE8 mitigates brain injury in a rat model of SAH by maintaining vascular endothelial integrity via TIGβ5/PI3K/CXCL12 signaling.Experimental brain research · 2021Article
- Article
- Blood-brain barrier permeability imaging as a predictor for delayed cerebral ischaemia following subarachnoid haemorrhage. A narrative review.Acta neurochirurgica · 2021Review
- Correlation of cardiac function and cerebral perfusion in a murine model of subarachnoid hemorrhage.Scientific reports · 2021Article
- Cerebrovascular pathophysiology of delayed cerebral ischemia after aneurysmal subarachnoid hemorrhage.Histology and histopathology · 2021Review
- Endothelial Regulation by Exogenous Annexin A1 in Inflammatory Response and BBB Integrity Following Traumatic Brain Injury.Frontiers in neuroscience · 2021Article
- Pituitary Adenylate Cyclase-Activating Polypeptide Attenuates Brain Edema by Protecting Blood-Brain Barrier and Glymphatic System After Subarachnoid Hemorrhage in Rats.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2020Article
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Authors and funding
7 authors at 4 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Development of vasogenic brain edema is a key event contributing to mortality after subarachnoid hemorrhage (SAH). The precise underlying mechanisms at the neurovascular level that lead to disruption of the blood-brain barrier (BBB) are still unknown. Activation of myosin light chain kinases (MLCK) may result in change of endothelial cell shape and opening of the intercellular gap with subsequent vascular leakage. Male C57Bl6 mice were subjected to endovascular perforation. Brain water content was determined by wet-dry ratio and BBB integrity by Evans-Blue extravasation. The specific MLCK inhibitor ML-7 was administered to the mice to determine the role of the contractile apparatus of the neurovascular unit in determining brain water content, BBB integrity, neurofunctional outcome, brain damage, and survival at 7 days after SAH. Inhibition of MLCK significantly reduced BBB permeability (Evans Blue extravasation - 28%) and significantly decreased edema formation in comparison with controls (- 2%). MLCK-treated mice showed reduced intracranial pressure (- 53%), improved neurological outcome at 24 h and 48 h after SAH, and reduced 7-day mortality. Tight junction proteins claudin-5 and zonula occludens-1 levels were not influenced by ML-7 at 24 h after insult. The effect of ML-7 on pMLC was confirmed in brain endothelial cell culture (bEnd.3 cells) subjected to 4-h oxygen-glucose deprivation. The present study indicates that MLCK contributes to blood-brain barrier dysfunction after SAH by a mechanism that does not involve modulation of tight junction protein levels, but via activation of the contractile apparatus of the endothelial cell skeleton. This underlying mechanism may be a promising target for the treatment of SAH.
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