ArticleTranslational stroke research2020
Mfsd2a Attenuates Blood-Brain Barrier Disruption After Sub-arachnoid Hemorrhage by Inhibiting Caveolae-Mediated Transcellular Transport in Rats.
Article in Translational stroke research, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.
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Who cites it
33 citing papers in PubMed, 61 citations in OpenAlex.
- MFSD2A in health and disease: lysolipid transport, barrier physiology, and translational boundaries.Molecular biomedicine · 2026Review
- Angiotensin III induces disruption of blood-brain barrier integrity in vitro in bEnd.3 brain endothelial cells.Hypertension research : official journal of the Japanese Society of Hypertension · 2026Article
- MFSD2A: a molecular nexus linking blood-brain barrier, lipid metabolism, and ischemia-reperfusion injury.Cellular & molecular biology letters · 2025Review
- Mfsd2a-Targeted Therapy for Ischemic Stroke: Mechanisms, Evidence, and Future Prospects.CNS neuroscience & therapeutics · 2025Review
- Phased blood-brain barrier disruption in ischaemic stroke: implications for therapy?Fluids and barriers of the CNS · 2025Review
- Caveolae-Mediated Transcytosis and Its Role in Neurological Disorders.Biomolecules · 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
- Channels and Transporters in Ischemic Brain Edema.Journal of inflammation research · 2025Review
- Article
- Endothelial Dysfunctions in Blood-Brain Barrier Breakdown in Alzheimer's Disease: From Mechanisms to Potential Therapies.CNS neuroscience & therapeutics · 2024Review
- Glial growth factor 2 treatment alleviates ischemia and reperfusion-damaged integrity of the blood-brain barrier through decreasing Mfsd2a/caveolin-1-mediated transcellular and Pdlim5/YAP/TAZ-mediated paracellular permeability.Acta pharmacologica Sinica · 2024Article
- Blood-brain barrier disruption: a culprit of cognitive decline?Fluids and barriers of the CNS · 2024Review
- GW0742 reduces mast cells degranulation and attenuates neurological impairments via PPARExperimental neurology · 2024Article
- Enhanced macromolecular substance extravasation through the blood-brain barrier via acoustic bubble-cell interactions.Ultrasonics sonochemistry · 2024Article
- Circadian Rhythm Regulator REV-ERBα Attenuates Neuroapoptosis in Early Brain Injury After Experimental Subarachnoid Hemorrhage in Rats.Neurochemical research · 2023Article
- The Role of Major Facilitator Superfamily Domain-Containing 2a in the Central Nervous System.Cellular and molecular neurobiology · 2023Review
- Transplantation of Umbilical Cord-Derived Mesenchymal Stem Cells Attenuates Surgical Wound-Induced Blood-Brain Barrier Dysfunction in Mice.Stem cells international · 2023Article
- Omega-3 polyunsaturated fatty acids alleviate early brain injury after traumatic brain injury by inhibiting neuroinflammation and necroptosis.Translational neuroscience · 2023Article
- Targeting Mfsd2a in hemorrhagic cerebrovascular diseases.Translational stroke research · 2022Article
- Review
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
Abstract
Blood-brain barrier (BBB) disruption is one of the critical mechanisms of brain injury induced by subarachnoid hemorrhage (SAH). Past studies have often focused on the tight junctions of endothelial cells. However, low transcellular transport levels also play an important role in the normal functioning of the BBB. Major facilitator superfamily domain-containing 2a (Mfsd2a) has been demonstrated to be essential for the maintenance of the normal BBB. Our present study aimed to explore the roles and mechanisms of Mfsd2a in BBB disruption after SAH. In this study, a prechiasmatic cistern single-injection model was used to produce experimental SAH in Sprague-Dawley rats. Specific small-interfering RNA and plasmids were used to downregulate and upregulate the expression of Mfsd2a prior to assessments in our SAH model. Omega-3 fatty acid deficiency diet was used to reduce DHA in rat brain. The expression level of Mfsd2a decreased significantly after SAH and reached its lowest level at 72 h post-SAH, which then gradually recovered. At 72 h after SAH, BBB function was disrupted; upregulation of Mfsd2a reversed this damage, whereas downregulation of Mfsd2a exacerbated this damage. These effects were primarily mediated through transcellular transport, especially for changes in caveolae compared to those of tight junctions. After stopping the supply of omega-3 fatty acids, the effect of Mfsd2a on inhibition of caveolae and protection of the blood-brain barrier was eliminated. Taken together, Mfsd2a inhibits caveolae-based transcellular transport by transporting omega-3 fatty acids to protect the BBB after SAH.
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Registered trials
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