ArticleMolecular neurobiology2022
Effect of TDP43-CTFs35 on Brain Endothelial Cell Functions in Cerebral Ischemic Injury.
Article in Molecular neurobiology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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9 citing papers in PubMed, 14 citations in OpenAlex.
- Targeting the Hippo pathway in pulmonary arterial hypertension: emerging pharmacological strategies.Journal of hypertension · 2026Review
- Stress granule phase transitions and neuronal fate in cerebral ischemia-reperfusion injury.Frontiers in molecular neuroscience · 2026Review
- Protective effect of sub-hypothermic mechanical perfusion combined with membrane lung oxygenation on a yorkshire model of brain injury after traumatic blood loss.Chinese journal of traumatology = Zhonghua chuang shang za zhi · 2025Article
- Total Flavones ofCurrent issues in molecular biology · 2025Article
- Activation of MST1 protects filtration barrier integrity of diabetic kidney disease in mice through restoring the tight junctions of glomerular endothelial cells.Acta pharmacologica Sinica · 2025Article
- Amyotrophic lateral sclerosis and frontotemporal dementia mutation reduces endothelial TDP-43 and causes blood-brain barrier defects.Science advances · 2025Article
- Acute severe hypoglycemia alters mouse brain microvascular proteome.Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism · 2024Article
- Establishment of a novel amyotrophic lateral sclerosis patient (Frontiers in cell and developmental biology · 2024Article
- Ablation of Siglec-E augments brain inflammation and ischemic injury.Journal of neuroinflammation · 2022Article
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Authors and funding
5 authors at 3 institutions in 2 countries.
Funding
Abstract
Pathological changes in the brain endothelium play an important role in the progression of ischemic stroke and the compromised BBB under ischemic stroke conditions cause neuronal damage. However, the pathophysiological mechanisms of the BBB under normal conditions and under ischemic stroke conditions have not been fully elucidated. The present study demonstrated that knockdown of TAR DNA-binding protein 43 (TDP-43) or overexpression of TDP43-CTFs35 inhibited tight junction protein expression, and mammalian sterile-20-like 1/2 (MST1/2) and YES-associated protein (YAP) phosphorylation in brain ECs and suppressed brain EC migration in vitro. The cytoplasmic TDP43-CTFs35 level was increased in brain ECs 24 h and 72 h after MCAO, but it disappeared 1 week after cerebral ischemia. The expression of tight junction proteins was also significantly deceased 24 h after MCAO and then gradually recovered at 72 h and 1 week after MCAO. The level of YAP phosphorylation was first significantly decreased 24 h after MCAO and then increased 72 h and 1 week after MCAO, accompanied by nuclear YAP translocation. The underlying mechanism is TDP43-CTFs35-mediated inhibition of Hippo signaling pathway activity through the dephosphorylation of MST1/2, which leads to the inhibition of YAP phosphorylation and the subsequent impairment of brain EC migration and tight junction protein expression. This study provides new insights into the mechanisms of brain vascular EC regulation, which may impact on BBB integrity after cerebral ischemic injury.
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