ArticleCNS neuroscience & therapeutics2019
Cathepsin B inhibition ameliorates leukocyte-endothelial adhesion in the BTBR mouse model of autism.
Article in CNS neuroscience & therapeutics, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed, 21 citations in OpenAlex.
- Article
- A Brief Overview of Neutrophils in Neurological Diseases.Biomolecules · 2023Review
- Possible Mechanisms of the Neuroprotective Actions of Date Palm Fruits Aqueous Extracts against Valproic Acid-Induced Autism in Rats.Current issues in molecular biology · 2023Article
- Extralysosomal cathepsin B in central nervous system: Mechanisms and therapeutic implications.Brain pathology (Zurich, Switzerland) · 2022Review
- Signalling pathways in autism spectrum disorder: mechanisms and therapeutic implications.Signal transduction and targeted therapy · 2022Review
- Central nervous system diseases related to pathological microglial phagocytosis.CNS neuroscience & therapeutics · 2021Review
- Proteomics Analysis of Tears and Saliva From Sjogren's Syndrome Patients.Frontiers in pharmacology · 2021Article
- The AMPAR antagonist perampanel protects the neurovascular unit against traumatic injury via regulating Sirt3.CNS neuroscience & therapeutics · 2021Article
- The Role of Cathepsins in Memory Functions and the Pathophysiology of Psychiatric Disorders.Frontiers in psychiatry · 2020Review
- Cathepsin B inhibition ameliorates leukocyte-endothelial adhesion in the BTBR mouse model of autism.CNS neuroscience & therapeutics · 2019Article
- Association of cathepsin B and cystatin C with an age-related pulmonary subclinical state in a healthy Chinese population.Therapeutic advances in respiratory diseaseArticle
Corrections and comments
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Authors and funding
11 authors at 4 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
aimsAutism spectrum disorder (ASD) is a wide range of neurodevelopmental disorders involving deficits in social interaction and communication. Unfortunately, autism remains a scientific and clinical challenge owing to the lack of understanding the cellular and molecular mechanisms underlying it. This study aimed to investigate the pathophysiological mechanism underlying leukocyte-endothelial adhesion in autism-related neurovascular inflammation.
methodsMale BTBR T+tf/J mice were used as an autism model. The dynamic pattern of leukocyte-endothelial adhesion in mouse cerebral vessels was detected by two-photon laser scanning microscopy (TPLSM). Using FACS, RT-PCR, and Western blotting, we explored the expression of cell adhesion molecules, the mRNA expression of endothelial chemokine, the protein levels of cathepsin B, and inflammatory mediators.
resultsWe found a significant increase in leukocyte-endothelial adhesion in BTBR mice, accompanied by elevated expression of the adhesion molecule neutrophils CD11b and endothelial ICAM-1. Our data further indicate that elevated neutrophil cathepsin B levels contribute to elevated endothelial chemokine CXCL7 levels in BTBR mice. The pharmacological inhibition of cathepsin B reverses the enhanced leukocyte-endothelial adhesion in the cerebral vessels of autistic mice.
conclusionOur results revealed the prominent role of cathepsin B in modulating leukocyte-endothelial adhesion during autism-related neurovascular inflammation and identified a promising novel approach for autism treatment.
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