ArticleClinics (Sao Paulo, Brazil)
Claudin-1 and Claudin-3 as Molecular Regulators of Myelination in Leukoaraiosis Patients.
Article in Clinics (Sao Paulo, Brazil). The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed, 8 citations in OpenAlex.
- Insights from TPPP3 and its family member proteins in neuronal diseases.Neural regeneration research · 2026Article
- Exerkine irisin mitigates cognitive impairment by suppressing gut-brain axis-mediated inflammation.Journal of advanced research · 2025Article
- Wireless In Situ Catalytic Electron Signaling-Mediated Transcriptomic Reprogramming for Neuron Regeneration via Adaptable Antennas.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Traumatic brain injury and post-injury sleep fragmentation differentially alter the microglial transcriptome.Frontiers in immunology · 2025Article
- Claudin-1 impairs blood-brain barrier by downregulating endothelial junctional proteins in traumatic brain injury.Tissue barriers · 2025Article
- Tight junction proteins in glial tumors development and progression.Frontiers in cellular neuroscience · 2025Review
- Developmental Cues and Molecular Drivers in Myelinogenesis: Revisiting Early Life to Re-Evaluate the Integrity of CNS Myelin.Current issues in molecular biology · 2022Review
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5 authors at 1 institution in 1 country.
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No grant is acknowledged in the PubMed record.
Abstract
objectivesLeukoaraiosis is described as white matter lesions that are associated with cognitive dysfunction, neurodegenerative disorders, etc. Myelin depletion is a salient pathological feature of, and the loss of oligodendrocytes is one of the most robust alterations evident in, white matter degeneration. Recent studies have revealed that claudin proteins are aberrantly expressed in leukoaraiosis and regulate oligodendrocyte activity. However, the roles of claudin-1 and claudin-3 in oligodendrocytes and leukoaraiosis are still not well-defined.
methodsQuantitative polymerase chain reaction was used to measure the expression of claudin-1 (CLDN1), claudin-3 (CLDN3), and myelinogenesis-related genes such as myelin basic protein (MBP), proteolipid protein (PLP), oligodendrocyte transcription factor 2 (OLIG2), and SRY-box transcription factor 10 (SOX10) in leukoaraiosis patients (n=122) and healthy controls (n=122). The expression of claudin-1 and claudin-3 was either ectopically silenced or augmented in Oli-neu oligodendrocytes, and colony formation, apoptosis, and migration assays were performed. Finally, the expression of myelin proteins was evaluated by western blotting.
resultsOur results revealed that in addition to SOX10, the expression levels of claudin-1, claudin-3, and myelinogenesis-related proteins were prominently downregulated in leukoaraiosis patients, compared to those in healthy controls. Furthermore, the growth and migration of Oli-neu cells were downregulated upon silencing claudin-1 or claudin-3. However, the overexpression of claudin-1 or claudin-3 resulted in the reduction of the degree of apoptosis in Oli-neu cells. In addition, claudin-1 and claudin-3 promoted the expression of MBP, OLIG2, PLP, and SOX10 at the translational level.
conclusionOur data has demonstrated that the abnormal expression of claudin-1 and claudin-3 regulates the pathological progression of leukoaraiosis by governing the viability and myelination of oligodendrocytes. These findings provide novel insights into the regulatory mechanisms underlying the roles of claudin-1 and claudin-3 in leukoaraiosis.
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