ArticleInternational journal of molecular medicine2023
Potential mechanism of TMEM2/CD44 in endoplasmic reticulum stress‑induced neuronal apoptosis in a rat model of traumatic brain injury.
Article in International journal of molecular medicine, 2023. 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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Who cites it
9 citing papers in PubMed, 16 citations in OpenAlex.
- After Traumatic Brain Injury, EPHA4 Enhances Endoplasmic Reticulum Stress to Promote M1 Microglial Polarization Through the MAPK Signaling Pathway.Mediators of inflammation · 2026Article
- Expression of CD44 and Its Spliced Variants: Innate and Inducible Roles in Nervous Tissue Cells and Their Environment.International journal of molecular sciences · 2025Review
- Hyaluronidases as Targets for the Treatment of Neurological Diseases.Proteoglycan research · 2025Article
- Review
- Research developments in the neurovascular unit and the blood‑brain barrier (Review).Biomedical reports · 2025Review
- Aquaporin‑1 regulates microglial polarization and inflammatory response in traumatic brain injury.International journal of molecular medicine · 2025Article
- Corticosterone effects induced by stress and immunity and inflammation: mechanisms of communication.Frontiers in endocrinology · 2025Review
- Hepatotoxicity assessment of innovative nutritional supplements based on olive-oil formulations enriched with natural antioxidants.Frontiers in nutrition · 2024Article
- Enriched environment may improve secondary brain injury after traumatic brain injury by regulating the TLR2/NF-κB signaling pathway.Journal of central nervous system disease · 2024Article
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Authors and funding
8 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Traumatic brain injury (TBI) can lead to the disruption of endoplasmic reticulum (ER) homeostasis in neurons and induce ER stress. Transmembrane protein 2 (TMEM2) may regulate ER stress through the p38/ERK signaling pathway, independent of the classic unfolded protein response (UPR) pathway. The present study examined the expression of TMEM2 following TBI in a rat model, in an aim to determine whether the mitogen‑activated protein kinase (MAPK) signaling pathway is controlled by TMEM2/CD44 to mitigate secondary brain injury. For this purpose, 89 Sprague‑Dawley rats were used to establish the model of TBI, and TMEM2 siRNA was used to silence TMEM2. Western blot analysis, immunofluorescence, TUNEL assay and Fluoro‑Jade C staining, the wet‑dry method and behavioral scoring were used for analyses. The results revealed that TMEM2 was activated following TBI in rats. The silencing of TMEM2 resulted in a significant increase in the levels of p38 and ERK (components of MAPK signaling), while brain edema, neuronal apoptosis and degeneration were significantly aggravated. TBI increased TMEM2/CD44‑aggravated brain edema and neurological impairment, possibly by regulating ERK and p38 signaling. TMEM2/CD44 may thus be a target for the prevention and control of TBI.
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