ArticleCell communication and signaling : CCS2019
Inhibition of T cell immunoglobulin and mucin-1 (TIM-1) protects against cerebral ischemia-reperfusion injury.
Article in Cell communication and signaling : CCS, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed, 19 citations in OpenAlex.
- A novel plasma proteomic signature predicts long-term incident heart failure risk among persons living with HIV.medRxiv : the preprint server for health sciences · 2026Article
- The effect of TIM1Cell death discovery · 2025Article
- The effect of TIM1Cell death & disease · 2025Article
- From acute tubular injury to tubular repair and chronic kidney diseases - KIM-1 as a promising biomarker for predicting renal tubular pathology.Current research in physiology · 2025Review
- Senescent Schwann cells induced by aging and chronic denervation impair axonal regeneration following peripheral nerve injury.EMBO molecular medicine · 2023Article
- Didymin Alleviates Cerebral Ischemia-Reperfusion Injury by Activating the PPAR Signaling Pathway.Yonsei medical journal · 2022Article
- miR-142 Targets TIM-1 in Human Endothelial Cells: Potential Implications for Stroke, COVID-19, Zika, Ebola, Dengue, and Other Viral Infections.International journal of molecular sciences · 2022Article
- Blockage of miR-485-5p on Cortical Neuronal Apoptosis Induced by Oxygen and Glucose Deprivation/Reoxygenation Through Inactivating MAPK Pathway.Neuromolecular medicine · 2021Article
- Tim-1 alleviates lupus nephritis-induced podocyte injury via regulating autophagy.Central-European journal of immunology · 2021Article
- Comprehensive Analysis of the Expression, Relationship to Immune Infiltration and Prognosis of TIM-1 in Cancer.Frontiers in oncology · 2020Article
- Histone Methylation Inhibitor DZNep Ameliorated the Renal Ischemia-Reperfusion InjuryFrontiers in medicine · 2020Article
- Correction to: Inhibition of T cell immunoglobulin and mucin-1 (TIM-1) protects against cerebral ischemia-reperfusion injury.Cell communication and signaling : CCS · 2019Article
Corrections and comments
- Erratum issued
Authors and funding
8 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundThe T cell Ig domain and mucin domain (TIM)-1 protein expressed on the surface of Th2 cells regulates the immune response by modulating cytokine production. The present study aimed to investigate the role and possible mechanism of TIM-1 in cerebral ischemia-reperfusion injury.
methodsWestern blot was used to detect TIM-1 and apoptosis-related protein expression, whereas TIM-1 mRNA was examined using quantitative real-time reverse transcription PCR. Flow cytometry and a TdT-mediated biotin-16-dUTP nick-end labeling (TUNEL) assay were used to detect the percentage of apoptotic cells and a pathological examination was performed. The migration of neutrophils and macrophages was analyzed by immunohistochemistry.
resultsOur results suggest that TIM-1 expression was transiently increased 24 h or 48 h following middle cerebral artery occlusion (MCAO)/reperfusion. The infarct size was markedly increased in MCAO, whereas treatment with a TIM-1-blocking mAb could reduce the infarct size. TIM-1 blocking mAb effectively reduced the number of neutrophils, macrophage functionality, cytokine (i.e., IL-6, IL-1β, and TNF-α) and chemokine (i.e., CXCL-1 and CXCL-2) production in the brain tissue. The effect of in vitro T cell damage on neurons was significantly reduced following treatment with a TIM-1 blocking mAb or the knockdown of TIM-1 in co-cultured T cells and neurons.
conclusionTake together, these results indicated that TIM-1 blockade ameliorated cerebral ischemia-reperfusion injury. Thus, TIM-1 disruption may serve as a novel target for therapy following MCAO.
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