The HIF-1/glial TIM-3 axis controls inflammation-associated brain damage under hypoxia
Open accessAbstract
Inflammation is closely related to the extent of damage following cerebral ischaemia, and the targeting of this inflammation has emerged as a promising therapeutic strategy. Here, we present that hypoxia-induced glial T-cell immunoglobulin and mucin domain protein (TIM)-3 can function as a modulator that links inflammation and subsequent brain damage after ischaemia. We find that TIM-3 is highly expressed in hypoxic brain regions of a mouse cerebral hypoxia-ischaemia (H/I) model. TIM-3 is distinctively upregulated in activated microglia and astrocytes, brain resident immune cells, in a hypoxia-inducible factor (HIF)-1-dependent manner. Notably, blockade of TIM-3 markedly reduces infarct size, neuronal cell death, oedema formation and neutrophil infiltration in H/I mice. Hypoxia-triggered neutrophil migration and infarction are also decreased in HIF-1α-deficient mice. Moreover, functional neurological deficits after H/I are significantly improved in both anti-TIM-3-treated mice and myeloid-specific HIF-1α-deficient mice. Further understanding of these insights could serve as the basis for broadening the therapeutic scope against hypoxia-associated brain diseases.
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B7H4 and TIM3 mRNA showed hypoxia-induced expression in vehicle-treated but not in 32-134D-treated Hepa1-6 cells (P < 0.05).
“B7H4 and TIM3 mRNA, which are encoded by the Vtcn1 and Havcr2 genes, respectively, and like PDL1, encode immune checkpoint receptors that are HIF regulated (51, 52) and associated with patient mortality in HCC (53), showed hypoxia-induced expression in vehicle-treated but not in 32-134D–treated cells (P < 0.05; Figure 3B).”
From HIF inhibitor 32-134D eradicates murine hepatocellular carcinoma in combination with anti-PD1 therapy (2022) · cites this paper as [52]
The Results section, “TIM-3 is elevated in a HIF-1-dependent manner under hypoxia” (page unavailable), reports increased TIM-3 transcripts under hypoxia and HIF-1-dependent regulation in glial cells. It does not report B7H4 expression or the vehicle-versus-32-134D result in Hepa1-6 cells. In the citing sentence, the citations accompany the HIF-regulation background statement; Figure 3B accompanies the cell-treatment result. (LLM, conf=0.88)
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Self-citation
- Authors
- Koh, H. S., Chang, C. Y., Jeon, S.-B., Yoon, H. J., Ahn, Y.-H., Kim, H.-S., Kim, I.-H., Jeon, S. H., Johnson, R. S., & Park, E. J.
- Affiliations
- Hallym University (KR)
- National Cancer Center (KR)
- University of Cambridge (GB)
- Corresponding author
- Park, Eun Jung
- ORCID
- Venue
- Nature Communications
- Published
- 2015-03-20
- Volume
- 6
- Issue
- 1
- Pages
- 6340-6340
- ISSN
- 2041-1723 (ISSN-L)
- PMC
- PMC4383004
- OpenAlex
- W2005158904
- Cited by
- 141
- References
- 69
- Citations by year
- 2026: 13 · 2025: 8 · 2024: 12 · 2023: 13 · 2022: 20 · 2021: 17 · 2020: 12 · 2019: 14 · 2018: 15 · 2017: 9 · 2016: 5 · 2015: 3
- FWCI
- 5.70
- Type
- journal article
- Language
- en
- Open access
- gold
- doi.org
- Locations
- Nature Communications (publishedVersion, cc-by)
- Europe PMC (PubMed Central) (publishedVersion, cc-by)
- PubMed Central (publishedVersion, cc-by)
- PubMed (publishedVersion)
- Apollo (University of Cambridge) (submittedVersion, cc-by)
- RePEc: Research Papers in Economics (submittedVersion)
- Apollo (cc-by)
- Funders
- Wellcome Trust (092738/Z/10/Z)
- National Research Foundation
- National Research Foundation of Korea
- Topics
- Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
- Life Sciences › Neuroscience › Neurology › Neurological Disease Mechanisms and Treatments
- Health Sciences › Medicine › Pediatrics, Perinatology and Child Health › Neonatal and fetal brain pathology
- Keywords
- TIM-3, HIF-1α, neuroinflammation, microglia, astrocytes, neutrophil infiltration, infarct size, brain oedema, neuronal cell death, myeloid cells, hypoxia
- MeSH terms
- Hepatitis A Virus Cellular Receptor 2, Animals, Astrocytes, Brain, Cell Movement, Cells, Cultured, Immunohistochemistry, Inflammation, Ligation, Magnetic Resonance Imaging, Mesencephalon, Neuroglia, Neutrophils, Receptors, Virus, RNA, Messenger, Carotid Artery, Common, Microglia, Reverse Transcriptase Polymerase Chain Reaction, Hypoxia-Ischemia, Brain, Mice, Hypoxia-Inducible Factor 1, alpha Subunit, In Vitro Techniques
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