ArticleCellular and molecular neurobiology2016
A New Role Discovered for IGTP: The Protective Effect of IGTP in ICH-Induced Neuronal Apoptosis.
Article in Cellular and molecular neurobiology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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3 citing papers in PubMed, 6 citations in OpenAlex.
- AUF1 modulates cellular senescence in auditory hair cells by regulating the transcription and alternative splicing of immune response genes.Molecular biology reports · 2026Article
- Echinocystic acid provides a neuroprotective effect via the PI3K/AKT pathway in intracerebral haemorrhage mice.Annals of translational medicine · 2020Article
- OTUB1 attenuates neuronal apoptosis after intracerebral hemorrhage.Molecular and cellular biochemistry · 2016Article
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Authors and funding
10 authors at 2 institutions in 1 country.
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No grant is acknowledged in the PubMed record.
Abstract
Interferon gamma-induced GTPase (IGTP), which is also named Irgm3, has been widely described in regulating host resistance against intracellular pathogens. Previous researches have demonstrated that IGTP exerts beneficial function during coxsackievirus B3 (CVB3) infection. However, little information is available regarding the role of IGTP in central nervous system. Here, our study revealed that IGTP may have an essential role during ICH-induced neuronal apoptosis. We found the expression level of IGTP adjacent to hematoma was strongly increased after ICH, accompanied with the up-regulation of proliferating cell nuclear antigen (PCNA), active-caspase-3, p-GSK-3β, and Bax. IGTP was also observed to be co-localized with PCNA in astrocytes and active-caspase-3 in neurons, indicating its association with astrocyte proliferation and neuronal apoptosis after ICH. Finally, in vitro study, knocking down IGTP with IGTP-specific siRNA promoted active-caspase-3, p-GSK-3β, and Bax expression, and led to more severe neuronal apoptosis after ICH. All these results above suggested that IGTP might play a critical role in protecting neurons from apoptosis after ICH.
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