ArticleEMBO molecular medicine2013
Role of stress-inducible protein-1 in recruitment of bone marrow derived cells into the ischemic brains.
Article in EMBO molecular medicine, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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Who cites it
18 citing papers in PubMed, 22 citations in OpenAlex.
- Role of HIF-1α-Activated IL-22/IL-22R1/Bmi1 Signaling Modulates the Self-Renewal of Cardiac Stem Cells in Acute Myocardial Ischemia.Stem cell reviews and reports · 2024Article
- Role of STAT3-FOXO3 Signaling in the Modulation of Neuroplasticity by PD-L1-HGF-Decorated Mesenchymal Stem Cell-Derived Exosomes in a Murine Stroke Model.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2024Article
- Astrocyte-Derived Extracellular Vesicles for Ischemic Stroke: Therapeutic Potential and Prospective.Aging and disease · 2024Review
- Stem cell-nanomedicine system as a theranostic bio-gadolinium agent for targeted neutron capture cancer therapy.Nature communications · 2023Article
- Genetic and Pharmacological Inhibition of Astrocytic Mysm1 Alleviates Depressive-Like Disorders by Promoting ATP Production.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2022Article
- The Hsp70-Hsp90 go-between Hop/Stip1/Sti1 is a proteostatic switch and may be a drug target in cancer and neurodegeneration.Cellular and molecular life sciences : CMLS · 2021Review
- Stress-induced phosphoprotein 1 restrains spinal cord ischaemia-reperfusion injury by modulating NF-κB signalling.Journal of cellular and molecular medicine · 2021Article
- Show Me Your Friends and I Tell You Who You Are: The Many Facets of Prion Protein in Stroke.Cells · 2020Review
- Potential role of CBX7 in regulating pluripotency of adult human pluripotent-like olfactory stem cells in stroke model.Cell death & disease · 2018Article
- Mechanisms of neuroprotection against ischemic insult by stress-inducible phosphoprotein-1/prion protein complex.Journal of neurochemistry · 2018Article
- The Hsp70/Hsp90 Chaperone Machinery in Neurodegenerative Diseases.Frontiers in neuroscience · 2017Review
- Article
- Cellular prion protein promotes post-ischemic neuronal survival, angioneurogenesis and enhances neural progenitor cell homing via proteasome inhibition.Cell death & disease · 2015Article
- Hyperactivity and attention deficits in mice with decreased levels of stress-inducible phosphoprotein 1 (STIP1).Disease models & mechanisms · 2015Article
- Cellular prion protein (PrP(C)) and its role in stress responses.International journal of clinical and experimental medicine · 2015Article
- The Cellular Prion Protein: A Player in Immunological Quiescence.Frontiers in immunology · 2015Review
- Exercise training enhanced SIRT1 longevity signaling replaces the IGF1 survival pathway to attenuate aging-induced rat heart apoptosis.Age (Dordrecht, Netherlands) · 2014Article
- Dynamic regulatory network reconstruction for Alzheimer's disease based on matrix decomposition techniques.Computational and mathematical methods in medicine · 2014Article
Corrections and comments
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Authors and funding
11 authors at 5 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Stress-inducible protein-1 (STI-1) is the proposed ligand for the cellular prion protein (PrP(C) ), which is thought to facilitate recovery following stroke. Whether STI-1 expression is affected by stroke and how its signalling facilitates recovery remain elusive. Brain slices from patients that died of ischemic stroke were collected for STI-1 immunohistochemistry. These findings were compared to results from cell cultures, mice with or without the PrP(C) knockout, and rats. Based on these findings, molecular and pharmacological interventions were administered to investigate the underlying mechanisms and to test the possibility for therapy in experimental stroke models. STI-1 was upregulated in the ischemic brains from humans and rodents. The increase in STI-1 expression in vivo was not cell-type specific, as it was found in neurons, glia and endothelial cells. Likewise, this increase in STI-1 expression can be mimicked by sublethal hypoxia in primary cortical cultures (PCCs) in vitro, and appear to have resulted from the direct binding of the hypoxia inducible factor-1α (HIF-1α) to the STI-1 promoter. Importantly, this STI-1 signalling promoted bone marrow derived cells (BMDCs) proliferation and migration in vitro and recruitment to the ischemic brain in vivo, and augmenting its signalling facilitated neurological recovery in part by recruiting BMDCs to the ischemic brain. Our results thus identified a novel mechanism by which ischemic insults can trigger a self-protective mechanism to facilitate recovery.
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