ArticleTranslational stroke research2021
Protective Effects of ShcA Protein Silencing for Photothrombotic Cerebral Infarction.
Article in Translational stroke research, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed, 21 citations in OpenAlex.
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- Pharmacological Inhibition of LRRK2 Exhibits Neuroprotective Activity in Mouse Photothrombotic Stroke Model.Experimental neurobiology · 2024Article
- Role of Estrogen-Related Receptor γ and PGC-1α/SIRT3 Pathway in Early Brain Injury After Subarachnoid Hemorrhage.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2023Article
- Targeting neuronal mitophagy in ischemic stroke: an update.Burns & trauma · 2023Review
- AMPK/MFF Activation: Role in Mitochondrial Fission and Mitophagy in Dry Eye.Investigative ophthalmology & visual science · 2022Article
- Pan-Cancer Study of SHC-Adaptor Protein 1 (SHC1) as a Diagnostic, Prognostic and Immunological Biomarker in Human Cancer.Frontiers in genetics · 2022Article
- Perampanel Reduces Brain Damage via Induction of M2 Microglia in a Neonatal Rat Stroke Model.International journal of nanomedicine · 2022Article
- Mitochondrial Quality Control: A Pathophysiological Mechanism and Therapeutic Target for Stroke.Frontiers in molecular neuroscience · 2021Review
- Mitochondrial Dynamics: A Potential Therapeutic Target for Ischemic Stroke.Frontiers in aging neuroscience · 2021Review
Corrections and comments
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Authors and funding
10 authors at 1 institution in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Reactive oxygen species (ROS) exacerbate stroke-induced cell damage. We found that ShcA, a protein that regulates ROS, is highly expressed in a Rose Bengal photothrombosis model. We investigated whether ShcA is essential for mitophagy in ROS-induced cellular damage and determined whether ROS exacerbate mitochondrial dysfunction via ShcA protein expression. Ischemic stroke was generated by Rose Bengal photothrombosis in mice. To silence ShcA protein expression in the mouse brain, ShcA-targeting siRNA-encapsulated nanoparticles were intrathecally injected into the cisterna magna. Upon staining with antibodies against ShcA counterpart caspase-3 or NeuN, we found that the ShcA protein expression was increased in apoptotic neurons. In addition, mitochondrial dysfunction and excessive mitophagy were evident in photothrombotic stroke tissue. Infarct volumes were significantly reduced, and neurological deficits were diminished in the ShcA siRNA nanoparticle-treated group, compared with the negative control siRNA nanoparticle-treated group. We confirmed that the reduction of ShcA expression by nanoparticle treatment rescued the expression of genes, associated with mitochondrial dynamics and mitophagy mediation in a stroke model. This study suggests that the regulation of ShcA protein expression can be a therapeutic target for reducing brain damage with mitochondrial dysfunction caused by thrombotic infarction.
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