ArticleNeuroscience2017
Neuron-specific SUMO knockdown suppresses global gene expression response and worsens functional outcome after transient forebrain ischemia in mice.
Article in Neuroscience, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
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Who cites it
22 citing papers in PubMed, 39 citations in OpenAlex.
- Dysregulation of protein SUMOylation networks in Huntington's disease R6/2 mouse striatum.Brain : a journal of neurology · 2025Article
- Ischemic Stroke and the Biological Hallmarks of Aging.Aging and disease · 2024Review
- TXNIP/NLRP3 aggravates global cerebral ischemia-reperfusion injury-induced cognitive decline in mice.Heliyon · 2024Article
- Integrative Analysis of Machine Learning and Molecule Docking Simulations for Ischemic Stroke Diagnosis and Therapy.Molecules (Basel, Switzerland) · 2023Article
- SUMOtherapeutics for Ischemic Stroke.Pharmaceuticals (Basel, Switzerland) · 2023Review
- Gene expression profiles and bioinformatics analysis in lung samples from ovalbumin-induced asthmatic mice.BMC pulmonary medicine · 2023Article
- The role of SUMOylation in the neurovascular dysfunction after acquired brain injury.Frontiers in pharmacology · 2023Review
- RNA editing of ion channels and receptors in physiology and neurological disorders.Oxford open neuroscience · 2022Review
- The Function of SUMOylation and Its Critical Roles in Cardiovascular Diseases and Potential Clinical Implications.International journal of molecular sciences · 2021Review
- SUMO1 Deficiency Exacerbates Neurological and Cardiac Dysfunction after Intracerebral Hemorrhage in Aged Mice.Translational stroke research · 2021Article
- Small ubiquitin-like modifier 2 (SUMO2) is critical for memory processes in mice.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2020Article
- Guanosine modulates SUMO2/3-ylation in neurons and astrocytes via adenosine receptors.Purinergic signalling · 2020Article
- A Critical Role for ISGylation, Ubiquitination and, SUMOylation in Brain Damage: Implications for Neuroprotection.Neurochemical research · 2020Review
- Role of pericyte-derived SENP1 in neuronal injury after brain ischemia.CNS neuroscience & therapeutics · 2020Article
- Resilience to Injury: A New Approach to Neuroprotection?Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2020Review
- The Role of Ubiquitin-Proteasome Pathway and Autophagy-Lysosome Pathway in Cerebral Ischemia.Oxidative medicine and cellular longevity · 2020Review
- Impaired capacity to restore proteostasis in the aged brain after ischemia: Implications for translational brain ischemia research.Neurochemistry international · 2019Review
- Aging Is Associated With Impaired Activation of Protein Homeostasis-Related Pathways After Cardiac Arrest in Mice.Journal of the American Heart Association · 2018Article
- Ubc9 overexpression and SUMO1 deficiency blunt inflammation after intestinal ischemia/reperfusion.Laboratory investigation; a journal of technical methods and pathology · 2018Article
- Quantitative high-throughput screening identifies cytoprotective molecules that enhance SUMO conjugation via the inhibition of SUMO-specific protease (SENP)2.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2018Article
Corrections and comments
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Authors and funding
9 authors at 3 institutions in 2 countries.
Funding
Abstract
Small ubiquitin-like modifier (SUMO) conjugation (SUMOylation) plays key roles in neurologic function in health and disease. Neuronal SUMOylation is essential for emotionality and cognition, and this pathway is dramatically activated in post-ischemic neurons, a neuroprotective response to ischemia. It is also known from cell culture studies that SUMOylation modulates gene expression. However, it remains unknown how SUMOylation regulates neuronal gene expression in vivo, in the physiologic state and after ischemia, and modulates post-ischemic recovery of neurologic function. To address these important questions, we used a SUMO1-3 knockdown (SUMO-KD) mouse in which a Thy-1 promoter drives expression of 3 distinct microRNAs against SUMO1-3 to silence SUMO expression specifically in neurons. Wild-type and SUMO-KD mice were subjected to transient forebrain ischemia. Microarray analysis was performed in hippocampal CA1 samples, and neurologic function was evaluated. SUMOylation had opposite effects on neuronal gene expression before and after ischemia. In the physiological state, most genes regulated by SUMOylation were up-regulated in SUMO-KD compared to wild-type mice. Brain ischemia/reperfusion significantly modulated the expression levels of more than 400 genes in wild-type mice, with a majority of those genes upregulated. The extent of this post-ischemic transcriptome change was suppressed in SUMO-KD mice. Moreover, SUMO-KD mice exhibited significantly worse functional outcome. This suggests that suppression of global gene expression response in post-ischemic brain due to SUMO knockdown has a negative effect on post-ischemic neurologic function. Together, our data provide a basis for future studies to mechanistically link SUMOylation to neurologic function in health and disease.
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Registered trials
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