ArticleJournal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism2014
CR8, a novel inhibitor of CDK, limits microglial activation, astrocytosis, neuronal loss, and neurologic dysfunction after experimental traumatic brain injury.
Article in Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers.
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Who cites it
37 citing papers in PubMed, 72 citations in OpenAlex.
- Research progress of anticancer drugs targeting CDK12.RSC medicinal chemistry · 2023Review
- Repeat mild traumatic brain injuries (RmTBI) modify nociception and disrupt orexinergic connectivity within the descending pain pathway.The journal of headache and pain · 2023Article
- Molecular Glues: The Adhesive Connecting Targeted Protein Degradation to the Clinic.Biochemistry · 2023Review
- Article
- HOXA11-AS aggravates microglia-induced neuroinflammation after traumatic brain injury.Neural regeneration research · 2022Article
- Neuroprotective and Anti-inflammatory Effects of Pioglitazone on Traumatic Brain Injury.Mediators of inflammation · 2022Review
- Eye Movements in Mild Traumatic Brain Injury: Clinical Challenges.Journal of eye movement research · 2022Article
- Acute colitis during chronic experimental traumatic brain injury in mice induces dysautonomia and persistent extraintestinal, systemic, and CNS inflammation with exacerbated neurological deficits.Journal of neuroinflammation · 2021Article
- Review
- Down-regulation of cyclin D2 in amyloid β toxicity, inflammation, and Alzheimer's disease.PloS one · 2021Article
- CDK inhibitors in cancer therapy, an overview of recent development.American journal of cancer research · 2021Review
- Core cell cycle machinery is crucially involved in both life and death of post-mitotic neurons.Cellular and molecular life sciences : CMLS · 2020Review
- Dementia, Depression, and Associated Brain Inflammatory Mechanisms after Spinal Cord Injury.Cells · 2020Review
- Pharmacological Inhibition of Cyclin-Dependent Kinases Triggers Anti-Fibrotic Effects in Hepatic Stellate Cells In Vitro.International journal of molecular sciences · 2020Article
- Cell cycle activation contributes to isoflurane-induced neurotoxicity in the developing brain and the protective effect of CR8.CNS neuroscience & therapeutics · 2019Article
- Comparing effects of CDK inhibition and E2F1/2 ablation on neuronal cell death pathways in vitro and after traumatic brain injury.Cell death & disease · 2018Article
- MicroRNA-711-Induced Downregulation of Angiopoietin-1 Mediates Neuronal Cell Death.Journal of neurotrauma · 2018Article
- Elucidating opportunities and pitfalls in the treatment of experimental traumatic brain injury to optimize and facilitate clinical translation.Neuroscience and biobehavioral reviews · 2018Review
- Cell cycle inhibition reduces inflammatory responses, neuronal loss, and cognitive deficits induced by hypobaria exposure following traumatic brain injury.Journal of neuroinflammation · 2016Article
- Simulated Aeromedical Evacuation Exacerbates Experimental Brain Injury.Journal of neurotrauma · 2016Article
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
Central nervous system injury causes a marked increase in the expression of cell cycle-related proteins. In this study, we show that cell cycle activation (CCA) is detected in mature neurons at 24 hours after rat lateral fluid percussion (LFP)-induced traumatic brain injury (TBI), as reflected by increased expression of cyclin G1, phosphorylated retinoblastoma (phospho-Rb), E2F1 and proliferating cell nuclear antigen (PCNA). These changes were associated with progressive cortical, hippocampal, and thalamic neuronal loss and microglial and astrocyte activation. Notably, we detected 5-bromo-2'-deoxyuridine (BrdU)-positive neurons, microglia, and astrocytes at 7 days, but not at 24 hours, suggesting that cell cycle reaches the S phase in these cell types at the latter time point. A delayed systemic post-LFP administration at 3 hours of CR8--a potent second-generation cyclin-dependent kinase (CDK) inhibitor--reduced CCA; cortical, hippocampal, and thalamic neuronal loss; and cortical microglial and astrocyte activation. Furthermore, CR8 treatment attenuated sensorimotor and cognitive deficits, alleviated depressive-like symptoms, and decreased lesion volume. These findings underscore the contribution of CCA to progressive neurodegeneration and chronic neuroinflammation following TBI, and demonstrate the neuroprotective potential of cell cycle inhibition in a clinically relevant experimental TBI model.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.