ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2012
Rit GTPase signaling promotes immature hippocampal neuronal survival.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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Who cites it
19 citing papers in PubMed, 28 citations in OpenAlex.
- Mechanism by which low-intensity focused ultrasound promotes angiogenesis and neurogenesis after traumatic brain injury in a rat model via the OXA/MAPK signaling pathway.Neural regeneration research · 2026Article
- Genetic backgrounds and genotype-phenotype relationships in anthropometric parameters of 116 Japanese individuals with Noonan syndrome.Clinical pediatric endocrinology : case reports and clinical investigations : official journal of the Japanese Society for Pediatric Endocrinology · 2024Article
- Article
- Multiomic characterization of oncogenic signaling mediated by wild-type and mutant RIT1.Science signaling · 2021Article
- The molecular functions of RIT1 and its contribution to human disease.The Biochemical journal · 2020Review
- The potential oncogenic role of the RAS-like GTP-binding gene RIT1 in glioblastoma.Cancer biomarkers : section A of Disease markers · 2020Article
- Small GTPase RIT1 in Mouse Retina; Cellular and Functional Analysis.Current eye research · 2018Article
- Central Infusion of Insulin-Like Growth Factor-1 Increases Hippocampal Neurogenesis and Improves Neurobehavioral Function after Traumatic Brain Injury.Journal of neurotrauma · 2018Article
- IGF-1 mediated Neurogenesis Involves a Novel RIT1/Akt/Sox2 Cascade.Scientific reports · 2017Article
- RIT1 GTPase Regulates Sox2 Transcriptional Activity and Hippocampal Neurogenesis.The Journal of biological chemistry · 2017Article
- Mutations in RIT1 cause Noonan syndrome with possible juvenile myelomonocytic leukemia but are not involved in acute lymphoblastic leukemia.European journal of human genetics : EJHG · 2016Article
- A Compact Blast-Induced Traumatic Brain Injury Model in Mice.Journal of neuropathology and experimental neurology · 2016Article
- Neurogenesis in the Hippocampus of Patients with Temporal Lobe Epilepsy.Current neurology and neuroscience reports · 2016Review
- Article
- Chronic Histopathological and Behavioral Outcomes of Experimental Traumatic Brain Injury in Adult Male Animals.Journal of neurotrauma · 2015Review
- Conditional overexpression of insulin-like growth factor-1 enhances hippocampal neurogenesis and restores immature neuron dendritic processes after traumatic brain injury.Journal of neuropathology and experimental neurology · 2014Article
- Traumatic brain injury using mouse models.Translational stroke research · 2014Review
- Rit subfamily small GTPases: regulators in neuronal differentiation and survival.Cellular signalling · 2013Review
- Rit GTPase regulates a p38 MAPK-dependent neuronal survival pathway.Neuroscience letters · 2012Article
Corrections and comments
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
Abstract
The molecular mechanisms governing the spontaneous recovery seen following brain injury remain elusive, but recent studies indicate that injury-induced stimulation of hippocampal neurogenesis contributes to the repair process. The therapeutic potential of endogenous neurogenesis is tempered by the demonstration that traumatic brain injury (TBI) results in the selective death of adult-born immature neurons, compromising the cell population poised to compensate for trauma-induced neuronal loss. Here, we identify the Ras-related GTPase, Rit, as a critical player in the survival of immature hippocampal neurons following brain injury. While Rit knock-out (Rit(-/-)) did not alter hippocampal development, hippocampal neural cultures derived from Rit(-/-) mice display increased cell death and blunted MAPK cascade activation in response to oxidative stress, without affecting BDNF-dependent signaling. When compared with wild-type hippocampal cultures, Rit loss rendered immature (Dcx(+)) neurons susceptible to oxidative damage, without altering the survival of neural progenitor (Nestin(+)) cells. Oxidative stress is a major contributor to neuronal cell death following brain injury. Consistent with the enhanced vulnerability of cultured Rit(-/-) immature neurons, Rit(-/-) mice exhibited a significantly greater loss of adult-born immature neurons within the dentate gyrus after TBI. In addition, post-TBI neuronal remodeling was blunted. Together, these data identify a new and unexpected role for Rit in injury-induced neurogenesis, functioning as a selective survival mechanism for immature hippocampal neurons within the subgranular zone of the dentate gyrus following TBI.
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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.