ArticleNeurochemical research2017
Upregulated Expression of TRIM32 Is Involved in Schwann Cell Differentiation, Migration and Neurite Outgrowth After Sciatic Nerve Crush.
Article in Neurochemical research, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed, 10 citations in OpenAlex.
- TRIM32 Inhibits NEK7 Ubiquitylation-Dependent Microglia Pyroptosis After Spinal Cord Injury.Molecular biotechnology · 2025Article
- Whole Exome Sequencing Study Identifies Novel Rare Risk Variants for Habitual Coffee Consumption Involved in Olfactory Receptor and Hyperphagia.Nutrients · 2022Article
- Knockdown of TRIM32 Protects Hippocampal Neurons from Oxygen-Glucose Deprivation-Induced Injury.Neurochemical research · 2019Article
- TRIM32 affects the recovery of motor function following spinal cord injury through regulating proliferation of glia.Oncotarget · 2017Article
- Global proteomics of Ubqln2-based murine models of ALS.The Journal of biological chemistryArticle
Corrections and comments
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Authors and funding
10 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Tripartite motif containing 32 (TRIM32), a member of the tripartite motif (TRIM) family, plays an indispensable role in myoblast proliferation. It also regulates neuron and skeletal muscle stem cell differentiation. Although it is of great importance, we know little about the roles of TRIM32 during peripheral nervous system injury. Here, we examined the dynamic changes of TRIM32 in acute sciatic nerve crush (SNC) model. After crush, TRIM32 rapidly increased and reached the climax at 1 week but then gradually declined to the normal level at 4 weeks post-injury. Meanwhile, we observed similar changes of Oct-6. What is more, we found co-localization of TRIM32 with S100 and Oct-6 in 1-week-injured tissues using double immunofluorescent staining. In further vitro experiments, enhancive expression of TRIM32 was detected during the process of cyclic adenosine monophosphate (cAMP)-induced Schwann cell differentiation and nerve growth factor (NGF)-induced PC12 cell neurite outgrowth. More interestingly, specific si-TRIM32-transfected RSC96 cells exhibited obvious reduction in the ability of migration. Taken together, we inferred that upregulated TRIM32 was not only involved in the differentiation and migration of Schwann cells but the neurite elongation after SNC.
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