{"title":"MiRNA-Mediated Regulation of S100B: A Review.","authors":"Animesh Dali, Suhana Basnyat, Rachel Delancey, Nipun Chopra","doi":"10.3390/neurosci6030075","DOIUrl":null,"url":null,"abstract":"<p><p>S100β is a significant signaling molecule and biomarker that is primarily expressed in the brain. At low physiological concentrations, S100β induces astrocyte maturation, microglial migration, and neural proliferation. However, high concentrations activate inflammatory and pro-apoptotic pathways. Due to this dual role, increased research is being invested into the role of S100β in neuronal homeostasis and inflammation. In fact, increased S100β expression is seen in many neuropathologies including Alzheimer's disease, Parkinson's disease, cerebral ischemia, and traumatic brain injury. High S100β is generally associated with worsened disease outcome. Here, we provide an overview of the structure and role of S100β in various pathways, particularly in the context of neurological disorders. Modulation of S100β levels also holds promise as a therapeutic strategy. Micro-RNAs (miRNA) post-transcriptionally regulate gene expression and provide a novel approach reduce excess S100β protein. However, much of this research is still in its infancy. We outline current studies identifying miRNA in human and animal models of various neurological disorders. S100β itself has several predicted miRNA interactions although most have not yet been directly validated. Together, we compile the literature identifying S100β and miRNAs to guide future research in this field. We also comment on the feasibility and future uses of miRNA for pharmaceutical regulation of S100β, particularly for neurological treatments.</p>","PeriodicalId":74294,"journal":{"name":"NeuroSci","volume":"6 3","pages":""},"PeriodicalIF":2.0000,"publicationDate":"2025-08-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12371975/pdf/","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"NeuroSci","FirstCategoryId":"1085","ListUrlMain":"https://doi.org/10.3390/neurosci6030075","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q3","JCRName":"CLINICAL NEUROLOGY","Score":null,"Total":0}
引用次数: 0
Abstract
S100β is a significant signaling molecule and biomarker that is primarily expressed in the brain. At low physiological concentrations, S100β induces astrocyte maturation, microglial migration, and neural proliferation. However, high concentrations activate inflammatory and pro-apoptotic pathways. Due to this dual role, increased research is being invested into the role of S100β in neuronal homeostasis and inflammation. In fact, increased S100β expression is seen in many neuropathologies including Alzheimer's disease, Parkinson's disease, cerebral ischemia, and traumatic brain injury. High S100β is generally associated with worsened disease outcome. Here, we provide an overview of the structure and role of S100β in various pathways, particularly in the context of neurological disorders. Modulation of S100β levels also holds promise as a therapeutic strategy. Micro-RNAs (miRNA) post-transcriptionally regulate gene expression and provide a novel approach reduce excess S100β protein. However, much of this research is still in its infancy. We outline current studies identifying miRNA in human and animal models of various neurological disorders. S100β itself has several predicted miRNA interactions although most have not yet been directly validated. Together, we compile the literature identifying S100β and miRNAs to guide future research in this field. We also comment on the feasibility and future uses of miRNA for pharmaceutical regulation of S100β, particularly for neurological treatments.