دورية أكاديمية
أعرض في EDS

Traumatic brain injury results in unique microglial and astrocyte transcriptomes enriched for type I interferon response.

التفاصيل البيبلوغرافية
العنوان: Traumatic brain injury results in unique microglial and astrocyte transcriptomes enriched for type I interferon response.
المؤلفون: Todd BP; Medical Scientist Training Program, University of Iowa, Iowa City, IA, USA., Chimenti MS; Iowa Institute of Human Genetics, Bioinformatics Division, University of Iowa, Iowa City, IA, USA., Luo Z; Department of Pediatrics, University of Iowa, Iowa City, IA, USA., Ferguson PJ; Department of Pediatrics, University of Iowa, Iowa City, IA, USA., Bassuk AG; Department of Pediatrics, University of Iowa, Iowa City, IA, USA. alexander-bassuk@uiowa.edu., Newell EA; Department of Pediatrics, University of Iowa, Iowa City, IA, USA. elizabeth-newell@uiowa.edu.
المصدر: Journal of neuroinflammation [J Neuroinflammation] 2021 Jul 05; Vol. 18 (1), pp. 151. Date of Electronic Publication: 2021 Jul 05.
نوع المنشور: Journal Article
اللغة: English
بيانات الدورية: Publisher: BioMed Central Country of Publication: England NLM ID: 101222974 Publication Model: Electronic Cited Medium: Internet ISSN: 1742-2094 (Electronic) Linking ISSN: 17422094 NLM ISO Abbreviation: J Neuroinflammation Subsets: MEDLINE
أسماء مطبوعة: Original Publication: [London] : BioMed Central, c2004-
مواضيع طبية MeSH: Astrocytes/*metabolism , Brain Injuries, Traumatic/*metabolism , Interferon Type I/*biosynthesis , Microglia/*metabolism , Transcriptome/*physiology, Animals ; Astrocytes/pathology ; Brain Injuries, Traumatic/genetics ; Brain Injuries, Traumatic/pathology ; Interferon Type I/genetics ; Male ; Mice ; Mice, Inbred C57BL ; Microglia/pathology
مستخلص: Background: Traumatic brain injury (TBI) is a leading cause of death and disability that lacks neuroprotective therapies. Following a TBI, secondary injury response pathways are activated and contribute to ongoing neurodegeneration. Microglia and astrocytes are critical neuroimmune modulators with early and persistent reactivity following a TBI. Although histologic glial reactivity is well established, a precise understanding of microglia and astrocyte function following trauma remains unknown.
Methods: Adult male C57BL/6J mice underwent either fluid percussion or sham injury. RNA sequencing of concurrently isolated microglia and astrocytes was conducted 7 days post-injury to evaluate cell-type-specific transcriptional responses to TBI. Dual in situ hybridization and immunofluorescence were used to validate the TBI-induced gene expression changes in microglia and astrocytes and to identify spatial orientation of cells expressing these genes. Comparative analysis was performed between our glial transcriptomes and those from prior reports in mild TBI and other neurologic diseases to determine if severe TBI induces unique states of microglial and astrocyte activation.
Results: Our findings revealed sustained, lineage-specific transcriptional changes in both microglia and astrocytes, with microglia showing a greater transcriptional response than astrocytes at this subacute time point. Microglia and astrocytes showed overlapping enrichment for genes related to type I interferon signaling and MHC class I antigen presentation. The microglia and astrocyte transcriptional response to severe TBI was distinct from prior reports in mild TBI and other neurodegenerative and neuroinflammatory diseases.
Conclusion: Concurrent lineage-specific analysis revealed novel TBI-specific transcriptional changes; these findings highlight the importance of cell-type-specific analysis of glial reactivity following TBI and may assist with the identification of novel, targeted therapies.
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معلومات مُعتمدة: K08 NS110829 United States NS NINDS NIH HHS; R01NS098590 United States NH NIH HHS; R01AR059730 United States NH NIH HHS; T32 GM139776 United States GM NIGMS NIH HHS; R01 NS098590 United States NS NINDS NIH HHS; T32 GM007337 United States GM NIGMS NIH HHS; K08NS110829 United States NS NINDS NIH HHS
فهرسة مساهمة: Keywords: Astrocytes; Microglia; Traumatic brain injury; Type I interferon
المشرفين على المادة: 0 (Interferon Type I)
تواريخ الأحداث: Date Created: 20210706 Date Completed: 20211216 Latest Revision: 20220716
رمز التحديث: 20231215
مُعرف محوري في PubMed: PMC8259035
DOI: 10.1186/s12974-021-02197-w
PMID: 34225752
قاعدة البيانات: MEDLINE
الوصف
تدمد:1742-2094
DOI:10.1186/s12974-021-02197-w