ArticleJournal of molecular neuroscience : MN2013
Müller glia cells activation in rat retina after optic nerve injury: spatiotemporal correlation with transcription initiation factor IIb.
Article in Journal of molecular neuroscience : MN, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed, 9 citations in OpenAlex.
- ABioMed research international · 2020Article
- Spatiotemporal Expression Changes of PACAP and Its Receptors in Retinal Ganglion Cells After Optic Nerve Crush.Journal of molecular neuroscience : MN · 2019Article
- Apobec1 Promotes Neurotoxicity-Induced Dedifferentiation of Müller Glial Cells.Neurochemical research · 2017Article
- Upregulation of SYF2 Relates to Retinal Ganglion Cell Apoptosis and Retinal Glia Cell Proliferation After Light-Induced Retinal Damage.Journal of molecular neuroscience : MN · 2015Article
- The expression changes of myelin and lymphocyte protein (MAL) following optic nerve crush in adult rats retinal ganglion cells.Journal of molecular neuroscience : MN · 2014Article
- A new paradigm for transcription factor TFIIB functionality.Scientific reports · 2014Article
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Authors and funding
11 authors at 4 institutions in 1 country.
Funding
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Abstract
Transcription initiation factor IIB (TFIIB) is an ideal factor to localize core promoters and plays a central role in the assembly of the pre-initiation complex. Previous studies showed that the assembly of TFIIB played an important role in rat ischemic brain injury. To elucidate the expression and possible functions of TFIIB in retina lesion and repair, we performed an optic nerve crush (ONC) model in adult rats. Western blot analysis and immunohistochemistry showed a significant upregulation of TFIIB in retina after ONC. Immunofluorescent labeling indicated that TFIIB was localized mainly in the Müller glia cells (MGCs); colocalization of TFIIB and proliferating cell nuclear antigen (PCNA) in the injured retina suggested that TFIIB might participate in MGCs proliferation. In addition, we also examined the expression of the retinal progenitor markers (Nestin and Pax6) whose changes were correlated with the expression of TFIIB. In vitro, we induced MGCs differentiation with brain nerve growth factor (BNGF) and found that TFIIB expression was increased in the differentiated process, which was collected with the expression of PCNA, Nestin, and Pax6. Additionally, knocking TFIIB down with siRNA inhibited the expression of PCNA, Nestin, and Pax6. Collectively, we hypothesized ONC-induced upregulation of TFIIB in the retina was associated with MGCs activation and differentiation.
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