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Gyorgy, B.

Publications and source records attributed to Gyorgy, B..

2 recordsLinked to original sources

Proliferative Capacity and Neural Lineage Commitment of Muller Glia in the Adult Human Retina

BackgroundThe mammalian retina lacks meaningful regenerative capacity, and degeneration usually leads to irreversible vision loss. Although lower vertebrates regenerate retinal neurons through Muller glia, this capacity has generally been considered absent in humans. This study investigated whether defined humoral cues alone are sufficient to unlock a latent neurogenic program in human Muller cells. MethodsLong-term organotypic retinal cultures were established from 39 adult donors. Cultures were treated with FGF-2 and GSK-3 inhibition to assess proliferation across the peripheral and central retina. Cellular responses were evaluated using single-cell transcriptomics and immunohistochemistry. ResultsFGF-2 treatment and GSK-3 inhibition induced robust proliferation across both peripheral and central retina, with 79.09 {+/-} 6.32% of dividing cells identified as Muller glia, some completing multiple cell cycles. Single-cell transcriptomics revealed activation of progenitor-like and neuronal differentiation pathways, whereas immunohistochemistry demonstrated expression of early and late neuronal markers spanning all major retinal lineages. Newly generated cells expressed markers of cone, rod, bipolar, horizontal, amacrine, and ganglion cell identities, together with evidence of early synaptogenesis. ConclusionsThese findings reveal an intrinsic regenerative potential in adult human Muller glia and show that defined humoral cues can activate a latent neurogenic program in these cells. This may have implications for future vision-restoration strategies in degenerative retinal disease.

neuroscience↗

TCF12 controls oligodendroglial cell proliferation and regulates signaling pathways conserved in gliomas

Diffuse gliomas are primary brain tumors originating from the transformation of glial cells. In particular, oligodendrocyte precursor cells constitute the major tumor-amplifying population in the gliomagenic process. We previously identified the TCF12 gene, encoding a transcription factor of the E protein family, as being recurrently mutated in oligodendrogliomas. In this study, we sought to understand the function of TCF12 in oligodendroglial cells, the glioma lineage of origin. We first describe TCF12 mRNA and protein expression pattern in oligodendroglial development in the mouse brain. Second, by TCF12 genome wide chromatin profiling in oligodendroglial cells, we show that TCF12 binds active promoters of genes involved in proliferation, translation/ribosomes, and pathways involved in oligodendrocyte development and cancer. Finally, we perform OPC-specific Tcf12 inactivation in vivo and demonstrate by immunofluorescence and transcriptomic analyses that TCF12 is transiently required for OPC proliferation but dispensable for oligodendrocyte differentiation. We further show that Tcf12 inactivation results in deregulation of biological processes that are also altered in oligodendrogliomas. Together, our data suggest that TCF12 directly regulates transcriptional programs in oligodendroglia development that are relevant in a glioma context.

neuroscience↗