穆勒胶质细胞
小胶质细胞
转录组
生物
斑马鱼
细胞生物学
视网膜再生
再生(生物学)
视网膜
细胞分裂
祖细胞
细胞
视网膜
细胞生长
神经胶质
神经科学
细胞命运测定
视网膜色素上皮
祖细胞
电池类型
细胞分化
基因表达
核糖核酸
干细胞
基因表达调控
基因
神经发生
机制(生物学)
作者
Soumitra Mitra,Sulochana Devi,Mi‐Sun Lee,Aresh Sahu,Jonathan Jui,Emil Kriukov,Petr Baranov,Daniel Goldman
标识
DOI:10.1073/pnas.2535044123
摘要
In the zebrafish retina, Müller glia (MG) respond to retinal injury by dividing and producing a multipotent progenitor for retinal repair. This cell division is regulated by microglia; however, the underlying mechanism remains unknown. Here, we report that MG-derived Il34 attracts microglia to sites of retinal injury where they stimulate MG proliferation via the release of cytokines, like M17, Spp1, Tnfa, and Tnfb. Remarkably, RNA sequencing analysis of MG's regeneration-associated transcriptome with and without microglia depletion suggests microglia stimulate MG proliferation by preferentially enhancing the expression of regeneration-associated genes involved in cell division-related processes. In contrast, genetic ablation of essentially all microglia from early development appears to reprogram MG, so they exhibit enhanced injury-dependent proliferation, but their survival is compromised. Our studies illustrate the profound effects MG-microglia cross talk can have on MG transcriptional programs related to cell division processes.
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