ArticleOncotarget2016
Lin28B promotes Müller glial cell de-differentiation and proliferation in the regenerative rat retinas.
Article in Oncotarget, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
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Who cites it
10 citing papers in PubMed, 14 citations in OpenAlex.
- The role of Lin28A and Lin28B in cancer beyond Let-7.FEBS letters · 2024Review
- Insight into the role of non-coding RNA in the diagnosis and treatment of retinitis pigmentosa.Non-coding RNA research · 2024Review
- Epigenetic mechanisms of Müller glial reprogramming mediating retinal regeneration.Frontiers in cell and developmental biology · 2023Review
- Therapeutic effects of mesenchymal stem cells-derived extracellular vesicles' miRNAs on retinal regeneration: a review.Stem cell research & therapy · 2021Review
- A Comparative Analysis of Reactive Müller Glia Gene Expression After Light Damage and microRNA-Depleted Müller Glia-Focus on microRNAs.Frontiers in cell and developmental biology · 2020Article
- Let-7 regulates cell cycle dynamics in the developing cerebral cortex and retina.Scientific reports · 2019Article
- Endogenous Mobilization of Bone-Marrow Cells Into the Murine Retina Induces Fusion-Mediated Reprogramming of Müller Glia Cells.EBioMedicine · 2018Article
- Synergistic neuroprotective effect of rasagiline and idebenone against retinal ischemia-reperfusion injury via the Lin28-let-7-Dicer pathway.Oncotarget · 2018Article
- Activation of liver X receptor delayed the retinal degeneration of rd1 mice through modulation of the immunological function of glia.Oncotarget · 2017Article
- Combined transplantation of human mesenchymal stem cells and human retinal progenitor cells into the subretinal space of RCS rats.Scientific reports · 2017Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Retinal regeneration and repair are severely impeded in higher mammalian animals. Although Müller cells can be activated and show some characteristics of progenitor cells when injured or under pathological conditions, they quickly form gliosis scars. Unfortunately, the basic mechanisms that impede retinal regeneration remain unknown. We studied retinas from Royal College of Surgeon (RCS) rats and found that let-7 family molecules, let-7e and let-7i, were significantly overexpressed in Müller cells of degenerative retinas. It demonstrated that down-regulation of the RNA binding protein Lin28B was one of the key factors leading to the overexpression of let-7e and let-7i. Lin28B ectopic expression in the Müller cells suppressed overexpression of let-7e and let-7i, stimulated and mobilized Müller glia de-differentiation, proliferation, promoted neuronal commitment, and inhibited glial fate acquisition of de-differentiated Müller cells. ERG recordings revealed that the amplitudes of a-wave and b-wave were improved significantly after Lin28B was delivered into the subretinal space of RCS rats. In summary, down-regulation of Lin28B as well as up-regulation of let-7e and let-7i may be the main factors that impede Müller cell de-differentiation and proliferation in the retina of RCS rats.
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Registered trials
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