Oct4 mediates Müller glia reprogramming and cell cycle exit during retina regeneration in zebrafish

Sharma, Poonam; Gupta, Shivangi; Chaudhary, Mansi; Mitra, Soumitra; Chawla, Bindia; Khursheed, M.; Ramachandran, Rajesh

doi:10.26508/lsa.201900548

Cited by 34 publications

(41 citation statements)

References 77 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“… 31 In a study on zebrafish, miR-200a was reported to be one of the most important functional miRNAs in retinal degeneration and it is essential in the Müller glia cellular reprogramming. 32 However, no previous work has been conducted on the effects of miR-200a in the development of DR.…”

Section: Discussionmentioning

confidence: 99%

Protective Role of microRNA-200a in Diabetic Retinopathy Through Downregulation of PDLIM1

Wan

Long

Jin

et al. 2021

JIR

View full text Add to dashboard Cite

Background Diabetic retinopathy (DR) is a most common microvascular complication and regarded as the leading cause of blindness in the working age population. The involvement of miR-200a in various disorders has become recognized, and the objective of this study was to identify the protective effect of miR-200a in the development of DR. Methods The contents of miR-200a and its potential target gene, PDZ and LIM domain protein 1 (PDLIM1), were detected in both in-vivo and in-vitro DR models. Retinal leakage and inflammatory factor concentrations were detected after vitreous injections of miR-200a/PDLIM1 vectors in mice. The cellular viability, apoptosis and cellular migration were investigated using trypan blue staining, flow cytometry and transwell assay with human retinal microvascular endothelial cells (HRMECs). Besides, the prediction and confirmation of miR-200a targeting PDLIM1 were conducted with bioinformation analyses and dual-luciferase reporter assay. Results Lower miR-200a and higher PDLIM1 levels were detected in both in-vivo and in-vitro DR models. Besides, it was found that miR-200a treatment would significantly inhibit retinal permeability and inflammatory factors. Through targeting PDLIM1, it was found that miR-200a could improve cellular viability, remit apoptotic status and reduce cellular migration significantly in high glucose-treated HRMECs. Conclusion Our results demonstrated that miR-200a could be used as a potential therapy target through down-regulating PDLIM1 in DR.

show abstract

Section: Discussionmentioning

confidence: 99%

Protective Role of microRNA-200a in Diabetic Retinopathy Through Downregulation of PDLIM1

Wan

Long

Jin

et al. 2021

JIR

View full text Add to dashboard Cite

show abstract

“…This gliotic state rapidly transitions to reprogramming. Reprogrammed Müller glia down-regulate a subset of glia-specific genes, e.g., rlbp1a and glul , upregulate genes that encode reprogramming factors, e.g., oct4, and upregulate genes indicative of retinal stem and progenitor cells, e.g., pax6a , sox2 , and rx1 [ 42 , 74 , 75 , 76 ]. The rapid and dynamic reprogramming of Müller glia is followed closely by their entry into the cell cycle, which is characterized by interkinetic nuclear migration and a single asymmetric cell division that produces a Müller glia-derived progenitor and a post-mitotic Müller glia [ 42 , 77 , 78 ].…”

Section: Quiescence Reprogramming and Proliferation In Müller Gliamentioning

confidence: 99%

Inflammation Regulates the Multi-Step Process of Retinal Regeneration in Zebrafish

Nagashima

Hitchcock

2021

Cells

View full text Add to dashboard Cite

The ability to regenerate tissues varies between species and between tissues within a species. Mammals have a limited ability to regenerate tissues, whereas zebrafish possess the ability to regenerate almost all tissues and organs, including fin, heart, kidney, brain, and retina. In the zebrafish brain, injury and cell death activate complex signaling networks that stimulate radial glia to reprogram into neural stem-like cells that repair the injury. In the retina, a popular model for investigating neuronal regeneration, Müller glia, radial glia unique to the retina, reprogram into stem-like cells and undergo a single asymmetric division to generate multi-potent retinal progenitors. Müller glia-derived progenitors then divide rapidly, numerically matching the magnitude of the cell death, and differentiate into the ablated neurons. Emerging evidence reveals that inflammation plays an essential role in this multi-step process of retinal regeneration. This review summarizes the current knowledge of the inflammatory events during retinal regeneration and highlights the mechanisms whereby inflammatory molecules regulate the quiescence and division of Müller glia, the proliferation of Müller glia-derived progenitors and the survival of regenerated neurons.

show abstract

“…In this process, miR-145 directly targets progranulin A-dependent hepatic outgrowth during embryonic development [ 29 ]. In addition, miR-145 and several regeneration-associated factors have been involved in an early panretinal induction of octamer-binding transcription factor 4, which is essential for Müller glia reprogramming and cell cycle exit in zebrafish [ 30 ]. Finally, miR-145 and other miRNAs assist Müller glial cells of the zebrafish retina in reprogramming and forming progenitors essential for regeneration upon injury [ 31 ].…”

Section: Introductionmentioning

confidence: 99%

Conservation of Zebrafish MicroRNA-145 and Its Role during Neural Crest Cell Development

Steeman

Rubiolo

Sánchez

et al. 2021

Genes

View full text Add to dashboard Cite

The neural crest is a multipotent cell population that develops from the dorsal neural fold of vertebrate embryos in order to migrate extensively and differentiate into a variety of tissues. A number of gene regulatory networks coordinating neural crest cell specification and differentiation have been extensively studied to date. Although several publications suggest a common role for microRNA-145 (miR-145) in molecular reprogramming for cell cycle regulation and/or cellular differentiation, little is known about its role during in vivo cranial neural crest development. By modifying miR-145 levels in zebrafish embryos, abnormal craniofacial development and aberrant pigmentation phenotypes were detected. By whole-mount in situ hybridization, changes in expression patterns of col2a1a and Sry-related HMG box (Sox) transcription factors sox9a and sox9b were observed in overexpressed miR-145 embryos. In agreement, zebrafish sox9b expression was downregulated by miR-145 overexpression. In silico and in vivo analysis of the sox9b 3′UTR revealed a conserved potential miR-145 binding site likely involved in its post-transcriptional regulation. Based on these findings, we speculate that miR-145 participates in the gene regulatory network governing zebrafish chondrocyte differentiation by controlling sox9b expression.

show abstract

Oct4 mediates Müller glia reprogramming and cell cycle exit during retina regeneration in zebrafish

Cited by 34 publications

References 77 publications

Protective Role of microRNA-200a in Diabetic Retinopathy Through Downregulation of PDLIM1

Protective Role of microRNA-200a in Diabetic Retinopathy Through Downregulation of PDLIM1

Inflammation Regulates the Multi-Step Process of Retinal Regeneration in Zebrafish

Conservation of Zebrafish MicroRNA-145 and Its Role during Neural Crest Cell Development

Contact Info

Product

Resources

About