Sox11b regulates the migration and fate determination of Müller glia-derived progenitors during retina regeneration in zebrafish

Song, Kaida; Cao, Lining; Lu, Bowen; Chen, Yuxi; Zhang, Shuqiang; Lu, Jianfeng; Xu, Hui

doi:10.4103/1673-5374.346550

Cited by 5 publications

(6 citation statements)

References 46 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Bringmann et al proposed that activation of p38 MAPKs ( Bringmann et al, 2009 ) is a possible mechanism to direct Müller cell migration, and the migratory effects of FGF-b are mediated through direct activation of p38 MAPKs, while EGF stimulates the EGF receptor tyrosine kinase that eventually activates p38 MAPKs. Recent findings also imply that Sox11b plays key roles in MGPC migration and fate determination during retina regeneration in zebrafish ( Song et al, 2023 ). Furthermore, studies confirmed that bFGF and insulin lead to the migration of Müller glia to the photoreceptor layer ( Goel and Dhingra, 2021 ).…”

Section: Discussionmentioning

confidence: 97%

RETRACTED: Comparison of the effects of EGF, FGF-b, and NGF on the proliferation, migration, and reprogramming of primary rat Müller cells

Liao,

2024

Front. Cell. Neurosci.

View full text Add to dashboard Cite

PurposeDuring the healing process of full-thickness macular holes (FTMHs), the closure and recovery of the hole depend on the migration, proliferation, and activation of Müller cells to promote the closure of holes and restoration of the photosensitive layer. In this study, we investigated the ability of the epidermal growth factor (EGF), fibroblast growth factor-basic (FGF-b), and nerve growth factor (NGF) to influence this process by regulating proliferation, migration, and reprogramming of primary rat Müller cells.MethodsCell proliferation was measured using CCK8 [2- (2-Methoxy-4-nitrophenyl)-3- (4-nitrophenyl)-5- (2,4-disulfophenyl)-2H-tetrazolium Sodium Salt] colorimetric assays and EdU [5-Ethynyl-2′-deoxyuridine] assays over 48 h. Cell migration was measured using scratch-wound assays and transwell migration assays over 48 h. In addition, we conducted Western blot assays and immunofluorescence assays on cells that were specially treated for 1, 3, and 5 days for cell reprogramming. The percentage of EdU-positive cells in Nestin-positive have also been tested by co-immunofluorescence (Co-IF) staining.ResultsEGF and FGF-b significantly promoted the proliferation of Müller cells (p < 0.05) at a concentration of 0–50 ng/mL, but NGF did not (p > 0.05), compared to untreated controls. Exogenous FGF-b and EGF promote the reprogramming of primary rat Müller cells, significantly enhancing the neural stem cell marker Nestin after stimulation on the 1st, 3rd, and 5th days, respectively. The expression of Müller cell marker Vimentin was significantly (p < 0.05) reduced during this period compared to the control group. However, there was no significant difference between the NGF and control groups. Furthermore, the EGF group expressed stronger Nestin expression than the SCM group. The Co-IF staining showed that early 50% of activated cells came from newly proliferating cells on the 5th day.ConclusionThese observations suggest that FGF-b can promote the activation of Müller cells in a short time and enhance the possessive features of neural stem cells, while EGF may act for a longer period of time. This may further the understanding of growth factor therapy in treating FTMHs, and Müller glia may be promising candidates for cell replacement therapy.

show abstract

Section: Discussionmentioning

confidence: 97%

RETRACTED: Comparison of the effects of EGF, FGF-b, and NGF on the proliferation, migration, and reprogramming of primary rat Müller cells

Liao,

2024

Front. Cell. Neurosci.

View full text Add to dashboard Cite

show abstract

“…A role for Sox11b in adult zebrafish regeneration was first implicated in a zebrafish model of congenital rod PR degeneration ( Morris et al, 2011 ). More recently, functional knockdown of Sox11b following acute damage to the retina was shown to affect the fate determination of MGPCs ( Song et al, 2023 ). However, it is role in chronic retinal damage models is unknown.…”

Section: Discussionmentioning

confidence: 99%

A comparative analysis of gene and protein expression in chronic and acute models of photoreceptor degeneration in adult zebrafish

Kramer,

Carthage,

Berry

et al. 2023

Front. Cell Dev. Biol.

View full text Add to dashboard Cite

Background: Adult zebrafish are capable of photoreceptor (PR) regeneration following acute phototoxic lesion (AL). We developed a chronic low light (CLL) exposure model that more accurately reflects chronic PR degeneration observed in many human retinal diseases.Methods: Here, we characterize the morphological and transcriptomic changes associated with acute and chronic models of PR degeneration at 8 time-points over a 28-day window using immunohistochemistry and 3′mRNA-seq.Results: We first observed a differential sensitivity of rod and cone PRs to CLL. Next, we found no evidence for Müller glia (MG) gliosis or regenerative cell-cycle re-entry in the CLL model, which is in contrast to the robust gliosis and proliferative response from resident MG in the AL model. Differential responses of microglia between the models was also observed. Transcriptomic comparisons between the models revealed gene-specific networks of PR regeneration and degeneration, including genes that are activated under conditions of chronic PR stress. Finally, we showed that CLL is at least partially reversible, allowing for rod and cone outer segment outgrowth and replacement of rod cell nuclei via an apparent upregulation of the existing rod neurogenesis mechanism.Discussion: Collectively, these data provide a direct comparison of the morphological and transcriptomic PR degeneration and regeneration models in zebrafish.

show abstract

“…Multiple pluripotent transcription factors, such as Sox2, Sox11, Oct4, Myc, and Klf4 are upregulated and expressed in MGPCs following retinal injury, and their expression is regulated by Ascl1a/Lin28/Let-7 signaling. 87 , 88 , 89 , 96 In zebrafish, gene knockdown and overexpression showed Sox2 is necessary and sufficient for Müller glia proliferation. 87 Oct4 and Myc are closely associated with epigenetic factors during the exit of the cell cycle.…”

Section: Regulators Mediating the Dedifferentiation And Proliferation...mentioning

confidence: 99%

“… 88 , 89 Sox11b regulates the migration and differentiation of MGPCs during retinal regeneration in zebrafish. 96 However, the role of these factors play in mammalian RMGCs is not clear. Previously, a single Sox2 is proved to reprogram astrocytes into proliferative neuroblasts in the adult mouse brain.…”

Section: Regulators Mediating the Dedifferentiation And Proliferation...mentioning

confidence: 99%

Genetic and epigenetic regulators of retinal Müller glial cell reprogramming

Xiao

Liao

Zou

2023

Advances in Ophthalmology Practice and Research

View full text Add to dashboard Cite

Sox11b regulates the migration and fate determination of Müller glia-derived progenitors during retina regeneration in zebrafish

Cited by 5 publications

References 46 publications

RETRACTED: Comparison of the effects of EGF, FGF-b, and NGF on the proliferation, migration, and reprogramming of primary rat Müller cells

RETRACTED: Comparison of the effects of EGF, FGF-b, and NGF on the proliferation, migration, and reprogramming of primary rat Müller cells

A comparative analysis of gene and protein expression in chronic and acute models of photoreceptor degeneration in adult zebrafish

Genetic and epigenetic regulators of retinal Müller glial cell reprogramming

Contact Info

Product

Resources

About