scholarly journals Photobiomodulation with 670 nm light ameliorates Müller cell-mediated activation of microglia and macrophages in retinal degeneration

2017 ◽  
Vol 165 ◽  
pp. 78-89 ◽  
Author(s):  
Yen-Zhen Lu ◽  
Riccardo Natoli ◽  
Michele Madigan ◽  
Nilisha Fernando ◽  
Kartik Saxena ◽  
...  
Keyword(s):  
Retinal Degeneration ◽  
Müller Cell ◽  
Muller Cell

scholarly journals Cone Photoreceptor Degeneration and Neuroinflammation in the Zebrafish Bardet-Biedl Syndrome 2 (bbs2) Mutant Does Not Lead to Retinal Regeneration

2020 ◽  
Vol 8 ◽  
Author(s):  
Ping Song ◽  
Joseph Fogerty ◽  
Lauren T. Cianciolo ◽  
Rachel Stupay ◽  
Brian D. Perkins
Keyword(s):  
Cell Proliferation ◽  
Inflammatory Response ◽  
Retinal Degeneration ◽  
Autosomal Recessive Disorder ◽  
Müller Cell ◽  
Cone Photoreceptor ◽  
Photoreceptor Degeneration ◽  
Retinal Regeneration ◽  
Bardet Biedl Syndrome ◽  
Muller Cell

Bardet-Biedl syndrome (BBS) is a heterogeneous and pleiotropic autosomal recessive disorder characterized by obesity, retinal degeneration, polydactyly, renal dysfunction, and mental retardation. BBS results from defects in primary and sensory cilia. Mutations in 21 genes have been linked to BBS and proteins encoded by 8 of these genes form a multiprotein complex termed the BBSome. Mutations in BBS2, a component of the BBSome, result in BBS as well as non-syndromic retinal degeneration in humans and rod degeneration in mice, but the role of BBS2 in cone photoreceptor survival is not clear. We used zebrafish bbs2–/– mutants to better understand how loss of bbs2 leads to photoreceptor degeneration. Zebrafish bbs2–/– mutants exhibited impaired visual function as larvae and adult zebrafish underwent progressive cone photoreceptor degeneration. Cone degeneration was accompanied by increased numbers of activated microglia, indicating an inflammatory response. Zebrafish exhibit a robust ability to regenerate lost photoreceptors following retinal damage, yet cone degeneration and inflammation was insufficient to trigger robust Müller cell proliferation. In contrast, high intensity light damage stimulated Müller cell proliferation and photoreceptor regeneration in both wild-type and bbs2–/– mutants, although the bbs2–/– mutants could only restore cones to pre-damaged densities. In summary, these findings suggest that cone degeneration leads to an inflammatory response in the retina and that BBS2 is necessary for cone survival. The zebrafish bbs2 mutant also represents an ideal model to identify mechanisms that will enhance retinal regeneration in degenerating diseases.

scholarly journals Müller cell metabolic chaos during retinal degeneration

2016 ◽  
Vol 150 ◽  
pp. 62-70 ◽  
Author(s):  
Rebecca L. Pfeiffer ◽  
Robert E. Marc ◽  
Mineo Kondo ◽  
Hiroko Terasaki ◽  
Bryan W. Jones
Keyword(s):  
Retinal Degeneration ◽  
Müller Cell ◽  
Muller Cell

The changes of potassium currents in RCS rat Müller cell during retinal degeneration

2012 ◽  
Vol 1427 ◽  
pp. 78-87 ◽  
Author(s):  
TongTao Zhao ◽  
YaoChen Li ◽  
ChuanHuang Weng ◽  
ZhengQin Yin
Keyword(s):  
Retinal Degeneration ◽  
Potassium Currents ◽  
Müller Cell ◽  
Rcs Rat ◽  
Muller Cell

scholarly journals Profiling of MicroRNAs Involved in Retinal Degeneration Caused by Selective Müller Cell Ablation

PLoS ONE ◽  
2015 ◽  
Vol 10 (3) ◽  
pp. e0118949 ◽  
Author(s):  
Sook Hyun Chung ◽  
Mark Gillies ◽  
Yuki Sugiyama ◽  
Ling Zhu ◽  
So-Ra Lee ◽  
...  
Keyword(s):  
Retinal Degeneration ◽  
Müller Cell ◽  
Cell Ablation ◽  
Muller Cell

scholarly journals Müller Cell Regulated Microglial Activation and Migration in Rats With N-Methyl-N-Nitrosourea-Induced Retinal Degeneration

2018 ◽  
Vol 12 ◽  
Author(s):  
Shuai Zhang ◽  
Shanshan Zhang ◽  
Wenqing Gong ◽  
Guopei Zhu ◽  
Songtao Wang ◽  
...  
Keyword(s):  
Retinal Degeneration ◽  
Microglial Activation ◽  
Müller Cell ◽  
Muller Cell ◽  
And Migration

Müller cell changes precede photoreceptor cell degeneration in the age-related retinal degeneration of the Fischer 344 rat

1995 ◽  
Vol 698 (1-2) ◽  
pp. 1-14 ◽  
Author(s):  
David A. DiLoreto ◽  
Mark R. Martzen ◽  
Constancia del Cerro ◽  
Paul D. Coleman ◽  
Manuel del Cerro
Keyword(s):  
Retinal Degeneration ◽  
Photoreceptor Cell ◽  
Müller Cell ◽  
Cell Degeneration ◽  
Fischer 344 ◽  
Age Related ◽  
Fischer 344 Rat ◽  
Muller Cell ◽  
Cell Changes

scholarly journals Reintroduction of DJ-1 in Müller Cells Inhibits Retinal Degeneration in the DJ-1 Deficient Retina

Antioxidants ◽  
2021 ◽  
Vol 10 (12) ◽  
pp. 1862
Author(s):  
Naouel Gharbi ◽  
Dagne Røise ◽  
Jorunn-Elise Førre ◽  
Amanda J. Edson ◽  
Helena A. Hushagen ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Retinal Degeneration ◽  
Light Exposure ◽  
Pigment Epithelium ◽  
Retinal Pigment ◽  
Müller Cells ◽  
Müller Cell ◽  
Muller Cells ◽  
Age Dependent ◽  
Muller Cell

The eye is continuously under oxidative stress due to high metabolic activity and reactive oxygen species generated by daily light exposure. The redox-sensitive protein DJ-1 has proven to be essential in order to protect retina and retinal pigment epithelium (RPE) from oxidative-stress-induced degeneration. Here, we analyzed the specific role of Müller cell DJ-1 in the adult zebrafish retina by re-establishing Müller-cell-specific DJ-1 expression in a DJ-1 knockout retina. Loss of DJ-1 resulted in an age-dependent retinal degeneration, including loss of cells in the ganglion cell layer, retinal thinning, photoreceptor disorganization and RPE cell dysfunction. The degenerative phenotype induced by the absence of DJ-1 was inhibited by solely expressing DJ-1 in Müller cells. The protective effect was dependent upon the cysteine-106 residue of DJ-1, which has been shown to be an oxidative sensor of DJ-1. In a label-free proteomics analysis of isolated retinas, we identified proteins differentially expressed after DJ-1 knockout, but with restored levels after Müller cell DJ-1 re-insertion. Our data show that Müller cell DJ-1 has a major role in protecting the retina from age-dependent oxidative stress.

Sign in / Sign up

Export Citation Format

Share Document