Neuronal and Glial Alterations in Complex Long-Term Rhegmatogenous Retinal Detachment

Ghosh, Fredrik; Johansson, K.

doi:10.3109/02713683.2012.663856

Cited by 12 publications

(12 citation statements)

References 25 publications

(20 reference statements)

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“…10A-F Within the model, the detached retina without tissue support (free-floating) displays progressive gliosis and apoptotic cell death in all nuclear layers with almost no surviving ganglion cells and cone photoreceptors after 60 hours in vitro. These findings are well in line with pathologic reactions reported in human eyes with advanced RRD [16,17]. In contrast to cones, rod photoreceptors in our model appear to be more resistant to the in vitro detachment evident by a substantial amount of surviving rhodopsin labeled cells even after 60 hours of detachment which is in accordance with previous clinical and experimental studies in vivo [5,18].…”

Section: Müller Cell Activationsupporting

confidence: 82%

In vitro biomechanical modulation—retinal detachment in a box

Ghosh

Arnér

Taylor

2015

Graefes Arch Clin Exp Ophthalmol

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Section: Müller Cell Activationsupporting

confidence: 82%

In vitro biomechanical modulation—retinal detachment in a box

Ghosh

Arnér

Taylor

2015

Graefes Arch Clin Exp Ophthalmol

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“…That not all the factors examined were detected in both, isolated Müller glia and retinal specimens may be due to the fact that Müller cells in culture may de‐differentiate and lose many of their typical physiological and functional features upon in vitro culture. Although in gliotic PVR retina there is severe loss of retinal neurons and predominance of reactive Müller glia expressing GFAP and CRALBP (Charteris et al, ; Ghosh and Johansson, ; Wickham et al, ), it is possible that factors expressed by Müller glia may be under‐represented in the retinal samples due to the presence of other retinal cell types.…”

Section: Discussionmentioning

confidence: 99%

Müller glia as an important source of cytokines and inflammatory factors present in the gliotic retina during proliferative vitreoretinopathy

Eastlake¹,

Banerjee²,

Angbohang³

et al. 2015

Glia

111

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Retinal gliosis is characterized by biochemical and physiological changes that often lead to Müller glia proliferation and hypertrophy and is a feature of many neuro‐degenerative and inflammatory diseases such as proliferative vitreoretinopathy (PVR). Although Müller glia are known to release inflammatory factors and cytokines, it is not clear whether cytokine production by these cells mirrors the pattern of factors present in the gliotic retina. Lysates from normal cadaveric retina and gliotic retinal specimens from patients undergoing retinectomy for treatment of PVR, the Müller cell line MIO‐M1 and four human Müller glial cell preparations isolated from normal retina were examined for their expression of cytokines and inflammatory factors using semi‐quantitative dot blot antibody arrays and quantitative arrays. Comparative analysis of the expression of inflammatory factors showed that in comparison with normal retina, gliotic retina exhibited greater than twofold increase in 24/102 factors examined by semiquantitative arrays, and a significant increase in 19 out of 27 factors assessed by quantitative methods (P < 0.05 to P < 0.001). It was observed that with the exception of some chemotactic factors, the majority of cytokines and inflammatory factors were produced by Müller glia in vitro and included G‐CSF, MCP‐1, PDGF‐bb, RANTES, VEGF, and TGFβ2. These results showed that a large number of inflammatory factors expressed by Müller glia in vitro are upregulated in the gliotic retina, suggesting that targeting the production of inflammatory factors by Müller glia may constitute a valid approach to prevent neural damage during retinal gliosis and this merits further investigations. GLIA 2016;64:495–506

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“…Wrinkling of the inner limiting membrane and formation of epiretinal membranes is also evident . Long-term rhegmatogenous retinal detachment also leads to retinal remodeling, characterized by the loss of first-and second-order retinal neurons, disruption of the entire retinal lamination and gliosis (Ghosh and Johansson, 2012).…”

Section: Phasementioning

confidence: 99%