Immunohistochemical Detection of CTGF in the Human Eye

Setten, G.‐B. van; Trost, Andrea; Schrödl, Falk; Kaser-Eichberger, Alexandra; Bogner, Barbara; Setten, Mercedes van; Heindl, Ludwig M.; Grabner, Günther; Reitsamer, Herbert A.

doi:10.3109/02713683.2016.1143014

Cited by 20 publications

(20 citation statements)

References 60 publications

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“…It was reported to induce the angio-fibrotic switch in diabetic retinopathy and to be involved in remodeling of the extracellular matrix in glaucoma. 88 – 90 …”

Section: Discussionmentioning

confidence: 99%

Retinal Degeneration Triggers the Activation of YAP/TEAD in Reactive Müller Cells

Hamon

Masson

Bitard

et al. 2017

Invest. Ophthalmol. Vis. Sci.

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PurposeDuring retinal degeneration, Müller glia cells respond to photoreceptor loss by undergoing reactive gliosis, with both detrimental and beneficial effects. Increasing our knowledge of the complex molecular response of Müller cells to retinal degeneration is thus essential for the development of new therapeutic strategies. The purpose of this work was to identify new factors involved in Müller cell response to photoreceptor cell death.MethodsWhole transcriptome sequencing was performed from wild-type and degenerating rd10 mouse retinas at P30. The changes in mRNA abundance for several differentially expressed genes were assessed by quantitative RT-PCR (RT-qPCR). Protein expression level and retinal cellular localization were determined by western blot and immunohistochemistry, respectively.ResultsPathway-level analysis from whole transcriptomic data revealed the Hippo/YAP pathway as one of the main signaling pathways altered in response to photoreceptor degeneration in rd10 retinas. We found that downstream effectors of this pathway, YAP and TEAD1, are specifically expressed in Müller cells and that their expression, at both the mRNA and protein levels, is increased in rd10 reactive Müller glia after the onset of photoreceptor degeneration. The expression of Ctgf and Cyr61, two target genes of the transcriptional YAP/TEAD complex, is also upregulated following photoreceptor loss.ConclusionsThis work reveals for the first time that YAP and TEAD1, key downstream effectors of the Hippo pathway, are specifically expressed in Müller cells. We also uncovered a deregulation of the expression and activity of Hippo/YAP pathway components in reactive Müller cells under pathologic conditions.

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“…It was reported to induce the angio-fibrotic switch in diabetic retinopathy and to be involved in remodeling of the extracellular matrix in glaucoma. 88 – 90 …”

Section: Discussionmentioning

confidence: 99%

Retinal Degeneration Triggers the Activation of YAP/TEAD in Reactive Müller Cells

Hamon

Masson

Bitard

et al. 2017

Invest. Ophthalmol. Vis. Sci.

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“…Furthermore, CTGF was also demonstrated as the matricellular proteins in glaucoma, which plays a role in fibrosis and increased extracellular matrix deposition . CTGF might be relevant for the development of elevated IOP, which is considered as a high‐risk factor in glaucoma pathogenesis . These results indicated high‐risk genes were key regulators in pathogenesis of glaucoma.…”

Section: Resultsmentioning

confidence: 89%

“…16 CTGF might be relevant for the development of elevated IOP, which is considered as a high-risk factor in glaucoma pathogenesis. 17 These results indicated high-risk genes were key regulators in pathogenesis of glaucoma.…”

Section: Identification Of Differentially Expressed Genesmentioning

confidence: 93%

Integrative transcriptomic and proteomic analysis reveals CD9/ITGA4/PI3K‐Akt axis mediates trabecular meshwork cell apoptosis in human glaucoma

Yan

Yang

Jiao

et al. 2019

J Cellular Molecular Medi

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Glaucoma has been the leading cause of irreversible blindness worldwide. High intraocular pressure (IOP) is a high‐risk factor of glaucoma, repression of which has been the important treatment of glaucoma in clinic. Trabecular meshwork is crucial for maintaining IOP in aqueous humour out‐flow system. It is urgent to reveal the molecular mechanism of trabecular meshwork in glaucoma. Previous studies found that some pathways were related to glaucoma, such as extracellular matrix (ECM)‐receptor interaction, phosphatidylinositol 3‐kinase (PI3K)‐protein kinase B (Akt) and apoptosis. To identify novel molecules in glaucoma, we performed high‐throughput transcriptome and proteome analysis to immortal human trabecular meshwork cells (iHTM) and glaucomatous human trabecular meshwork cells (GTM3), respectively. Twenty‐six up‐regulated genes/proteins and 59 down‐regulated genes/proteins were identified as the high‐risk factors based on differential analysis, including some known factors of glaucoma. Furthermore, a glaucoma‐related protein‐protein interaction (PPI) network was constructed for investigating the function roles of risk factors. Some genes were identified as potential regulator in the pathogenesis of glaucoma based on the topology analysis and module analysis to the network. Importantly, we identified and demonstrated that CD9 played key roles in glaucoma by biological experiment. CD9 is down‐regulated in glaucoma, overexpression of CD9 can active integrin α4 (ITGA4), PI3K and Akt, which lead to the decreased apoptosis and attenuate glaucoma. All these results provide a novel molecular therapy of glaucoma.

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“…However, previous studies have reported high intra-and inter-observer repeatability (19). Although we excluded patients with systemic hypertension, the absence of diastolic blood pressure measurements is another limitation of our study (20).…”

Section: Discussionmentioning

confidence: 90%

Macular choroidal thickness in patients with ocular hypertension as assessed by enhanced depth imaging optical coherence tomography

Topçu-Yılmaz¹

2019

Beyoglu Eye J

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The aim of this study was to evaluate the macular choroidal thickness (CT) in patients with ocular hypertension (OHT) using spectral domain optical coherence tomography (SD-OCT) and compare the results with healthy individuals. Methods: Thirty eyes of 30 patients newly diagnosed with OHT and 24 eyes of 24 healthy controls were included in this cross-sectional study. After a detailed ophthalmological examination, macular CT was measured with enhanced depth imaging optical coherence tomography (EDI-OCT) (Cirrus HD-OCT, Carl Zeiss Meditec AG, Jena, Germany) at the fovea and at positions 500 µ, 1000 µ, 1500 µ nasal and temporal to the fovea. The Mann-Whitney U test was used to compare the CT measurements between groups. The correlation between the mean deviation, pattern standard deviation, and retinal nerve fiber layer thickness (RNFL) and CT was evaluated with the Spearman correlation coefficient. Statistical significance was accepted as p<0.05. Results: The mean CT in the OHT group was significantly thinner than that of the controls at locations 1000 µ (250.13±69.53µ vs 275.92±47.34µ; p=0.02) and 1500µ (236.03±65.44µ vs 265.46±47.56µ; p=0.009) temporal to the fovea. The CT at the other measurement points was also thinner in eyes with OHT, but the difference failed to reach statistical significance. A moderately negative correlation was detected between the mean deviation and CT at locations 1000µ (r=-0.42; p=0.03) and 1500µ (r=-0.44; p=0.02) temporal to the fovea There was a moderate correlation between the average RNFL thickness and CT at locations 500µ (r=0.44; p=0.03), 1000µ (r=0.42; p=0.04) and 1500µ (r=0.56; p=0.005) temporal to the fovea. Conclusion: In the present study, the macular CT was thinner in patients with OHT and this thinning was statistically significant at the temporal macula. A longitudinal, prospective study involving multiple EDI-OCT measurements is required to further understand the relationship.

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Immunohistochemical Detection of CTGF in the Human Eye

Cited by 20 publications

References 60 publications

Retinal Degeneration Triggers the Activation of YAP/TEAD in Reactive Müller Cells

Retinal Degeneration Triggers the Activation of YAP/TEAD in Reactive Müller Cells

Integrative transcriptomic and proteomic analysis reveals CD9/ITGA4/PI3K‐Akt axis mediates trabecular meshwork cell apoptosis in human glaucoma

Macular choroidal thickness in patients with ocular hypertension as assessed by enhanced depth imaging optical coherence tomography

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