Retinal ganglion cell line apoptosis induced by hydrostatic pressure

Agar, Ashish; Li, Shaojuan; Agarwal, Neeraj; Coroneo, Minas T.; Hill, Mark A.

doi:10.1016/j.brainres.2006.02.061

Cited by 75 publications

(72 citation statements)

References 42 publications

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“…In this study, our results showed that the viability of cells in treatment reduced relative to the increase in hydrostatic pressure and time and resulted in an increase in cell death. Therefore, hydrostatic pressure as a cell death inducer (Agar et al, 2006) increased the percentage of cell deaths and decreased the percentage of cell viability in mMSCs. According to our results, it seems that hydrostatic pressure can improve length of neurite in mouse bone marrow-derived mesenchymal stem cells in an amount-dependent manner.…”

Section: Discussionmentioning

confidence: 95%

“…This study was undertaken to evaluate the effect of hydrostatic pressure on staurosporine-induced neural differentiation in mouse bone marrow-derived mesenchymal stem cells. Previous studies have shown that pressure alone may act as a stimulus for apoptosis in neuronal cell cultures (Agar et al, 2000;Agar et al, 2006). Hydrostatic pressure induces apoptosis in differentiated PC12 cells as identifi ed by DNA fragmentation, chromatin condensation, retraction of neuronal process and cell shrinkage (Sadri et al, 2008).…”

Section: Discussionmentioning

confidence: 99%

“…The unpressurized control cell groups were treated identically within a chamber, but with no pressure applied. The cell culture pressure chamber used in this study is an established model (Agar et al, 2000;Agar et al, 2006) that allows a gas mix to be pressurized to a constant ambient hydrostatic pressure ranging from 0-200 ± 2.25 mmHg over the pressure period. After pressurization, the pressure was restored to the atmospheric value, and the culture plates were removed from the pressure chamber for analysis.…”

Section: Experimental Protocolmentioning

confidence: 99%

“…Namely biological and pharmacological techniques (1), mechanical cues (2), and external mechanical and electrical forces (3) have been used to regulate mMSCs differentiation (Titushkin et al, 2010). Brown (2000) suggested that a significant factor in nerve regeneration is the mechanical environment.…”

Section: Introductionmentioning

confidence: 99%

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The effect of hydrostatic pressure on staurosporine-induced neural differentiation in mouse bone marrow‑derived mesenchymal stem cells

Javanmard¹,

Azadbakht²,

Pourmoradi³

2016

BLL

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In this study, the role of hydrostatic pressure on staurosporine-induced neural differentiation in mouse bone marrow mesenchymal stem cells were investigated. The cells were cultured in treatment medium containing 100 nM of staurosporine for 4 hours; then the cells were affected by hydrostatic pressure (0, 25,50, 100 mmHg). The percentage of cell viability by trypan blue staining and the percentage of cell death by Hoechst/PI differential staining were assessed. We obtained the total neurite length. Expression of β-tubulin III and GFAP (Glial fi brillary acidic protein) proteins were also analyzed by immunocytochemistry. The percentage of cell viability in treatments decreased relative to the increase in hydrostatic pressure and time (p < 0.05). The results revealed that total neurite length increased in cells treated with 25 mmHg hydrostatic pressure and decreased in those treated with 100 mmHg hydrostatic pressure (p < 0.05). Low hydrostatic pressure as a mechanical force can improve neural differentiation in mMSCs (mouse mesenchymal stem cells) (Tab. 3, Fig. 7, Ref. 30). Text in PDF www.elis.sk.

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Section: Discussionmentioning

confidence: 95%

Section: Discussionmentioning

confidence: 99%

Section: Experimental Protocolmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

See 2 more Smart Citations

The effect of hydrostatic pressure on staurosporine-induced neural differentiation in mouse bone marrow‑derived mesenchymal stem cells

Javanmard¹,

Azadbakht²,

Pourmoradi³

2016

BLL

View full text Add to dashboard Cite

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“…On the other hand, there are situations where acute cell stress is predominant, ie, in cases of acute glaucoma or in end-stage glaucoma patients needing glaucoma-filtering surgery, where the risk of "wipeout" (loss of the central visual field) is feared. 67,68 In such cases, minocycline might offer a new option to protect affected eyes from further damage.…”

Section: Discussionmentioning

confidence: 99%

Minocycline is cytoprotective in human trabecular meshwork cells and optic nerve head astrocytes by increasing expression of XIAP, Survivin and Bcl‐2

Kernt

Neubauer

et al. 2007

Acta Ophthalmologica Scandinavica

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Introduction: Primary open-angle glaucoma (POAG) is one of the leading causes of blindness. Activation of optic nerve head astrocytes (ONHA) and loss of trabecular meshwork cells (TMC) are pathognomonic for this neurodegenerative disease. Oxidative stress and elevated levels of transforming growth factor beta (TGFβ) play an important role in the pathogenesis of POAG. This study investigates the possible antiapoptotic and cytoprotective effects of minocycline on TMC and ONHA under oxidative stress and increased TGFβ levels. Methods: TMC and ONHA were treated with minocycline 1-150 µM. Possible toxic effects and IC 50 were evaluated after 48 hours. Cell proliferation and viability were examined in order to assess the protective effects of minocycline on TMC and ONHA. Expression of Bcl-2, XIAP, and survivin, as well as their mRNA expression, were assessed by real time polymerase chain reaction (RT-PCR) and Western Blot analysis 48 hours after treatment with minocycline alone and additional incubation with TGFβ-2 or oxidative stress. Results: Minocycline 1-75 µM showed no toxic effects on TMC and ONHA. Under conditions of oxidative stress, both TMC and ONHA showed an increase in viability and an ability to proliferate when treated with minocycline 20-40 µM. RT-PCR and Western blotting yielded an overexpression of Bcl-2, XIAP, and survivin when TMC or ONHA were treated with minocycline 20-40 µM under conditions of oxidative stress and when additionally incubated with TGFβ-2. Conclusion: Minocycline up to 75 µM does not have toxic effects on TMC and ONHA. Treatment with minocycline 20-40 µM led to increased viability and proliferation under oxidative stress and TGFβ-2, as well as overexpression of Bcl-2, XIAP, and survivin. This protective pathway may help to prevent apoptotic cell death of TMC and ONHA and therefore be a promising approach to avoidance of progression of glaucomatous degeneration.

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A lab‐on‐a‐chip model of glaucoma

et al. 2020

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Glaucoma is a collective term used to define a group of neurodegenerative processes affecting the entire visual pathway best distinguished by progressive, irreversible destruction, and death of retinal ganglion cells (RGCs). The disease spectrum is estimated to affect more than 100 million people worldwide by the year of 2040 (Tham et al., 2014). The primary risk factor for progression and development of glaucoma is elevated intraocular pressure (IOP). IOP is regulated by the balance between aqueous humor secretion into

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Retinal ganglion cell line apoptosis induced by hydrostatic pressure

Cited by 75 publications

References 42 publications

The effect of hydrostatic pressure on staurosporine-induced neural differentiation in mouse bone marrow‑derived mesenchymal stem cells

The effect of hydrostatic pressure on staurosporine-induced neural differentiation in mouse bone marrow‑derived mesenchymal stem cells

Minocycline is cytoprotective in human trabecular meshwork cells and optic nerve head astrocytes by increasing expression of XIAP, Survivin and Bcl‐2

A lab‐on‐a‐chip model of glaucoma

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