Proteomics analysis of N-methyl-d-aspartate-induced cell death in retinal and optic nerves

2021 ◽  
pp. 104427
Author(s):  
Lingge Suo ◽  
Wanwei Dai ◽  
Xuhao Chen ◽  
Xuejiao Qin ◽  
Guanlin Li ◽  
...  
Keyword(s):  
Cell Death ◽  
Proteomics Analysis ◽  
Optic Nerves

scholarly journals Minocycline reduces inflammatory response and cell death in a S100B retina degeneration model

2020 ◽  
Vol 17 (1) ◽  
Author(s):  
Pia Grotegut ◽  
Natarajan Perumal ◽  
Sandra Kuehn ◽  
Andreas Smit ◽  
H. Burkhard Dick ◽  
...  
Keyword(s):  
Cell Death ◽  
Body Weight ◽  
Optic Nerve ◽  
Inflammatory Response ◽  
Negative Impact ◽  
Dependent Manner ◽  
Label Free ◽  
Proteomics Analysis ◽  
Concentration Dependent Manner ◽  
Minocycline Treatment

Abstract Background Previous studies noted that intravitreal injection of S100B triggered a glaucoma-like degeneration of retina and optic nerve as well as microglia activation after 14 days. The precise role of microglia in our intravitreal S100B model is still unclear. Hence, microglia were inhibited through minocycline. The aim is to investigate whether microglia have a significant influence on the degeneration process or whether they are only a side effect in the model studied here. Methods Minocycline was applied daily in rats by intraperitoneal injection using two different concentrations (13.5 mg/kg body weight, 25 mg/kg body weight). One day after treatment start, S100B or PBS was intravitreally injected in one eye per rat. The naïve groups received no injections. This resulted in a total of five groups (naïve n = 14, PBS n = 14, S100B n = 13, 13.5 mg/kg mino n = 15, 25 mg/kg mino n = 15). At day 14, electroretinogram measurements were performed, followed by immunofluorescence and label-free quantitative proteomics analysis. The focus of these investigations was on the survival of RGCs as well as their axons, the response of the microglia, and the identification of further pathological modes of action of S100B. Results The best signal transmission was detected via ERG in the 13.5 mg/kg mino group. The inhibition of the microglia protected optic nerve neurofilaments and decreased the negative impact of S100B on RGCs. However, the minocycline treatment could not trigger complete protection of RGCs. Furthermore, in retina and optic nerve, the minocycline treatment reduced the number and activity of S100B-triggered microglia in a concentration-dependent manner. Proteomics analysis showed that S100B application led to numerous metabolic functions and cellular stress, mainly an increased inflammatory response, glycolysis, and mitochondrial dysfunction, which caused oxidative stress in the retina. Importantly, the protective capability of lower dose of minocycline was unraveled by suppressing the apoptotic, inflammatory, and the altered metabolic processes caused by S100B insult in the retina. Conclusion Intravitreally injected S100B not only led to a pro-inflammatory microglial reaction, but also a mitochondrial and metabolic dysfunction. Also, these results suggest that an excessive microglial response may be a significant degenerative factor, but not the only trigger for increased cell death.

Proteomics Analysis of Rice Lesion Mimic Mutant (spl1) Reveals Tightly Localized Probenazole-Induced Protein (PBZ1) in Cells Undergoing Programmed Cell Death

2008 ◽  
Vol 7 (4) ◽  
pp. 1750-1760 ◽  
Author(s):  
Sun Tae Kim ◽  
Sang Gon Kim ◽  
Young Hyun Kang ◽  
Yiming Wang ◽  
Jae-Yean Kim ◽  
...  
Keyword(s):  
Cell Death ◽  
Programmed Cell Death ◽  
Proteomics Analysis ◽  
Lesion Mimic ◽  
Lesion Mimic Mutant ◽  
In Cells

Proteomics analysis of lung reveals inflammation and cell death induced by atmospheric H2S exposure in pig

2020 ◽  
Vol 191 ◽  
pp. 110204
Author(s):  
Zhen Liu ◽  
Qin Fu ◽  
Shanlong Tang ◽  
Yanjiao Xie ◽  
Qingshi Meng ◽  
...  
Keyword(s):  
Cell Death ◽  
Proteomics Analysis

scholarly journals Rat Optic Nerve Oligodendrocytes Develop in the Absence of Viable Retinal Ganglion Cell Axons

1999 ◽  
Vol 146 (6) ◽  
pp. 1365-1374 ◽  
Author(s):  
H. Ueda ◽  
J.M. Levine ◽  
R.H. Miller ◽  
B.D. Trapp
Keyword(s):  
Cell Death ◽  
Optic Nerve ◽  
Ganglion Cell ◽  
Retinal Ganglion Cell ◽  
Basic Protein ◽  
Retinal Ganglion ◽  
Optic Nerves ◽  
Temporal And Spatial Patterns ◽  
Longitudinal Orientation ◽  
Temporal And Spatial

Retinal ganglion cell axons and axonal electrical activity have been considered essential for migration, proliferation, and survival of oligodendrocyte lineage cells in the optic nerve. To define axonal requirements during oligodendrogenesis, the developmental appearance of oligodendrocyte progenitors and oligodendrocytes were compared between normal and transected optic nerves. In the absence of viable axons, oligodendrocyte precursors migrated along the length of the nerve and subsequently multiplied and differentiated into myelin basic protein–positive oligodendrocytes at similar densities and with similar temporal and spatial patterns as in control nerves. Since transected optic nerves failed to grow radially, the number of oligodendrocyte lineage cells was reduced compared with control nerves. However, the mitotic indices of progenitors and the percentage of oligodendrocytes undergoing programmed cell death were similar in control and transected optic nerves. Oligodendrocytes lacked their normal longitudinal orientation, developed fewer, shorter processes, and failed to form myelin in the transected nerves. These data indicate that normal densities of oligodendrocytes can develop in the absence of viable retinal ganglion axons, and support the possibility that axons assure their own myelination by regulating the number of myelin internodes formed by individual oligodendrocytes.

scholarly journals A Proteomics Analysis to Evaluate Cytotoxicity in NRK-52E Cells Caused by Unmodified Nano-Fe3O4

2014 ◽  
Vol 2014 ◽  
pp. 1-9 ◽  
Author(s):  
Yi-Reng Lin ◽  
Chao-Jen Kuo ◽  
Hugo You-Hsien Lin ◽  
Chin-Jen Wu ◽  
Shih-Shin Liang
Keyword(s):  
Cell Death ◽  
Cell Lines ◽  
Rat Kidney ◽  
Antagonistic Effect ◽  
Chaperone Proteins ◽  
Protective Effects ◽  
Proteomics Analysis ◽  
Cellular Environment ◽  
Nano Fe3o4 ◽  
Related Proteins

We synthesized unmodified Fe3O4nanoparticles (NPs) with particles size from 10 nm to 100 nm. We cultured NRK-52E cell lines (rat, kidney) and treated with Fe3O4NPs to investigate and evaluate the cytotoxicity of NPs for NRK-52E cells. Through global proteomics analysis using dimethyl labeling techniques and liquid phase chromatography coupled with a tandem mass spectrometer (LC-MS/MS), we characterized 435 proteins including the programmed cell death related proteins, ras-related proteins, glutathione related proteins, and the chaperone proteins such as heat shock proteins, serpin H1, protein disulfide-isomerase A4, endoplasmin, and endoplasmic reticulum resident proteins. From the statistical data of identified proteins, we believed that NPs treatment causes cell death and promotes expression of ras-related proteins. In order to avoid apoptosis, NRK-52E cell lines induce a series of protective effects such as glutathione related proteins to reduce reactive oxygen species (ROS), and chaperone proteins to recycle damaged proteins. We suggested that, in the indigenous cellular environment, Fe3O4NPs treatment induced an antagonistic effect for cell lines to go to which avoids apoptosis.

DNA nick end labeling: a reliable marker for apoptosis?

1995 ◽  
Vol 53 ◽  
pp. 962-963
Author(s):  
Anne F. Bushnell ◽  
Sarah Webster ◽  
Lynn S. Perlmutter
Keyword(s):  
Cell Death ◽  
Cultured Cells ◽  
Apoptotic Cell ◽  
Morphological Characteristics ◽  
Detection Methods ◽  
Tissue Preparation ◽  
Preparation Methods ◽  
Dna Laddering ◽  
Disease States ◽  
Reliable Marker

Apoptosis, or programmed cell death, is an important mechanism in development and in diverse disease states. The morphological characteristics of apoptosis were first identified using the electron microscope. Since then, DNA laddering on agarose gels was found to correlate well with apoptotic cell death in cultured cells of dissimilar origins. Recently numerous DNA nick end labeling methods have been developed in an attempt to visualize, at the light microscopic level, the apoptotic cells responsible for DNA laddering.The present studies were designed to compare various tissue processing techniques and staining methods to assess the occurrence of apoptosis in post mortem tissue from Alzheimer's diseased (AD) and control human brains by DNA nick end labeling methods. Three tissue preparation methods and two commercial DNA nick end labeling kits were evaluated: the Apoptag kit from Oncor and the Biotin-21 dUTP 3' end labeling kit from Clontech. The detection methods of the two kits differed in that the Oncor kit used digoxigenin dUTP and anti-digoxigenin-peroxidase and the Clontech used biotinylated dUTP and avidinperoxidase. Both used 3-3' diaminobenzidine (DAB) for final color development.

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