Lipopolysaccharide (LPS) potentiates hydrogen peroxide toxicity in T98G astrocytoma cells by suppression of anti-oxidative and growth factor gene expression

Yue, Gang; Shi, Guoqing; Azaro, Marco A.; Yang, Qifeng; Hu, Guohong; Luo, Minjie; Yin, Kingsley; Nagele, Robert G.; Fine, Daniel H.; Yang, Jin Ming; Li, Honghua

doi:10.1186/1471-2164-9-608

Cited by 9 publications

(5 citation statements)

References 61 publications

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“…Our discovery that expression of Cytochrome b561, an abundant transmembrane protein from neuroendocrine vesicles is selectively increased in castration recurrent tumors of CWR22 tumor model is an important observation. Based on the data presented here, altered Cytochrome b561 expression does not appear to represent neuro-endocrine cells per se which is reminiscent of earlier and recent observations, where Cytochrome b561 is expressed in tumor cells lines of diverse tissue types [12,21,22]. On the basis of accumulating evidence of sustained androgen receptor signaling during the progression of CaP in response to androgen ablation [2,23], we propose that AR signaling activation may lead to the Cytochrome b561 expression in CRPC.…”

Section: Discussionsupporting

confidence: 53%

Elevated expression of the cytochrome b561, a neuroendocrine vesicle protein, in castration resistant prostate tumors

Srivastava

Mousses

Dobi

et al. 2010

CBM

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Evaluation of gene expression profiles in CWR22 prostate tumor xenografts in nude mice revealed overexpression of the Cytochrome b561, a transmembrane electron transport protein abundant in neuroendocrine vesicles, in the castration recurrent prostate cancers (CRPC). Four fold higher levels of the Cytochrome b561 was present in highly metastatic and androgen refractory LNCaP/C4-2 prostate cancer cells in comparison to androgen responsive and non-metastatic LNCaP cells. In LNCaP cells, Cytochrome b561 expression was induced by the synthetic androgen, R1881. Of note, Cytochrome b561 expression pattern correlated with known androgen regulated genes in epithelial transcriptome of primary prostate tumors. Taken together, these novel findings suggest that the expression of Cytochrome b561, is androgen regulated in the context of CaP cells and its increased expression in CRPC reflects increased androgen receptor signaling in tumor cells. These observations warrant further evaluation of functions and biomarker potential of Cytochrome b561 in CRPC.

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Section: Discussionsupporting

confidence: 53%

Elevated expression of the cytochrome b561, a neuroendocrine vesicle protein, in castration resistant prostate tumors

Srivastava

Mousses

Dobi

et al. 2010

CBM

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“…Independent of the LPS concentration [0, 2.5, 5, 10, and 100 μg/mL], there was no cytotoxic effect on cells isolated from the dermis and epidermis of the equine hoof. On the one hand, previous studies showed no cytotoxic effect of LPS on equine macrophage cell line (eCAS) [ 33 ] or astrocytes cell line [ 34 ] and even demonstrated an increased proliferation of human fibroblasts and keratinocytes after LPS treatment [ 35 ]. On the other hand, it was reported that LPS inhibited the cell growth of mesenchymal cell lines, epithelial cells and significantly decreased the viability of mouse macrophage cell line (RAW 264.7) [ 36 ].…”

Section: Discussionmentioning

confidence: 99%

Concentration Dependent Influence of Lipopolysaccharides on Separation of Hoof Explants and Supernatant Lactic Acid Concentration in an Ex Vivo/In Vitro Laminitis Model

Reisinger¹,

Schaumberger²,

Nagl³

et al. 2015

PLoS ONE

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Laminitis is one of the most common diseases in horses. It is not only painful for the animal, but also has a significant financial impact on the equine industry. This multifactorial disease affects the connective tissue of the hoof. However, the pathogenesis of laminitis is still not fully understood. Endotoxins, also known as lipopolysaccharides (LPS), and bacterial exotoxins seem to play an important role during the development of laminitis. The aim of our study was to investigate the effect of increasing LPS concentrations (0, 2.5, 5, 10, and 100 μg/mL) on cell viability of isolated epidermal and dermal hoof cells as well as on the tissue integrity of hoof explants. Furthermore, glucose, acetic acid, lactic acid, and propionic acid concentrations in explant supernatants were measured to evaluate the energy metabolism in the hoof tissue. LPS did not exhibit cytotoxic effects on epidermal or dermal cells. Force required to separate LPS treated hoof explants decreased in a concentration dependent manner. Specifically, explants incubated with 10 and 100 μg/mL needed significantly less force to separate compared to control explants. Lactic acid concentrations were significantly decreased in explants incubated with 5, 10, or 100 μg/mL LPS, while glucose, acetic acid and propionic acid concentrations were unaffected by LPS treatment. Our study indicates that LPS has no cytotoxic effect on epidermal and dermal cells isolated from hoof tissue, but impairs integrity of hoof explants. In addition, LPS led to an alteration of the lactic acid production in the lamellar tissue. Since our data highlight that LPS can affect the integrity of the equine hoof tissue in vitro, endotoxins should be further explored for their contribution to facilitate the development of laminitis.

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“…T98G cells were grown as monolayer cultures in Dulbecco’s Modified Eagle’s Medium (DMEM, Gibco), supplemented with 10% fetal bovine serum (FBS, Gibco), 100 IU/ml penicillin and 100 μg/ml streptomycin (Gibco) [35,36]. All cells were grown at 37°C in a humidified atmosphere of 95% O 2 and 5% CO 2 .…”

Section: Methodsmentioning

confidence: 99%

Loss of GSK-3 Causes Abnormal Astrogenesis and Behavior in Mice

Jung

Kim

2015

Mol Neurobiol

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Altered activity of glycogen synthase kinase-3 (GSK-3) is associated with psychiatric diseases and neurodegenerative diseases. GSK-3 is a key regulator in multiple aspects of neuronal differentiation in the brain. However, little is known about the role of GSK-3 in astrocyte development. To examine the role of GSK-3 in astrocytes, we generated a conditional knockout mouse using a GFAP-cre driver, in which the GSK-3 alpha and beta genes are deleted in astrocytes. We found that GFAP-cre-mediated GSK-3 deletion led to a larger brain. The number and size of astrocytes were increased in GSK-3 mutant brains. The levels of GFAP and phospho-STAT3, indicators of astrogenesis, were elevated in GSK-3 mutants. Furthermore, we found upregulation of astrocyte regulatory molecules such as phospho-AKT, phospho-S6, and cyclin D in GSK-3 mutant brains. Finally, GSK-3 mutant mice exhibited aberrant anxiety and social behavior. Our results suggest that GSK-3 plays a significant role in astrocyte development and behavioral control in mice.

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Lipopolysaccharide (LPS) potentiates hydrogen peroxide toxicity in T98G astrocytoma cells by suppression of anti-oxidative and growth factor gene expression

Cited by 9 publications

References 61 publications

Elevated expression of the cytochrome b561, a neuroendocrine vesicle protein, in castration resistant prostate tumors

Elevated expression of the cytochrome b561, a neuroendocrine vesicle protein, in castration resistant prostate tumors

Concentration Dependent Influence of Lipopolysaccharides on Separation of Hoof Explants and Supernatant Lactic Acid Concentration in an Ex Vivo/In Vitro Laminitis Model

Loss of GSK-3 Causes Abnormal Astrogenesis and Behavior in Mice

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