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10.1186/1471-2164-9-608 http://scihub22266oqcxt.onion/10.1186/1471-2164-9-608 19087328/?report=reader!2631585!19087328     free     free     free Deprecated: Implicit conversion from float 229.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 229.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 229.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 229.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 229.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 229.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 229.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 263.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 263.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 263.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 263.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 263.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 263.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 263.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 296.79999999999995 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       BMC+Genomics 2008 ; 9 (ä): 608 Nephropedia Template TP {{tp|p=19087328|t=2008. Lipopolysaccharide (LPS) potentiates hydrogen peroxide toxicity in T98G astrocytoma cells by suppression of anti-oxidative and growth factor gene expression |pdf=|usr=}}{{19087328}} gab.com Text Lipopolysaccharide (LPS) potentiates hydrogen peroxide toxicity in T98G astrocytoma cells by suppression of anti-oxidative and growth factor gene expression JO: BMC Genomics http://www.kidney.de/pget.php?&tw=1&pmid=19087328 #FOAvip BACKGROUND: Lipopolysaccharide (LPS) is a cell wall component of Gram-negative bacteria with proved role in pathogenesis of sepsis. Brain injury was observed with both patients dead from sepsis and animal septic models. However, in vitro administration of LPS has not shown obvious cell damage to astrocytes and other relative cell lines while it does cause endothelial cell death in vitro. These observations make it difficult to understand the role of LPS in brain parenchymal injury. RESULTS: To test the hypothesis that LPS may cause biological changes in astrocytes and make the cells to become vulnerable to reactive oxygen species, a recently developed highly sensitive and highly specific system for large-scale gene expression profiling was used to examine the gene expression profile of a group of 1,135 selected genes in a cell line, T98G, a derivative of human glioblastoma of astrocytic origin. By pre-treating T98G cells with different dose of LPS, it was found that LPS treatment caused a broad alteration in gene expression profile, but did not cause obvious cell death. However, after short exposure to H2O2, cell death was dramatically increased in the LPS pretreated samples. Interestingly, cell death was highly correlated with down-regulated expression of antioxidant genes such as cytochrome b561, glutathione s-transferase a4 and protein kinase C-epsilon. On the other hand, expression of genes encoding growth factors was significantly suppressed. These changes indicate that LPS treatment may suppress the anti-oxidative machinery, decrease the viability of the T98G cells and make the cells more sensitive to H2O2 stress. CONCLUSION: These results provide very meaningful clue for further exploring and understanding the mechanism underlying astrocyte injury in sepsis in vivo, and insight for why LPS could cause astrocyte injury in vivo, but not in vitro. It will also shed light on the therapeutic strategy of sepsis. Twit Text FOAVip Lipopolysaccharide (LPS) potentiates hydrogen peroxide toxicity in T98G astrocytoma cells by suppression of anti-oxidative and growth factor gene expression ????BMC Genomics http://www.kidney.de/pget.php?&tw=1&pmid=19087328 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=19087328 #FOAvip English Wikipedia <ref>{{Cite pmid|19087328}}</ref> Lipopolysaccharide (LPS) potentiates hydrogen peroxide toxicity in T98G astrocytoma cells by suppression of anti-oxidative and growth factor gene expression #MMPMID19087328 Yue G; Shi G; Azaro MA; Yang Q; Hu G; Luo M; Yin K; Nagele RG; Fine DH; Yang JM; Li H BMC Genomics 2008[Dec]; 9 (ä): 608 PMID19087328show ga BACKGROUND: Lipopolysaccharide (LPS) is a cell wall component of Gram-negative bacteria with proved role in pathogenesis of sepsis. Brain injury was observed with both patients dead from sepsis and animal septic models. However, in vitro administration of LPS has not shown obvious cell damage to astrocytes and other relative cell lines while it does cause endothelial cell death in vitro. These observations make it difficult to understand the role of LPS in brain parenchymal injury. RESULTS: To test the hypothesis that LPS may cause biological changes in astrocytes and make the cells to become vulnerable to reactive oxygen species, a recently developed highly sensitive and highly specific system for large-scale gene expression profiling was used to examine the gene expression profile of a group of 1,135 selected genes in a cell line, T98G, a derivative of human glioblastoma of astrocytic origin. By pre-treating T98G cells with different dose of LPS, it was found that LPS treatment caused a broad alteration in gene expression profile, but did not cause obvious cell death. However, after short exposure to H2O2, cell death was dramatically increased in the LPS pretreated samples. Interestingly, cell death was highly correlated with down-regulated expression of antioxidant genes such as cytochrome b561, glutathione s-transferase a4 and protein kinase C-epsilon. On the other hand, expression of genes encoding growth factors was significantly suppressed. These changes indicate that LPS treatment may suppress the anti-oxidative machinery, decrease the viability of the T98G cells and make the cells more sensitive to H2O2 stress. CONCLUSION: These results provide very meaningful clue for further exploring and understanding the mechanism underlying astrocyte injury in sepsis in vivo, and insight for why LPS could cause astrocyte injury in vivo, but not in vitro. It will also shed light on the therapeutic strategy of sepsis. |Antioxidants/*metabolism[MESH] |Astrocytes/drug effects/*metabolism[MESH] |Astrocytoma[MESH] |Cell Death[MESH] |Cell Line, Tumor[MESH] |Gene Expression[MESH] |Gene Expression Profiling[MESH] |Humans[MESH] |Hydrogen Peroxide/*toxicity[MESH] |Intercellular Signaling Peptides and Proteins/genetics/*metabolism[MESH] |Lipopolysaccharides/*pharmacology[MESH] |Oxidation-Reduction[MESH] |Oxidative Stress[MESH]Lipopolysaccharide (LPS) potentiates hydrogen peroxide toxicity in T98(epmc).pdf DeepDyve Pubget Overpricing