Differential expression of genes in HepG2 cells caused by UC001kfo RNAi as shown by RNA-seq

2017 ◽  
Vol 37 (4) ◽  
pp. 510-515 ◽  
Author(s):  
Yan-feng Pan ◽  
Tong Su ◽  
Li-dan Chen ◽  
Tao Qin
Keyword(s):  
Differential Expression ◽  
Hepg2 Cells ◽  
Rna Seq ◽  
Expression Of Genes ◽  
Differential Expression Of Genes

scholarly journals Genetic deletion of Sphk2 confers protection against Pseudomonas aeruginosa mediated differential expression of genes related to virulent infection and inflammation in mouse lung

2019 ◽  
Author(s):  
David Lenin Ebenezer ◽  
Panfeng Fu ◽  
Yashaswin Krishnan ◽  
Mark Maienschein-Cline ◽  
Hong Hu ◽  
...  
Keyword(s):  
Signal Transduction ◽  
Pseudomonas Aeruginosa ◽  
Differential Expression ◽  
Lung Inflammation ◽  
Mouse Lung ◽  
Rna Seq ◽  
Wild Type ◽  
Expression Of Genes ◽  
Whole Transcriptome ◽  
Differential Expression Of Genes

Abstract BACKGROUND Pseudomonas aeruginosa (PA) is an opportunistic Gram-negative bacterium that causes serious life threatening and nosocomial infections including pneumonia. PA has the ability to alter host genome to facilitate its invasion, thus increasing the virulence of the organism. Sphingosine-1- phosphate (S1P), a bioactive lipid, is known to play a key role in facilitating infection. Sphingosine kinases (SPHK) 1&2 phosphorylate sphingosine to generate S1P in mammalian cells. We reported earlier that Sphk2-/- mice offered significant protection against lung inflammation, compared to wild type (WT) animals. Therefore, we profiled the differential expression of genes between the protected group of Sphk2-/- and the wild type controls to better understand the underlying protective mechanisms related to the Sphk2 deletion in lung inflammatory injury. Whole transcriptome shotgun sequencing (RNA-Seq) was performed on mouse lung tissue using NextSeq 500 sequencing system. RESULTS: Two-way analysis of variance (ANOVA) analysis was performed and differentially expressed genes following PA infection were identified using whole transcriptome of Sphk2-/- mice and their WT counterparts. Pathway (PW) enrichment analyses of the RNA seq data identified several signaling pathways that are likely to play a crucial role in pneumonia caused by PA such as those involved in: 1. Immune response to PA infection and NF-κB signal transduction; 2. PKC signal transduction; 3. Impact on epigenetic regulation; 4. Epithelial sodium channel pathway; 5. Mucin expression; and 6. Bacterial infection related pathways. Our genomic data suggests a potential role for SPHK2 in PA-induced pneumonia through elevated expression of inflammatory genes in lung tissue. Further, validation by RT-PCR on 10 differentially expressed genes showed 100% concordance in terms of vectoral changes as well as significant fold change. CONCLUSION: Using Sphk2-/- mice and differential gene expression analysis, we have shown here that S1P/SPHK2 signaling could play a key role in promoting PA pneumonia. The identified genes promote inflammation and suppress others that naturally inhibit inflammation and host defense. Thus, targeting SPHK2/S1P signaling in PA-induced lung inflammation could serve as a potential therapy to combat PA-induced pneumonia. Key Words: Pseudomonas aeruginosa; Lung infection; Sphingosine kinase 2; Sphingolipids; Gene Profiling; Resistance to Infection

scholarly journals Genetic deletion of Sphk2 confers protection against Pseudomonas aeruginosa mediated differential expression of genes related to virulent infection and inflammation in mouse lung

BMC Genomics ◽  
2019 ◽  
Vol 20 (1) ◽  
Author(s):  
David L. Ebenezer ◽  
Panfeng Fu ◽  
Yashaswin Krishnan ◽  
Mark Maienschein-Cline ◽  
Hong Hu ◽  
...  
Keyword(s):  
Signal Transduction ◽  
Pseudomonas Aeruginosa ◽  
Differential Expression ◽  
Lung Inflammation ◽  
Mouse Lung ◽  
Rna Seq ◽  
Wild Type ◽  
Expression Of Genes ◽  
Whole Transcriptome ◽  
Differential Expression Of Genes

Abstract Background Pseudomonas aeruginosa (PA) is an opportunistic Gram-negative bacterium that causes serious life threatening and nosocomial infections including pneumonia. PA has the ability to alter host genome to facilitate its invasion, thus increasing the virulence of the organism. Sphingosine-1- phosphate (S1P), a bioactive lipid, is known to play a key role in facilitating infection. Sphingosine kinases (SPHK) 1&2 phosphorylate sphingosine to generate S1P in mammalian cells. We reported earlier that Sphk2−/− mice offered significant protection against lung inflammation, compared to wild type (WT) animals. Therefore, we profiled the differential expression of genes between the protected group of Sphk2−/− and the wild type controls to better understand the underlying protective mechanisms related to the Sphk2 deletion in lung inflammatory injury. Whole transcriptome shotgun sequencing (RNA-Seq) was performed on mouse lung tissue using NextSeq 500 sequencing system. Results Two-way analysis of variance (ANOVA) analysis was performed and differentially expressed genes following PA infection were identified using whole transcriptome of Sphk2−/− mice and their WT counterparts. Pathway (PW) enrichment analyses of the RNA seq data identified several signaling pathways that are likely to play a crucial role in pneumonia caused by PA such as those involved in: 1. Immune response to PA infection and NF-κB signal transduction; 2. PKC signal transduction; 3. Impact on epigenetic regulation; 4. Epithelial sodium channel pathway; 5. Mucin expression; and 6. Bacterial infection related pathways. Our genomic data suggests a potential role for SPHK2 in PA-induced pneumonia through elevated expression of inflammatory genes in lung tissue. Further, validation by RT-PCR on 10 differentially expressed genes showed 100% concordance in terms of vectoral changes as well as significant fold change. Conclusion Using Sphk2−/− mice and differential gene expression analysis, we have shown here that S1P/SPHK2 signaling could play a key role in promoting PA pneumonia. The identified genes promote inflammation and suppress others that naturally inhibit inflammation and host defense. Thus, targeting SPHK2/S1P signaling in PA-induced lung inflammation could serve as a potential therapy to combat PA-induced pneumonia.

scholarly journals Genetic deletion of Sphk2 confers protection against Pseudomonas aeruginosa mediated differential expression of genes related to virulent infection and inflammation in mouse lung

2019 ◽  
Author(s):  
David Lenin Ebenezer ◽  
Panfeng Fu ◽  
Yashaswin Krishnan ◽  
Mark Maienschein-Cline ◽  
Hong Hu ◽  
...  
Keyword(s):  
Signal Transduction ◽  
Pseudomonas Aeruginosa ◽  
Differential Expression ◽  
Lung Inflammation ◽  
Mouse Lung ◽  
Rna Seq ◽  
Wild Type ◽  
Expression Of Genes ◽  
Whole Transcriptome ◽  
Differential Expression Of Genes

Abstract BACKGROUND Pseudomonas aeruginosa (PA) is an opportunistic Gram-negative bacteria that causes serious life threatening and nosocomial infections including pneumonia. PA has the ability to alter host genome to facilitate its invasion thus increasing the virulence of the organism. Sphingosine-1 phosphate (S1P), a bioactive lipid is known to play a key role in facilitating infection. Sphingosine kinases (SPHK)1&2 phosphorylate sphingosine to generate S1P in mammalian cells. We reported earlier that Sphk2-/- mice offered significant protection against lung inflammation, compared to wild type (WT) animals. Therefore, we profiled the differential expression of genes between the protected group of Sphk2-/- and the wild type controls to better understand the underlying protective mechanisms Sphk2 deletion in lung inflammatory injury. Whole transcriptome shotgun sequencing (RNA seq) was performed on mouse lung tissue using NextSeq 500 sequencing system. RESULTS: Two-way ANOVA analysis was performed and differentially expressed genes following PA infection were identified using whole transcriptome of Sphk2-/- mice and their wild WT counterparts. Pathway (PW) enrichment analyses of the RNA seq data identified several signaling pathways that are likely to play a crucial role in pneumonia caused by PA such as those involved in: 1. Immune response to PA infection and NF-κB signal transduction; 2. PKC signal transduction; 3. Impact on epigenetic regulation; 4. Epithelial sodium channel pathway; 5. Mucin expression; and 6. Bacterial infection related pathways. Our data clearly suggests a role for SPHK2 in PA-induced pneumonia through elevated expression of inflammatory genes in lung tissue. Further, validation by RT-PCR on 10 differentially expressed genes showed 100% concordance in terms of vectoral changes, and 70% of genes showed concordance for significant fold change. CONCLUSION: Using Sphk2-/- mice and differential gene expression analysis, we have shown here that S1P/SPHK2 signaling plays a key role in promoting PA pneumonia. The identified genes promote inflammation, and suppress others that naturally inhibit inflammation and host defense. We therefore propose a key role for SPHK2/S1P signaling in PA-induced lung inflammation, and could serve as a potential therapeutic target to combat PA-induced pneumonia.

scholarly journals Evidence for increased thermogenesis in female C57BL/6J mice housed aboard the international space station

2021 ◽  
Vol 7 (1) ◽  
Author(s):  
Carmen P. Wong ◽  
Urszula T. Iwaniec ◽  
Russell T. Turner
Keyword(s):  
Adipose Tissue ◽  
Differential Expression ◽  
International Space Station ◽  
Space Station ◽  
Interscapular Brown Adipose Tissue ◽  
International Space ◽  
Expression Of Genes ◽  
Brown Adipose ◽  
Differential Expression Of Genes ◽  
Shivering Thermogenesis

AbstractSixteen-week-old female C57BL/6J mice were sacrificed aboard the International Space Station after 37 days of flight (RR-1 mission) and frozen carcasses returned to Earth. RNA was isolated from interscapular brown adipose tissue (BAT) and gonadal white adipose tissue (WAT). Spaceflight resulted in differential expression of genes in BAT consistent with increased non-shivering thermogenesis and differential expression of genes in WAT consistent with increased glucose uptake and metabolism, adipogenesis, and β-oxidation.

Differential expression of genes that encode glycolysis enzymes in kidney and lung cancer in humans

2013 ◽  
Vol 49 (7) ◽  
pp. 707-716 ◽  
Author(s):  
N. Yu. Oparina ◽  
A. V. Snezhkina ◽  
A. F. Sadritdinova ◽  
V. A. Veselovskii ◽  
A. A. Dmitriev ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Differential Expression ◽  
Expression Of Genes ◽  
Differential Expression Of Genes

Immature versus Mature Dura Mater: II. Differential Expression of Genes Important to Calvarial Reossification

2000 ◽  
Vol 106 (3) ◽  
pp. 639
Author(s):  
Joshua A. Greenwald ◽  
Babak J. Mehrara ◽  
Jason A. Spector ◽  
Peter J. Fagenholz ◽  
Pierre B. Saadeh ◽  
...  
Keyword(s):  
Differential Expression ◽  
Dura Mater ◽  
Expression Of Genes ◽  
Differential Expression Of Genes
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