Gene expression profiles of four heat shock proteins in response to different acute stresses in shrimp, Litopenaeus vannamei

2012 ◽  
Vol 156 (3-4) ◽  
pp. 211-220 ◽  
Author(s):  
Zhaoying Qian ◽  
Xiaolin Liu ◽  
Lijun Wang ◽  
Xianzong Wang ◽  
Yang Li ◽  
...  
Keyword(s):  
Gene Expression ◽  
Heat Shock ◽  
Heat Shock Proteins ◽  
Litopenaeus Vannamei ◽  
Expression Profiles ◽  
Gene Expression Profiles ◽  
Shock Proteins

scholarly journals Gene Expression in Porphyromonas gingivalis after Contact with Human Epithelial Cells

2005 ◽  
Vol 73 (4) ◽  
pp. 2327-2335 ◽  
Author(s):  
Yumiko Hosogi ◽  
Margaret J. Duncan
Keyword(s):  
Gene Expression ◽  
Epithelial Cells ◽  
Porphyromonas Gingivalis ◽  
Expression Profiles ◽  
Gene Expression Profiles ◽  
Cell Types ◽  
Adverse Conditions ◽  
Human Epithelial Cells ◽  
Host Epithelium ◽  
Shock Proteins

ABSTRACT Porphyromonas gingivalis, a gram-negative oral anaerobe, is strongly associated with adult periodontitis. The adherence of the organism to host epithelium signals changes in both cell types as bacteria initiate infection and colonization and epithelial cells rally their defenses. We hypothesized that the expression of a defined set of P. gingivalis genes would be consistently up-regulated during infection of HEp-2 human epithelial cells. P. gingivalis genome microarrays were used to compare the gene expression profiles of bacteria that adhered to HEp-2 cells and bacteria that were incubated alone. Genes whose expression was temporally up-regulated included those involved in the oxidative stress response and those encoding heat shock proteins that are essential to maintaining cell viability under adverse conditions. The results suggest that contact with epithelial cells induces in P. gingivalis stress-responsive pathways that promote the survival of the bacterium.

Exertional heat injury and gene expression changes: a DNA microarray analysis study

2004 ◽  
Vol 96 (5) ◽  
pp. 1943-1953 ◽  
Author(s):  
Larry A. Sonna ◽  
C. Bruce Wenger ◽  
Scott Flinn ◽  
Holly K. Sheldon ◽  
Michael N. Sawka ◽  
...  
Keyword(s):  
Gene Expression ◽  
Stress Response ◽  
Heat Shock ◽  
Heat Shock Proteins ◽  
Molecular Evidence ◽  
Peripheral Blood Mononuclear ◽  
Heat Injury ◽  
Shock Proteins

This study examined gene expression changes associated with exertional heat injury (EHI) in vivo and compared these changes to in vitro heat shock responses previously reported by our laboratory. Peripheral blood mononuclear cell (PBMC) RNA was obtained from four male Marine recruits (ages 17-19 yr) who presented with symptoms consistent with EHI, core temperatures ranging from 39.3 to 42.5°C, and elevations in serum enzymes such as creatine kinase. Controls were age- and gender-matched Marines from whom samples were obtained before and several days after an intense field-training exercise in the heat (“The Crucible”). Expression analysis was performed on Affymetrix arrays (containing ∼12,600 sequences) from pooled samples obtained at three times for EHI group (at presentation, 2-3 h after cooling, and 1-2 days later) and compared with control values (average signals from two chips representing pre- and post-Crucible samples). After post hoc filtering, the analysis identified 361 transcripts that had twofold or greater increases in expression at one or more of the time points assayed and 331 transcripts that had twofold or greater decreases in expression. The affected transcripts included sequences previously shown to be heat-shock responsive in PBMCs in vitro (including both heat shock proteins and non-heat shock proteins), a number of sequences whose changes in expression had not previously been noted as a result of in vitro heat shock in PBMCs (including several interferon-induced sequences), and several nonspecific stress response genes (including ubiquitin C and dual-specificity phosphatase-1). We conclude that EHI produces a broad stress response that is detectable in PBMCs and that heat stress per se can only account for some of the observed changes in transcript expression. The molecular evidence from these patients is thus consistent with the hypothesis that EHI can result from cumulative effects of multiple adverse interacting stimuli.

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