Gene expression profiling of the response to thermal injury in human cells

Dinh, Hong-Khanh B.; Zhao, Bin; Schuschereba, Steven T.; Merrill, Gerald A.; Bowman, Phillip D.

doi:10.1152/physiolgenomics.2001.7.1.3

Cited by 34 publications

(24 citation statements)

References 40 publications

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“…An experiment reported in 1996 (94) used an array containing 1,000 genes to examine changes in gene expression in human T cells and demonstrated the feasibility of using this technology to identify new candidate heatresponsive genes. Another study involved exposing cultured human retinal pigment epithelial cells to sublethal heat shock (55°C for 3 s) (25). In a third, mice were immersed in 43°C water for 20 min and changes in gene expression in testes were examined (91).…”

Section: Changes In Expression Of Other Genes As a Results Of Heat Stressmentioning

confidence: 99%

Invited Review: Effects of heat and cold stress on mammalian gene expression

Sonna

Fujita

Gaffin

et al. 2002

Journal of Applied Physiology

547

409

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This review examines the effects of thermal stress on gene expression, with special emphasis on changes in the expression of genes other than heat shock proteins (HSPs). There are ∼50 genes not traditionally considered to be HSPs that have been shown, by conventional techniques, to change expression as a result of heat stress, and there are <20 genes (including HSPs) that have been shown to be affected by cold. These numbers will likely become much larger as gene chip array and proteomic technologies are applied to the study of the cell stress response. Several mechanisms have been identified by which gene expression may be altered by heat and cold stress. The similarities and differences between the cellular responses to heat and cold may yield key insights into how cells, and by extension tissues and organisms, survive and adapt to stress.

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Section: Changes In Expression Of Other Genes As a Results Of Heat Stressmentioning

confidence: 99%

Invited Review: Effects of heat and cold stress on mammalian gene expression

Sonna

Fujita

Gaffin

et al. 2002

Journal of Applied Physiology

547

409

View full text Add to dashboard Cite

show abstract

“…Studies in which gene expression is analyzed by cDNA microarrays during the recovery phase after exposure to HS have demonstrated that HS modifies expression of many genes in addition to the classic HSPs, including those involved in regulation of transcription, growth, DNA repair, apoptosis, signaling, and cytoskeletal function (Dinh et al, 2001;Murray et al, 2004;Sonna et al, 2002a,b).…”

Section: Hsp and Heat Shock Factor-1mentioning

confidence: 99%

CXC Chemokines: A New Family of Heat-Shock Proteins?

Nagarsekar

Hasday

Singh

2005

Immunological Investigations

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The heat shock (HS) response is a generalized stress response that is characterized by the induced synthesis of a family of proteins referred to as heat shock proteins (HSPs). These proteins protect cells from a myriad of stressful insults in part by functioning as chaperones for denatured proteins. Increasing evidence suggests that the stress response is not limited to the HSP family of genes, but includes numerous other genes that are regulated by HS through the activation of the stress-activated transcription factor, heat shock factor-1 (HSF-1). Based on observations from our own in vivo hyperthermia models, we hypothesized that the CXC chemokine family of neutrophil activators and chemoattractants might be a previously unrecognized class of HS-responsive genes. Analysis of the promoters of the CXC family of chemokines in both human and mouse showed that they share a common promoter organization in which multiple copies of the HSF-1 binding sequence (heat shock response element, HRE) are present in the 5'-upstream flanking region of each of these genes. We have reviewed previous work from our own laboratory and others demonstrating a strong correlation between activation of HSPs and generation of CXC chemokines. Although rigorous experimental evidence is still required to support this hypothesis, this strong and consistent correlation between expression of HSPs and CXC chemokines in vivo and in vitro model systems suggests that the putative HREs present in the CXC chemokine genes are functionally active. We speculate that the activation of the HS response during febrile range hyperthermia, inflammation, infection and injury directly enhances expression of the CXC chemokines, thereby augmenting neutrophil delivery to sites of infection and injury during febrile illnesses.

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“…Recent DNA microarray and computational microarray analyzing technologies have provided a view of the expression (9,(14)(15)(16)(17)(18)(19)(20)(21)(22)(23)(24)(25). It is well known that cancer cells exposed to HT of more than 42.5˚C will undergo cell death, whereas exposure to MHT conditions, i.e., temperatures up to 42.5˚C, produces only slight or no cytotoxicity (26).…”

Section: Introductionmentioning

confidence: 99%

Gene networks related to the cell death elicited by hyperthermia in human oral squamous cell carcinoma HSC-3 cells

Tabuchi

Wada

Furusawa³

et al. 2011

Int J Mol Med

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Abstract. Local hyperthermia (HT) for various types of malignant tumors has shown promising antitumor effects. To confirm the detailed molecular mechanism underlying cell death induced by HT, gene expression patterns and gene networks in human oral squamous cell carcinoma (OSCC) cells were examined using a combination of DNA microarray and bioinformatics tools. OSCC HSC-3 cells were treated with HT at 44˚C for 90 min or mild hyperthermia (MHT) at 42˚C for 90 min, followed by culturing at 37˚C for 0-24 h. Treatment of cells with HT prevented cell proliferation (62%) and induced cell death (17%), whereas these alterations were not observed in cells treated with MHT. Microarray analysis revealed substantial differences with respect to gene expression patterns and biological function for the two different hyperthermic treatments. Moreover, we identified the temperature-specific gene networks D and H that were obtained from significantly up-regulated genes in the HT and MHT conditions, respectively, using Ingenuity pathway analysis tools. Gene network D, which contains 14 genes such as ATF3, DUSP1 and JUN, was associated with relevant biological functions including cell death and cellular movement. Gene network H, which contains 13 genes such as BAG3, DNAJB1 and HSPA1B, was associated with cellular function and maintenance and cellular assembly and organization. These findings provide a basis for understanding the detailed molecular mechanisms of cell death elicited by HT in human OSCC cells. IntroductionIn the treatment of oral squamous cell carcinoma (OSCC), treatment outcomes have improved in the past two decades due to progress in reconstructive techniques, stereotactic radiotherapy, new anticancer drugs such as taxanes, and combinations of these therapeutic modalities (1). Nonetheless, it is well known that patients with advanced tumors or tumor recurrence have a poor prognosis with a median survival period less than one year (2). Local hyperthermia (HT) for various malignant tumors including OSCC has been recognized as an effective and attractive tool with the advantages of relatively few side effects and slight damage to normal tissue. Combinations of HT with chemotherapy, radiotherapy or both have been clinically used for patients with cancer in various organs, and their antitumor effects have been verified by many clinical trials (3-7).In general, HT elicits a wide spectrum of stress responses such as induction of heat shock proteins (HSPs), protein aggregation, an imbalance of protein homeostasis, DNA and RNA damage, reactive oxygen species production, cell growth arrest and cell death in mammalian cells (8,9). In particular, HSPs, which are induced by heat, behave as molecular chaperones and exert strong cytoprotective effects that prevent cell death. The treatment of cells with HT induces numerous signal transduction pathways which contribute variously to cell death and survival (10-12). Although many biological processes are affected by HT, the overall responses to HT in mammalian cells remain unknown.Re...

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Gene expression profiling of the response to thermal injury in human cells

Cited by 34 publications

References 40 publications

Invited Review: Effects of heat and cold stress on mammalian gene expression

Invited Review: Effects of heat and cold stress on mammalian gene expression

CXC Chemokines: A New Family of Heat-Shock Proteins?

Gene networks related to the cell death elicited by hyperthermia in human oral squamous cell carcinoma HSC-3 cells

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