Abstract
The gene expression kinetics for human cells exposed to hyperthermic stress are not well characterized. In this study, we identified and characterized the genes that are differentially expressed in human epidermal keratinocyte (HEK) cells exposed to hyperthermic stress. In order to obtain temporal gene expression kinetics, we exposed HEK cells to a heat stress protocol (44 °C for 40 min) and used messenger RNA (mRNA) microarrays at 0 h, 4 h and 24 h post-exposure. Bioinformatics software was employed to characterize the chief biological processes and canonical pathways associated with these heat stress genes. The data shows that the genes encoding for heat shock proteins (HSPs) that function to prevent further protein denaturation and aggregation, such as HSP40, HSP70 and HSP105, exhibit maximal expression immediately after exposure to hyperthermic stress. In contrast, the smaller HSPs, such as HSP10 and HSP27, which function in mitochondrial protein biogenesis and cellular adaptation, exhibit maximal expression during the “recovery phase”, roughly 24 h post-exposure. These data suggest that the temporal expression kinetics for each particular HSP appears to correlate with the cellular function that is required at each time point. In summary, these data provide additional insight regarding the expression kinetics of genes that are triggered in HEK cells exposed to hyperthermic stress.
Highlights
Human beings frequently encounter a wide variety of hyperthermic stressors
After confirming that the human epidermal keratinocyte (HEK) cells survived post-exposure, we sought to test whether our selected hyperthermic stress protocol induced an appreciable transcriptional stress response To investigate the transcriptional stress response, we exposed HEK cells to hyperthermic stress and used microarray gene chips to quantify the expression level of genes at 0, 4 and 24 h post-exposure (Figure 1A)
We examined the temporal gene expression kinetics for HEK cells exposed to hyperthermic stress
Summary
Human beings frequently encounter a wide variety of hyperthermic stressors. Common examples include exposure to hot conducting objects, elevated environmental temperatures, as well as electromagnetic radiation from the sun and numerous man-made sources, such as lasers, communication devices and imaging systems [1,2,3,4,5,6,7,8,9,10]. The CSR is immediately activated in response to stress stimuli, and a hallmark of this response is the robust transcriptional expression of hundreds of diverse genes These genes encode for a multitude of proteins involved in many important functions, including cellular survival, deoxyribonucleic acid (DNA) sensing and repair, redox regulation, proteolysis, molecular chaperoning, cell cycle control and apoptosis [12,13]. We used bioinformatics software to characterize the chief biological processes and canonical pathways associated with these genes These data provide valuable new insights that give us a much clearer picture of the genes and intracellular signaling pathways that are triggered in human cells exposed to hyperthermic stress. Values were calculated in relation to β-actin and normalized to a separate RNA calibrator
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