The time-profile of the PBMC HSP70 response to in vitro heat shock appears temperature-dependent

Abstract

Heat shock proteins (HSPs) are synthesised by cells subsequent to a stress exposure and are known to confer protection to the cell in response to a second challenge. HSP induction and decay are correlated to thermotolerance and may therefore be used as a biomarker of thermal history. The current study tested the temperature-dependent nature of the heat shock response and characterised its time profile of induction. Whole blood from 6 healthy males (Age: 26 +/- (SD) 2 yrs; Body mass 74.2 +/- 3.8 kgs; VO(2max): 49.1 +/- 4.0 ml.kg(-1).min(-1)) were isolated and exposed to in vitro heat shock (HS) at 37, 38, 39, 40, and 41 degrees C for a period of 90 min. After HS the temperature was returned to 37 degrees C and intracellular HSP70 was quantified from the leukocytes at 0, 2, 4, and 6 h after heat treatment. The concentration of HSP70 was not different between temperatures (P > 0.05), but the time-profile of HSP70 synthesis appeared temperature-dependent. At control (37 degrees C) and lower temperatures (38-39 degrees C) the mean HSP70 concentration increased up to 4 h post HS (P < 0.05) and then returned towards baseline values by 6 h post HS. With in vitro hyperthermic conditions (40-41 degrees C), the time-profile was characterised by a sharp rise in HSP70 levels immediately after treatment (P < 0.05 for 40 degrees C at 0 h), followed by a progressive decline over time. The results suggest a temperature-dependent time-profile of HSP70 synthesis. In addition, the temperature at which HSP70 is inducted might be lower than 37 degrees C.

Whole‐genome expression analysis in primary human keratinocyte cell cultures exposed to 60 GHz radiation

“…Using real-time RT-PCR, we verified that a 1 8C rise does not induce heat shock protein 70 and heat shock protein 27 (HSP70 and HSP27, respectively) expression in human keratinocytes (data not shown). These results confirm data from literature, showing that such a small temperature increase does not trigger a thermal biological response [Lovell et al, 2007]. This was confirmed by the DNA microarray analysis.…”

The effect of 15 consecutive days of heat–exercise acclimation on heat shock protein 70

“…Furthermore, lower levels of serum Hsp70 were measured after the second day of exercise compared to the first, indicating initial desensitisation of the heat shock response, which represents the development of thermotolerance. Thus, our data is consistent with previous studies conducted on thermotolerance in humans (Riabowol et al 1988;Walsh et al 2001;Marshall et al 2006;Lovell et al 2007). Furthermore, the increase in serum Hsp70 during exercise was inversely correlated to the resting values of serum Hsp70.…”

“…Whilst there are numerous human studies looking at Hsp70 during thermotolerance and exercise (Riabowol et al 1988;Walsh et al 2001;Fehrenbach et al 2005;Marshall et al 2006;Lovell et al 2007), there have been very few human studies monitoring the Hsp70 response during actual heat acclimation and exercise. Thermotolerance is defined as the organism's ability to survive an otherwise lethal heat stress from prior heat exposure, and heat acclimation is defined as the body's ability to perform continuous work in an elevated, but non-lethal, environmental temperature (Moseley 1997).…”

“…It is well known that heat and exercise greatly accelerate the synthesis of the inducible Hsp, especially Hsp70 (Riabowol et al 1988;Walsh et al 2001;Marshall et al 2006;Lovell et al 2007). Hsp70 is thought to have both a cellular (Welch and Feramisco 1984) and systemic protective role (Walsh et al 2001;Broquet et al 2003;Hunter-Lavin et al 2004).…”

Exercise-induced dehydration with and without environmental heat stress results in increased oxidative stress

“…While in the current study we found only a trend (p = 0.08) for TBARS (an indirect measure of MDA) to increase during dehydration, the increases in MDA from Paik et al (2009) were similar to GSSG increases in our own study. Our contradictory findings to the literature is most likely due to a myriad of factors, including lower stress levels incurred during cycle exercise rather than running (Byrne et al 2004), shorter duration of exposure to heat (Lovell et al 2007), increased scavenging activity of catalase (Mena et al 1991), or lack of specificity of the TBARS assay (Fisher-Wellman and Bloomer 2009). However, the current study and previous work (Paik et al 2009) implies that hydration state can influence markers of lipid peroxidation, warranting further investigation.…”