Acclimatory-phase specificity of gene expression during the course of heat acclimation and superimposed hypohydration in the rat hypothalamus

Abstract

The induction of the heat-acclimated phenotype involves reprogramming the expression of genes encoding both constitutive and inducible proteins. In this investigation, we studied the global genomic response in the hypothalamus during heat acclimation, with and without combined hypohydration stress. Rats were acclimated for 2 days (STHA) or for 30 days (LTHA) at 34 degrees C. Hypohydration (10% decrease in body weight) was attained by water deprivation. 32P-labeled RNA samples from the hypothalamus were hybridized onto cDNA Atlas array (Clontech no. 1.2) membranes. Clustering and functional analyses of the expression profile of a battery of genes representing various central regulatory functions of body homeostasis demonstrated a biphasic acclimation profile with a transient upregulation of genes encoding ion channels, transporters, and transmitter signaling upon STHA. After LTHA, most genes returned to their preacclimation expression levels. In both STHA and LTHA, genes encoding hormones and neuropeptides, linked with metabolic rate and food intake, were downregulated. This genomic profile, demonstrating an enhanced transcription of genes linked with neuronal excitability during STHA and enhanced metabolic efficiency upon LTHA, is consistent with our previously established integrative acclimation model. The response to hypohydration was characterized by an upregulation of a large number of genes primarily associated with the regulation of ion channels, cell volume, and neuronal excitability. During STHA, the response was transiently desensitized, recovering upon LTHA. We conclude that hypohydration overrides the heat acclimatory status. It is notable that STHA and hypohydration gene profiles are analogous with the physiological profile described in the response to various types of brain injury.

Light Interference (LI) as a possible stressor altering HSP70 and its gene expression levels in brain and liver tissues of Golden Spiny Mice

“…Moreover, it is claimed that repeated exposure to a stressor may decrease the severity of the response, thus causing an adaptation. Stress response activates molecular mechanisms that, as a consequence, alternate physiological and behavioural reactions to the stressor (de Nadal et al, 2011;Schwimmer et al, 2006). The results of our study show that SLI acclimation of 30min each night caused an increase in gene expression and protein levels of HSP70 in brain tissue, while in hepatic tissue only protein levels were elevated.…”

Exercise-heat acclimation in humans alters baseline levels and ex vivo heat inducibility of HSP72 and HSP90 in peripheral blood mononuclear cells

“…Animal models of HA demonstrate altered gene expression profiles in critical tissues (13,31), including genes encoding elements of the heat shock response. Activation of such genes by HA also confers protection against ischemia-reperfusion injury in the rat heart (13).…”

Heat acclimation and exercise training interact when combined in an overriding and trade-off manner: physiologic-genomic linkage

“…TRI reagent (Molecular Research Center) was used to extract total RNA. The quantity and quality of the RNA were determined from its absorbance at 260 and 280 nm (Nano Drop, NP-1000) and by denaturing 1% agarose gel electrophoresis (16,34). The probes were labeled for 1 h by reverse transcription of total RNA (3 g) at 42°C in a primer mix (Clontech) containing [ 32 P]dATP (Amersham Biosciences, Buckinghamshire, UK).…”

“…The membranes were exposed for 4, 12, and 24 h to a phosphor screen and detected using a Bioimaging Analyzer BAS2000 (Fuji Photo Film). Atlas Image 2.01 software (Clontech) was used to record spot pixel density and for background subtraction before further analysis (16,34).…”