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PubMed1997

Heat shock activates c-Src tyrosine kinases and phosphatidylinositol 3-kinase in NIH3T3 fibroblasts.

There is increasing evidence that cellular responses to stress are in part regulated by protein kinases, although specific mechanisms are not well defined. The purpose of these experiments was to investigate potential upstream signaling events activated during heat shock in NIH3T3 fibroblasts. Experiments were designed to ask whether heat shock activates p60 c-Src tyrosine kinase or phosphatidylinositol 3-kinase (PI 3-kinase). Using in vitro protein kinase activity assays, it was demonstrated that heat shock stimulates c-Src and PI 3-kinase activity in a time-dependent manner. Also, there was increased PI 3-kinase activity in anti-phosphotyrosine and anti-c-Src immunoprecipitated immunocomplexes from heated cells. Heat shock activated mitogen-activated protein kinase (MAPK) and p70 S6 kinase (S6K) in these cells. The role of PI 3-kinase in regulating heat shock activation of MAPK and p70 S6K was investigated using wortmannin, a specific pharmacological inhibitor of PI 3-kinase. The results demonstrated that wortmannin inhibited heat shock activation of p70 S6K but only partially inhibited heat activation of MAPK. A dominant negative Raf mutant inhibited activation of MAPK by heat shock but did not inhibit heat shock stimulation of p70 S6K. Genistein, a tyrosine kinase inhibitor, and suramin, a growth factor receptor inhibitor, both inhibited heat shock stimulation of MAPK activity and tyrosine phosphorylation of MAPK. Furthermore, a selective epidermal growth factor receptor (EGFR) inhibitor, tryphostin AG1478, and a dominant negative EGFR mutant also inhibited heat shock activation of MAPK. Heat shock induced EGFR phosphorylation. These results suggest that early upstream signaling events in response to heat stress may involve activation of PI 3-kinase and tyrosine kinases, such as c-Src, and a growth factor receptor, such as EGFR; activation of important downstream pathways, such as MAPK and p70 S6K, occur by divergent signaling mechanisms similar to growth factor stimulation.

3T3 Cells↗

PubMed1991

Aging and heat tolerance at rest or during work.

Collectively, the literature on heat tolerance suggests that middle-aged (45-64 year old) men and women are more work-heat intolerant, and suffer more physiological strain during heat acclimation, than do younger individuals. However, it is unclear whether the age differences in work-heat intolerance and physiological strain during heat acclimation are related to age per se or associated with other factors such as certain disease states, decreased physical activity, and/or lowered aerobic fitness. In contrast, the work-heat tolerance and physiological responses during heat acclimation of habitually active or aerobically trained middle-aged men are the same or better than younger individuals. The reviewed studies emphasize the importance of aerobic fitness and pertinent morphological factors, such as body fat, body weight, and surface area in maintaining work-heat tolerance with aging. Recent studies suggest that middle-aged and older men and women may be more susceptible to greater heat strain at physiologically significant levels of dehydration than those younger. However, additional research appears necessary to support this hypothesis. When the effects of chronic debilitating diseases in the elderly (greater than 64 years old) are minimized, their heat tolerance and thermoregulatory responses are comparable to those younger. In fact, healthy and well-acclimated elderly men and women appear to perform as well as those younger during desert walks in dry heat. This review shall discuss experimental observations from previously published studies concerning aging and heat tolerance or the physiological heat strain during heat acclimation at rest or during work; and, will suggest future research efforts needed to advance the area.

Acclimatization↗

PubMedDate not supplied

Aging and human heat tolerance.

Collectively, the literature on heat tolerance suggests that middle-aged (45- to 64-year-old) men and women are more work-heat-intolerant and suffer more physiological strain during heat acclimation than younger individuals. However, it is unclear whether the age differences in work-heat intolerance and physiological strain during heat acclimation are related to age per se or associated with other factors such as certain disease states, decreased physical activity, or lowered aerobic fitness. In contrast, the work-heat tolerance and physiological responses during heat acclimation of habitually active or aerobically trained middle-aged men are the same as or better than younger individuals. The reviewed studies emphasize the importance of aerobic fitness and pertinent morphological factors, such as body fat, body weight, and surface area in maintaining work-heat tolerance with aging. Recent studies suggest that middle-aged and older men and women may be more susceptible to greater heat strain at physiologically significant levels of dehydration than those younger. However, additional research appears necessary to support this hypothesis. When the effects of chronic debilitating diseases in the elderly (64 years old and older) are minimized, their heat tolerance and thermoregulatory responses are comparable to those of younger individuals. In fact, healthy and well acclimated elderly men and women appear to perform as well as younger individuals during desert walks in dry heat. This review discusses experimental observations from previously published studies concerning aging and heat tolerance or the physiological heat strain during heat acclimation at rest or during work; and it suggests future research efforts needed to understand this topic better.

Aging↗

PubMed1983

Influence of a prior heat treatment on the enhancement by hyperthermia of X-ray-induced inactivation of cultured mammalian cells.

The effect of prior heat treatment on thermal enhancement of radiation effects in treatments of cultured M8013S cells, derived from a transplantable murine mammary carcinoma, combining X-irradiation and 30 min at 43 degrees C up to 45 min at 45 degrees C in medium without serum have been studied. Prior heat treatment induces resistance to combined heat-irradiation treatments. A treatment of 30 min at 43 degrees C without prior heat treatment led to a thermal enhancement ratio of 2.2. With a prior 30 min at 43 degrees C treatment 6 hours before the combined heat-irradiation treatment, this ratio was decreased to 1.6. The relative resistance to combined treatments is very probably the result of the thermotolerant state of the cells induced by the prior heat treatment. The effects seem to be predominantly on the shoulder of the radiation survival curve. The resistance decays when the prior heat treatment is given longer than 24 hours before the combined heat-irradiation treatment. However, in the thermotolerant state large thermal enhancement ratios can be observed, this in spite of the resistance. A treatment of 45 min at 45 degrees C, 6 hours after a prior 30 min 43 degrees C treatment, led to an enhancement ratio of 6.0 both in medium with and without serum. Without prior heat treatment, the relative survival after 45 min at 45 degrees C is too low to enable determination of thermal enhancement of radiation effects. The sensitivity of the cells to a single heat treatment appeared to be dependent on nutritional conditions. Cells treated in medium without serum were more sensitive to heat. The sensitivity of preheated thermotolerant cells to a relatively short (up to 3 hours at 43 degrees C) heat treatment appeared to be rather independent of nutritional conditions, but the sensitivity of these cells to prolonged heat treatment (longer than 4 hours at 43 degrees C) was very dependent on the nutritional state. The presence of serum (and possibly other components in complete culture medium) made thermotolerant cells much more resistant to these long heat treatments. The present results may be important for clinical application of hyperthermia in combination with radiotherapy. They may provide guidelines concerning the intervals to be applied in fractionated treatments.

Adenocarcinoma↗

PubMed1997

Postanesthetic vasoconstriction slows peripheral-to-core transfer of cutaneous heat, thereby isolating the core thermal compartment.

UNLABELLED: Forced-air warming during anesthesia increases core temperature comparably with and without thermoregulatory vasoconstriction. In contrast, postoperative forced-air warming may be no more effective than passive insulation. Nonthermoregulatory anesthesia-induced vasodilation may thus influence heat transfer. We compared postanesthetic core rewarming rates in volunteers given cotton blankets or forced air. Additionally, we compared increases in peripheral and core heat contents in the postanesthetic period with data previously acquired during anesthesia to determine how much vasomotion alters intercompartmental heat transfer. Six men were anesthetized and cooled passively until their core temperatures reached 34 degrees C. Anesthesia was then discontinued, and shivering was prevented by giving meperidine. On one day, the volunteers were covered with warmed blankets for 2 h; on the other, volunteers were warmed with forced air. Peripheral tissue heat contents were determined from intramuscular and skin thermocouples. Predicted changes in core temperature were calculated assuming that increases in body heat content were evenly distributed. Predicted changes were thus those that would be expected if vasomotor activity did not impair peripheral-to-core transfer of applied heat. These results were compared with those obtained previously in a similar study of anesthetized volunteers. Body heat content increased 159 +/- 35 kcal (mean +/- SD) more during forced-air than during blanket warming (P < 0.001). Both peripheral and core temperatures increased significantly faster during active warming: 3.3 +/- 0.7 degrees C and 1.1 +/- 0.4 degrees C, respectively. Nonetheless, predicted core temperature increase during forced-air warming exceeded the actual temperature increase by 0.8 +/- 0.3 degree C (P < 0.001). Vasoconstriction thus isolated core tissues from heat applied to the periphery, with the result that core heat content increased 32 +/- 12 kcal less than expected after 2 h of forced-air warming (P < 0.001). In contrast, predicted and actual core temperatures differed only slightly in the anesthetized volunteers previously studied. In contrast to four previous studies, our results indicate that forced-air warming increases core temperature faster than warm blankets. Postanesthetic vasoconstriction nonetheless impeded peripheral-to-core heat transfer, with the result that core temperatures in the two groups differed less than might be expected based on systemic heat balance estimates. IMPLICATIONS: Comparing intercompartmental heat flow in our previous and current studies suggests that anesthetic-induced vasodilation influences intercompartmental heat transfer and distribution of body heat more than thermoregulatory shunt vasomotion.

Adult↗

PubMed2004

Effects of a circulating-water garment and forced-air warming on body heat content and core temperature.

BACKGROUND: Forced-air warming is sometimes unable to maintain perioperative normothermia. Therefore, the authors compared heat transfer, regional heat distribution, and core rewarming of forced-air warming with a novel circulating-water garment. METHODS: Nine volunteers were each evaluated on two randomly ordered study days. They were anesthetized and cooled to a core temperature near 34 degrees C. The volunteers were subsequently warmed for 2.5 h with either a circulating-water garment or a forced-air cover. Overall, heat balance was determined from the difference between cutaneous heat loss (thermal flux transducers) and metabolic heat production (oxygen consumption). Average arm and leg (peripheral) tissue temperatures were determined from 18 intramuscular needle thermocouples, 15 skin thermal flux transducers, and "deep" hand and foot thermometers. RESULTS: Heat production (approximately 60 kcal/h) and loss (approximately 45 kcal/h) were similar with each treatment before warming. The increases in heat transfer across anterior portions of the skin surface were similar with each warming system (approximately 65 kcal/h). Forced-air warming had no effect on posterior heat transfer, whereas circulating-water transferred 21+/-9 kcal/h through the posterior skin surface after a half hour of warming. Over 2.5 h, circulating water thus increased body heat content 56% more than forced air. Core temperatures thus increased faster than with circulating water than forced air, especially during the first hour, with the result that core temperature was 1.1 degrees +/- 0.7 degrees C greater after 2.5 h (P < 0.001). Peripheral tissue heat content increased twice as much as core heat content with each device, but the core-to-peripheral tissue temperature gradient remained positive throughout the study. CONCLUSIONS: The circulating-water system transferred more heat than forced air, with the difference resulting largely from posterior heating. Circulating water rewarmed patients 0.4 degrees C/h faster than forced air. A substantial peripheral-to-core tissue temperature gradient with each device indicated that peripheral tissues insulated the core, thus slowing heat transfer.

Body Temperature↗

PubMed1990

Expression of the Heat Shock Response in a Tomato Interspecific Hybrid Is Not Intermediate between the Two Parental Responses.

While it is apparent that the heat shock response is ubiquitous, variabilities in the nature of the heat shock response between closely related species have not been well characterized. The heat shock response of three genotypes of tomato, Lycopersicon esculentum, Lycopersicon pennellii, and the interspecific sexual hybrid was characterized. The two parental genotypes differed in the nature of the heat shock proteins synthesized; the speciesspecific heat shock proteins were identified following in vivo labeling of leaf tissue with [(35)S]methionine and cysteine. The duration of, and recovery from, heat shock varied between the two species: L. esculentum tissue recovered more rapidly and protein synthesis persisted longer during a heat shock than in the wild species, L. pennellii. Both species induced heat shock protein synthesis at 35 degrees C and synthesis was maximal at 37 degrees C. The response of the F1 to heat shock was intermediate to the parental responses for duration of, and recovery from, heat shock. In other aspects, the response of the F1 to heat shock was not intermediate to the parental responses: the F1 induced only half of the L. esculentum specific heat shock proteins, and all of the L. pennellii specific heat shock proteins. A discussion of the inheritance of the regulation of the heat shock response is presented.

Journal Article↗

PubMed2000

Heat production in human skeletal muscle at the onset of intense dynamic exercise.

1. We hypothesised that heat production of human skeletal muscle at a given high power output would gradually increase as heat liberation per mole of ATP produced rises when energy is derived from oxidation compared to phosphocreatine (PCr) breakdown and glycogenolysis. 2. Five young volunteers performed 180 s of intense dynamic knee-extensor exercise ( approximately 80 W) while estimates of muscle heat production, power output, oxygen uptake, lactate release, lactate accumulation and ATP and PCr hydrolysis were made. Heat production was determined continuously by (i) measuring heat storage in the contracting muscles, (ii) measuring heat removal to the body core by the circulation, and (iii) estimating heat transfer to the skin by convection and conductance as well as to the body core by lymph drainage. 3. The rate of heat storage in knee-extensor muscles was highest during the first 45 s of exercise (70-80 J s-1) and declined gradually to 14 +/- 10 J s-1 at 180 s. 4. The rate of heat removal by blood was negligible during the first 10 s of exercise, rising gradually to 112 +/- 14 J s-1 at 180 s. The estimated rate of heat release to skin and heat removal via lymph flow was < 2 J s-1 during the first 5 s and increased progressively to 24 +/- 1 J s-1 at 180 s. The rate of heat production increased significantly throughout exercise, being 107 % higher at 180 s compared to the initial 5 s, with half of the increase occurring during the first 38 s, while power output remained essentially constant. 5. The contribution of muscle oxygen uptake and net lactate release to total energy turnover increased curvilinearly from 32 % and 2 %, respectively, during the first 30 s to 86 % and 8 %, respectively, during the last 30 s of exercise. The combined energy contribution from net ATP hydrolysis, net PCr hydrolysis and muscle lactate accumulation is estimated to decline from 37 % to 3 % comparing the same time intervals. 6. The magnitude and rate of elevation in heat production by human skeletal muscle during exercise in vivo could be the result of the enhanced heat liberation during ATP production when aerobic metabolism gradually becomes dominant after PCr and glycogenolysis have initially provided most of the energy.

Adenosine Triphosphate↗

PubMed1987

The kinetics of heat production in response to active shortening in frog skeletal muscle.

1. Tension and heat production were measured at 0 degree C in sartorius muscles from Rana temporaria in response to two extents of shortening at five velocities. Shortening was from approximately 2.4 to 2.2 microns, 2.4 to 2.3 microns and 2.3 to 2.2 micron at velocities per half-sarcomere from 0.2 to 1.56 micron s-1. 2. Tension became approximately constant at all velocities. Records of heat rate obtained by differentiating traces from which thermoelastic heat had been subtracted became negative early in shortening and then rose. Heat rate became constant during shortening only at the lowest velocity and was still rising at the end of shortening at higher velocities. The highest heat rate occurred at the end of shortening at the two highest velocities. At the end of shortening at all velocities heat rate gradually approached the isometric level measured at the short length, the half-time for decline being largest following the slowest larger shortening. 3. Heat produced as a consequence of shortening but not associated with tension recovery was determined by subtracting shortening heat measured in response to two extents of shortening to the same muscle length. The differences in shortening heat continued to increase after shortening ended, and more of the extra heat produced in response to shortening appeared after the end of rapid shortening than during shortening itself. 4. Shortening heat coefficients calculated in different ways were similar to coefficients determined in previous studies. Coefficients calculated from measurements that excluded heat produced by tension recovery and allowed for continued production of heat by processes initiated by shortening were found to increase linearly with the force maintained during shortening. 5. The results show that the kinetics of heat production during and after shortening are very sensitive to the speed of shortening and that steady rates of energy liberation are not attained during shortening of less than or equal to 10% of muscle length at velocities greater than or equal to 12% of maximum velocity.

Animals↗

PubMed1990

Comparison of heat and mechanical receptive fields of cutaneous C-fiber nociceptors in monkey.

1. Receptive-field properties were investigated in cutaneous C-fiber nociceptive afferents (CMH) responsive to mechanical and heat stimuli. Teased-fiber techniques were used to record from 28 CMHs that innervated the hairy skin of upper or lower limb in anesthetized monkeys. 2. The response to mechanical stimuli was studied with the use of calibrated von Frey probes. The response to heat stimuli was studied with the use of a laser thermal stimulator that provided stepped increases in skin temperature with rise times to the desired temperature near 100 ms. The size of the receptive field (RF) for mechanical stimuli was determined by use of a suprathreshold stimulus that consisted of a 0.5-mm-diam probe that exerted a 200-mN force (10 bar). The size of the heat RF was determined by use of a 49 degrees C stimulus applied to a 7.5-mm-diam area for 1 s. 3. Heat thresholds were determined with an ascending series of stimulus intensities and were found to be stable over many hours: they ranged from 37 to 46 degrees C (mean, 41.1 degrees C). Mechanical thresholds ranged from 1.3 to 7.3 bar (mean, 3.3 bar). There was no correlation between mechanical and heat thresholds. Both thresholds extended well below the corresponding psychophysical pain thresholds in the literature. This suggests that spatial and/or temporal summation of C-fiber input are important for pain induced by either stimulus modality. 4. Mechanical RF diameters ranged from 3.3 to 9.6 mm (mean, 4.7 mm); heat RF diameters ranged from punctate (less than 1 mm) to 9.5 mm (mean, 4.3 mm). There was a significant linear correlation between mechanical and heat RF sizes with a slope of one. The distance between the center of the mechanical RF and the center of the heat RF along one axis ranged from 0 to 1.1 mm (mean, 0.4 mm). These data indicate that the heat RFs coincided with the mechanical RFs. 5. Within the mechanical RF determined with the suprathreshold stimuli, all CMHs had one or more punctate areas of maximal mechanical sensitivity where mechanical threshold was lowest. Heat excitability extended greater than 2 mm beyond these mechanically sensitive spots. Because lateral transmission of the heat stimulus is small, this indicates that heat transduction occurs outside the regions of maximal mechanical sensitivity. 6. Both the threshold to heat and the response magnitude at suprathreshold intensities depended on the percentage of the RF area overlapped by the heat stimulus. This indicates that multiple transducer sites probably contribute to the total evoked response.(ABSTRACT TRUNCATED AT 400 WORDS)

Action Potentials↗

PubMed2002

The relationship between heat flow and vasculature in the dorsal fin of wild bottlenose dolphins Tursiops truncatus.

The dorsal fin of the bottlenose dolphin Tursiops truncatus contains blood vessels that function either to conserve or to dissipate body heat. Prior studies have demonstrated that heat flux, measured from a single position on the dorsal fin, decreases during body cooling and diving bradycardia and increases after exercise and at the termination of the dive response. While prior studies attributed changes in heat flux to changes in the pattern of blood flow, none directly investigated the influence of vascular structures on heat flux across the dorsal fin. In this study we examined whether heat flux is higher directly over a superficial vein, compared to a position away from a vein, and investigated the temporal relationship between heart rate, respiration and heat flux. Simultaneous records of heat flux and skin temperature at three positions on the dorsal fins of 19 wild bottlenose dolphins (with the fin in air and submerged) were collected, together with heart rate and respiration. When the fin was submerged, heat flux values were highest over superficial veins, usually at the distal tip, suggesting convective delivery of heat, via blood, to the skin's surface. Conversely, in air there was no relationship between heat flux and superficial vasculature. The mean difference in heat flux (48 W m(-2)) measured between the three fin positions was often equal to or greater than the heat flux that had been recorded from a single position after exercising and diving in prior studies. Tachycardia at a respiratory event was not temporally related to an increase in heat flux across the dorsal fin. This study suggests that the dorsal fin is a spatially heterogeneous thermal surface and that patterns of heat flux are strongly influenced by underlying vasculature.

Animals↗

PubMed1999

Thermoregulatory responses to acute heat loads in rats following spontaneous running.

Earlier studies showed that spontaneous exercise training in rodents shifted their core temperature and thermoeffector thresholds to high levels. The present study investigated heat loss and heat production responses to acute heat loads of exercise-trained rats. The exercise-trained rats were allowed to run in a running wheel freely for 6 months, while the sedentary controls were denied access to the wheel during the same period. Then, they were loosely restrained and put in a direct calorimeter. After thermal equilibrium had been attained, they were warmed for 30 min with an intraperitoneal electric heater (internal heating). At least 2 h later, the rats were externally warmed for 90 min by raising the ambient temperature from 24 to 38C (external warming). Hypothalamic temperature (Thy), evaporative and nonevaporative heat loss (R+C+K) and heat production were measured. Internal and external heating significantly increased Thy. During internal heating, the magnitude of the increase in Thy was significantly smaller and the amount of increase in (R+C+K) was significantly greater in the exercise-trained rats than in the controls. The slope showing the relationship between Thy and (R+C+K) in the trained rats was significantly steeper than that in the controls. During external warming, the magnitude of increase in Thy of the exercise-trained rats was significantly greater than that of the controls. The slope showing the relationship between Thy and (R+C+K) in the trained rats was not different from that in the controls. Changes in evaporative heat loss and heat production during the two types of heat load did not differ between the two groups. The results suggest that, in rats, exercise training with voluntary running improves heat tolerance through enhancing nonevaporative heat loss response. However, this may be the case only when the rats are subjected to a direct internal heat load.

Animals↗

PubMed2001

Effects of calcium on antioxidant activities and water relations associated with heat tolerance in two cool-season grasses.

Calcium (Ca2+) may be involved in plant tolerance to heat stress by regulating antioxidant metabolism or/and water relations. This study was designed to examine whether external Ca2+ treatment would improve heat tolerance in two C(3), cool-season grass species, tall fescue (Festuca arundinacea L.) and Kentucky bluegrass (Poa pratensis L.), and to determine the physiological mechanisms of Ca2+ effects on grass tolerance to heat stress. Grasses were treated with CaCl(2) (10 mM) or H(2)O by foliar application and then exposed to heat stress (35/30 degrees C) in growth chambers. Some of the Ca2+ -untreated plants were maintained at 20/15 degrees C as the temperature control. Heat stress reduced grass quality, relative water content (RWC), and chlorophyll (Chl) content of leaves in both species, but Ca2+ treatment increased all three factors under heat stress. The Ca2+ concentration in cell saps increased with heat stress and with external Ca2+ treatment in both species. Osmotic potential increased with heat stress, but external Ca2+ treatment had no effect. Osmotic adjustment increased during short-term heat stress, but then decreased with a prolonged period of stress; it was not influenced by Ca2+ treatment. The activity of superoxide dismutase (SOD) in both species increased transiently at 12 d of heat stress and then remained at a level similar to that of the control. External Ca2+ treatment had no effect on SOD activity. The activities of catalase (CAT), ascorbate peroxidase (AP), and glutathione reductase (GR) of both species decreased during heat stress. Plants treated with Ca2+ under heat stress had higher CAT, GR and AP activities than untreated plants. Lesser amounts of malondialdehyde (MDA) accumulated in Ca2+ -treated plants than in untreated plants during extended periods of heat stress. The results suggested that exogenous Ca2+ treatment enhanced heat tolerance in both tall fescue and Kentucky bluegrass. This enhancement was related to the maintenance of antioxidant activities and a decrease in membrane lipid peroxidation, but not to the regulation of osmotic potential and osmotic adjustment.

Antioxidants↗

PubMed2004

[Dynamics of heat balance during growing season of broadleaved Korean pine forest in Changbai Mountains].

Based on the gradient measurement of microclimate factors, radiation and soil heat flux from late May to early October, 2001 and by the method of Bowen ratio-energy balance (BREB), this paper estimated the latent heat and sensible heat above the broadleaved Korean pine forest in Changbai Mountains. The energy storage of forest air and vegetative was calculated, and the seasonal variations of heat balance components of the forest were analyzed. The results showed that the net radiation of the forest and the solar radiation were linearly correlated. All the heat balance components had the similar characteristics of diurnal variation to the net radiation, showing curves positive at daytime and negative at night, and the terms ranged as net radiation > latent heat > sensible heat > storage. The time of keeping positive terms in a day became shorter from June to October as influenced by shinning time. The highest net radiation was in June and the lowest in October. The monthly averaged net radiation was 0-527 and 0-(-)121 W x m(-2), and the latent heat was 0-441 and 0-(-)81 W x m(-2) for day and night, respectively. Sensible heat was 0-80 and 0-(-)26 W x m(-2), and energy storage was 0-44 and 0-(-)26 W x m(-2) for day and night, respectively. The ratio of latent heat to net radiation at daytime decreased gradually from August to October, and the ratio of sensible heat and energy storage increased correspondingly. Especially 2-3 days after the first severe frost, a sudden drop of latent heat and a sudden bounce of sensible heat appeared. The instruments and measurement methods of heat flux were also concisely discussed in this paper.

China↗

PubMed2002

Induced thermotolerance in bovine two-cell embryos and the role of heat shock protein 70 in embryonic development.

Induced thermotolerance is a phenomenon whereby exposure to a mild heat shock can induce heat shock proteins (HSP) and other cellular changes to make cells more resistant to a subsequent, more severe heat shock. Given that the 2-cell bovine embryo is very sensitive to heat shock, but can also produce HSP70 in response to elevated temperature, experiments were conducted to test whether 2-cell embryos could be made to undergo induced thermotolerance. Another objective was to test the role of the heat-inducible form of heat shock protein 70 (HSP70i) in development and sensitivity of bovine embryos to heat shock. To test for induced thermotolerance, 2-cell bovine embryos were first exposed to a mild heat shock (40 degrees C for 1 hr, or 41 degrees C or 42 degrees C for 80 min), allowed to recover at 38.5 degrees C and 5% (v/v) CO2 for 2 hr, and then exposed to a severe heat shock (41 degrees C for 4.5, 6, or 12 hr). Regardless of the conditions, previous exposure to mild heat shock did not reduce the deleterious effect of heat shock on development of embryos to the blastocyst stage. The role of HSP70i in embryonic development was tested in two experiments by culturing embryos with a monoclonal antibody to the inducible form of HSP70. At both 38.5 degrees C and 41 degrees C, the proportion of 2-cell embryos that developed to blastocyst was reduced (P < 0.05) by addition of anti-HSP70i to the culture medium. In contrast, sensitivity to heat shock was not generally increased by addition of antibody. In conclusion, bovine 2-cell embryos appear incapable of induced thermotolerance. Lack of capacity for induced thermotolerance could explain in part the increased sensitivity of 2-cell embryos to heat shock as compared to embryos at later stages of development. Results also implicate a role for HSP70i in normal development of bovine embryos.

Animals↗

PubMed1995

Induction of heat shock gene expression in colonic epithelial cells after incubation with Escherichia coli or endotoxin.

OBJECTIVE: The universal cellular response to stress is the expression of a family of genes known as heat shock or stress proteins. We investigated whether bacteria or bacterial products (endotoxin) can induce heat shock protein expression in human enterocytes. DESIGN: Controlled, in vitro study. SETTING: Cell culture laboratory. SUBJECTS: Human Caco-2 enterocyte cell line. MEASUREMENTS AND MAIN RESULTS: Incubation of confluent monolayers of Caco-2 cells with Escherichia coli C25 (1 x 10(9) bacteria/mL) for 1 hr at 37 degrees C was found to induce the expression of the 72-kilodalton molecular weight heat shock protein gene (heat shock protein-72), the major inducible form of the 70-kilodalton molecular weight heat shock protein family of stress proteins, as detected by Western blot analysis. The level of heat shock protein-72 induction after incubation with E. coli was similar to the response of Caco-2 cells to heat shock at 43 degrees C for 1 hr. The induction of heat shock protein-72 gene expression by E. coli was not purely due to the process of phagocytosis, since incubation of Caco-2 cells with latex beads (1 micron) failed to induce heat shock gene expression. To elucidate the possible mechanism of heat shock protein-72 induction mediated by bacteria, Caco-2 cells were incubated with E. coli endotoxin (200 micrograms/mL) for 1 hr at 37 degrees C. Such treatment was also found to induce the synthesis of heat shock protein-72. CONCLUSIONS: These results demonstrate that bacteria and/or bacterial products induce the heat shock gene expression in Caco-2 cells. Since intestinal epithelial cells are constantly in contact with bacteria and bacterial products, we speculate that the heat shock gene expression may be part of the natural mechanism of protection for these cells in the potentially harmful environment that may be present in the intestinal tract.

Adenocarcinoma↗

PubMed2005

Heat shock-mediated regulation of MKP-1.

Heat shock modulates cellular proinflammatory responses, and we have been interested in elucidating the mechanisms that govern this modulation. The dual specific phosphatase, MAP kinase phosphatase-1 (MKP-1), is an important modulator of cellular inflammatory responses, and we recently reported that heat shock increases expression of MKP-1. Herein we sought to elucidate the mechanisms by which heat shock modulates MKP-1 gene expression. Subjecting RAW264.7 macrophages to heat shock increased MKP-1 gene expression in a time-dependent manner. Transfection with a wild-type murine MKP-1 promoter luciferase reporter plasmid demonstrated that heat shock activates the MKP-1 promoter. When the reporter plasmid was transfected into heat shock factor-1 (HSF-1)-null fibroblasts, the MKP-1 promoter was activated in response to heat shock in a manner similar to that of wild-type fibroblasts with intact HSF-1. Site-directed mutagenesis of two potential heat shock elements in the MKP-1 promoter demonstrated that both sites are required for basal promoter activity. mRNA stability assays demonstrated that heat shock increased MKP-1 mRNA stability compared with cells maintained at 37 degrees C. Inhibition of p38 MAP kinase activity inhibited heat shock-mediated expression of MKP-1. These data demonstrate that heat shock regulates MKP-1 gene expression at both the transcriptional and posttranscriptional levels. Transcriptional mechanisms are HSF-1 independent but are dependent on putative heat shock elements in the MKP-1 promoter. Posttranscriptional mechanisms involve increased stability of MKP-1 mRNA that is partially dependent on p38 MAP kinase activity. These data demonstrate another potential mechanism by which heat shock can modulate inflammation-related signal transduction.

Animals↗

PubMed1997

Intracellular distribution of heat-induced stress glycoproteins.

Cellular heat stress results in elevated heat-shock protein (HSP) synthesis and in thermotolerance development. Recently, we demonstrated that protein glycosylation is also an integral part of the stress response with the identification of two major stress glycoproteins, GP50, associated with thermotolerance, and P-SG67, the "prompt" stress glycoprotein induced immediately during acute heat stress. In the present study, we characterized the subcellular location and redistribution of these proteins during the cellular injury and recovery phase. In unheated and heated CHO cells, both stress glycoproteins were present in each subcellular fraction isolated by differential centrifugation. However, the subcellular redistribution in the course of cellular recovery after heat stress was specific for each stress glycoprotein. GP50 was present in all subcellular fractions before heat stress, but showed relatively little redistribution after heat stress. By 24 h of recovery following stress, GP50 showed partial depletion from lysosomes and microsomes, and was mainly present in the mitochondria. Glycosylated P-SG67 was redistributed in a more complex fashion. It was seen predominantly in the lysosomes and microsomes immediately following heat-stress, but after 6 h of recovery following heat stress, it largely disappeared from the microsomes and was present mainly in the cytosol. By 24 h of recovery following heat stress, it was found predominantly in the nucleus-rich fraction and mitochondria. The localization of GP50 and P-SG67 by subcellular fractionation is consistent with immunolocalization studies and contrasts with the translocation of HSP70 after heat stress from cytosol to nuclei and nucleoli. These results reflect a characteristic distribution for each stress glycoprotein; their presence in virtually all subcellular fractions suggests multifunctional roles for the various stress glycoproteins in the cellular heat stress response.

Animals↗