<b>Induction of heat shock protein 70 genes in human lymphocytes during fever therapy</b>

Dressel, Ralf; Heine, Lutz; Elsner, Leslie; Geginat, Gernot; Gefeller, Olaf; Kölmel, K. F.; Günther, E

doi:10.1046/j.1365-2362.1996.169319.x

Cited by 5 publications

(6 citation statements)

References 23 publications

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“…Hybridization of the mRNA probes for ␤-F 1 -ATPase (11), ANT 1 (36,44), and HSP70-1 (16) is similar to that observed in human (10,36,44), rat (11,35), mouse (16), or rabbit tissues (14) and is illustrated in Fig. 3.…”

Section: ␤-F 1 -Atpase Ant 1 and Hsp70-1 Mrnassupporting

confidence: 57%

“…␤-F 1 -ATPase mRNA levels were detected using a 1.8-kb cDNA fragment cloned from human HeLa cell line (ATCC) (11,36,46,47). HSP70-1 mRNA levels were detected using a 1.7-kb cDNA fragment cloned from human hippocampus (ATCC) (10,16,23,35). To compare different mRNA levels in the same myocardial sample, we analyzed aliquots of 15 µg total RNA from the myocardium by means of sequentially reprobing the membranes with 28S, ANT 1 , ␤-F 1 -ATPase, and HSP70-1 cDNA probes.…”

Section: Rna Isolationmentioning

confidence: 99%

“…Cardiac function and ATP preservation were measured to demonstrate that improved ischemic resistance occurred in this model. Additionally, Northern blot analyses of expression of an inducible heat shock protein (HSP70-1) gene (10,16,23), as well as genes regulating major constitutive mitochondrial membrane proteins [adenine nucleotide translocator isoform 1 (ANT 1 ) and ␤-subunit F 1 -adenosinetriphosphatase (␤-F 1 -ATPase)] (11,36,44,47) were performed to index signaling for mitochondrial biogenesis and cold adaptation. …”

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confidence: 99%

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Hypothermia preserves function and signaling for mitochondrial biogenesis during subsequent ischemia

Xue

Song

et al. 1998

American Journal of Physiology-Heart and Circulatory Physiology

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preserves function and signaling for mitochondrial biogenesis during subsequent ischemia. Am. J. Physiol. 274 (Heart Circ. Physiol. 43): H786-H793, 1998.-Hypothermia is known to protect myocardium during ischemia, but its role in induction of a protective stress response before ischemia has not been evaluated. As cold incites stress responses in other tissues, including heat shock protein induction and signaling mitochondrial biogenesis, we postulated that hypothermia in perfused hearts would produce similar phenomena while reducing injury during subsequent ischemia. Studies were performed in isolated perfused rabbit hearts (n ϭ 77): a control group (C) and a hypothermic group (H) subjected to decreasing infusate temperature from 37 to 31°C over 20 min. Subsequent ischemia during cardioplegic arrest at 34°C for 120 min was followed by reperfusion. At 15 min of reperfusion, recovery of left ventricular developed pressure (LVDP), maximum first derivative of left ventricular pressure (LV dP/dt max ), LV ϪdP/dt max , and the product of heart rate and LVDP was significantly increased in H (P Ͻ 0.01) compared with C hearts. Ischemic contracture started later in H (97.5 Ϯ 3.6 min) than in C (67.3 Ϯ 3.3 min) hearts. Myocardial ATP preservation and repletion during ischemia and reperfusion were higher in H than in C hearts. mRNA levels of the nuclear-encoded mitochondrial proteins adenine nucleotide translocase isoform 1 (ANT 1 ) and ␤-F 1 -adenosinetriphosphatase (␤-F 1 -ATPase) normalized to 28S RNA decreased in C hearts but were preserved in H hearts after reperfusion. Inducible heat shock protein (HSP70-1) mRNA was elevated nearly 4-fold after ischemia in C hearts and 12-fold in H hearts. These data indicate that hypothermia preserves myocardial function and ATP stores during subsequent ischemia and reperfusion. Signaling for mitochondrial biogenesis indexed by ANT 1 and ␤-F 1 -ATPase mRNA levels is also preserved during a marked increase in HSP70-1 mRNA.adenine nucleotide translocase isoform 1; ␤-F 1 -adenosinetriphosphatase; cold adaptation; inducible heat shock protein; myocardial reperfusion COLD-INDUCED STRESS is a phenomenon associated with an increase in inducible heat shock protein expression in various tissues (31,32). Particularly in brown adipose tissue, cold-induced stress or hypothermia also induces mitochondrial biogenesis (20,29,30). At the transcriptional level this is characterized by coordinated increases in expression of nuclear-and mitochondrial-encoded genes regulating mitochondrial membrane proteins (28). Although this signaling has been well characterized in brown adipose fat, it remains relatively unexplored in other mammalian tissues. This is surprising because stress responses in the heart secondary to heat shock or ischemia have been a major focus of investigation with respect to enhancement of tissue resistance to subsequent ischemia (14,21,33,35,40). Furthermore, hypothermia either singly or accompanied by cardioplegia is regularly employed in myocardial protection during heart surgery. T...

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Section: ␤-F 1 -Atpase Ant 1 and Hsp70-1 Mrnassupporting

confidence: 57%

Section: Rna Isolationmentioning

confidence: 99%

mentioning

confidence: 99%

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Hypothermia preserves function and signaling for mitochondrial biogenesis during subsequent ischemia

Xue

Song

et al. 1998

American Journal of Physiology-Heart and Circulatory Physiology

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“…Induction of HSP70-1 and HSP70-2 was analyzed by in situ hybridization in lymphocytes from patients undergoing fever therapy for metastatic malignant melanoma. Lymphocytes assayed immediately before fever induction were negative, but lymphocytes collected 4-6 h later, i.e., at the temperature maximum of Ն39°C, showed HSP70 induction in one-half of the patients [Dressel et al, 1996]. In positive Fig.…”

Section: Expression Of Hsp70-1 and Hsp70-2 Mrna After Induction In Vivomentioning

confidence: 95%

“…Induction of heat shock response was tested in patients undergoing fever therapy for metastatic melanoma in the Department of Dermatology, University Hospital Göttingen [Dressel et al, 1996]. Lymphocytes were obtained (see above) after fever induction by injection of bacterial lysates, and induction of HSP70 genes was tested by in situ hybridization as described above.…”

Section: Patients and Induction Of Fevermentioning

confidence: 99%

Heat-induced expression of MHC-linked HSP70 genes in lymphocytes varies at the single-cell level

Ralf

Günther

1999

J. Cell. Biochem.

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The expression of MHC-linked heat shock protein 70 (HSP70) genes HSP70-1 and HSP70-2 has been studied in human and rat lymphocytes and Concanavalin A (con A)-induced lymphoblasts by in situ hybridization and flow cytometry. In in vitro experiments transcripts of these genes were observed only after heat shock, and mitogen stimulation per se did not lead to induction. Heat shock-induced expression of HSP70-1 and HSP70-2 mRNA varied at the single-cell level. The fraction of HSP70-positive lymphocytes increased continuously with the severity of heat shock. However, 15-35% of the cells always remained HSP70 transcript negative. After fever induction in vivo similar variation of HSP70-1 and HSP70-2 mRNA expression could also be observed. Analysis of heat shocked lymphocytes by flow cytometry demonstrated that HSP70 induction varied also at the protein level, a fraction of cells always remaining unresponsive. Thus, HSP70 induction does not appear to occur in each cell and to a similar extent when a given cell population is exposed to the same stress.

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Reduced Susceptibility of Electroporated Tumor Cell Lines to Killing by Cytotoxic Lymphocytes

Dressel

Baraki

Langer

et al. 1998

Biochemical and Biophysical Research Communications

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Induction of heat shock protein 70 genes in human lymphocytes during fever therapy

Cited by 5 publications

References 23 publications

Hypothermia preserves function and signaling for mitochondrial biogenesis during subsequent ischemia

Hypothermia preserves function and signaling for mitochondrial biogenesis during subsequent ischemia

Heat-induced expression of MHC-linked HSP70 genes in lymphocytes varies at the single-cell level

Reduced Susceptibility of Electroporated Tumor Cell Lines to Killing by Cytotoxic Lymphocytes

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