Long‐term effects of hypothermia on neuronal cell death <scp>and</scp> the concentration of apoptotic proteins after incomplete cerebral ischemia <scp>and</scp> reperfusion in rats

Eberspächer, Eva; Werner, Christian; Engelhard, Kristin; Pape, Monika; Laacke, Lien; Winner, D.; Hollweck, Regina; Hutzler, Peter; Kochs, Eberhard

doi:10.1111/j.1399-6576.2005.00649.x

Cited by 39 publications

(24 citation statements)

References 42 publications

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“…It lowers metabolic rate, limits edema formation, and interrupts necrosis/apoptosis. 29,30 In addition, hypothermia reduces intracellular calcium rises after ischemia; the mechanism of this effect is not clear. Hypothermia may impair glutamate-mediated calcium influx or directly inhibit calcium-mediated effects on calcium/calmodulin kinase.…”

Section: Introductionmentioning

confidence: 99%

Induced Hypothermia for Acute Stroke

Hemmen

Lyden

2007

Stroke

101

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Section: Introductionmentioning

confidence: 99%

Induced Hypothermia for Acute Stroke

Hemmen

Lyden

2007

Stroke

101

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“…A similar pre-mitochondrial effect of mild hypothermia has been described after cerebral ischemia [42,54]. which could be explained by elevated Bcl-2 and Bcl-X L levels and a decrease of Bax and Bak [55,56]. The effect of RT on the expression levels of Bcl-2 proteins is currently under investigation in Jurkat cells, although we should not expect dramatic changes in such short periods of time, as already demonstrated in ischemia models [54,57].…”

Section: Discussionmentioning

confidence: 53%

The extrinsic and intrinsic apoptotic pathways are differentially affected by temperature upstream of mitochondrial damage

2006

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It is well known that mild hypothermia prevents neuronal cell death following cerebral ischemia, although it can also cause apoptosis in other cell types. Thus, incubation at room temperature (RT) has been shown to induce apoptosis in hematopoietic cells, including Jurkat T leukemia cells. To further understand the apoptotic events that can be activated at RT, we compared the induction of apoptosis by several apoptotic insults in Jurkat cells stimulated at 37 degrees C or RT. Retinoid-related molecules, which induce apoptosis via the intrinsic pathway, failed to induce apoptosis when cells were treated at RT, as determined by various apoptotic parameters including cytochrome c release and activation of caspase 3. In contrast, most apoptotic events were enhanced by lower temperatures when cells were stimulated with anti-Fas antibody via the extrinsic pathway. Ultraviolet radiation produced partial effects at RT, correlating with its capacity to activate both pathways. Our results indicate that the core caspase machinery is operational under mild hypothermia conditions. Experiments using purified recombinant caspases and cell-free assays confirmed that caspases are fully functional at RT. Other hallmark events of apoptosis, such as phosphatidylserine externalization and formation of apoptotic bodies were variably affected by RT in a stimulus-dependent manner, suggesting the existence of critical steps that are sensitive to temperature. Thus, analysis of apoptosis at RT might be useful to (i) discriminate between the extrinsic and intrinsic pathways in Jurkat cells treated with prospective stimuli, and (ii) to unravel temperature-sensitive steps of apoptotic signaling cascades.

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“…Laboratory in vivo models of cerebral ischemia show that when hypothermia is not delayed (Eberspacher et al, 2005), delayed by minutes (Ikonomidou et al, 1989;Baker et al, 1992;Colbourne et al, 2000Colbourne et al, , 2003Zhang et al, 2011) or hours (Krieger and Yenari, 2004;Roelfsema et al, 2004;Tsutsumi et al, 2004), protection can result. However, fewer studies have looked at the permanence of hypothermic protection.…”

Section: Delayed Application Of Hypothermia Can Be Detrimental After mentioning

confidence: 99%

Limitations of Mild, Moderate, and Profound Hypothermia in Protecting Developing Hippocampal Neurons After Simulated Ischemia

Gregersen

Lee

Gabatto

et al. 2013

Therapeutic Hypothermia and Temperature Management

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Long‐term effects of hypothermia on neuronal cell death and the concentration of apoptotic proteins after incomplete cerebral ischemia and reperfusion in rats

Cited by 39 publications

References 42 publications

Induced Hypothermia for Acute Stroke

Induced Hypothermia for Acute Stroke

The extrinsic and intrinsic apoptotic pathways are differentially affected by temperature upstream of mitochondrial damage

Limitations of Mild, Moderate, and Profound Hypothermia in Protecting Developing Hippocampal Neurons After Simulated Ischemia

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