Influence of hypothermia on post-ischemic inflammation: Role of nuclear factor kappa B (NFκB)

Yenari, Midori A.; Han, Hyung Soo

doi:10.1016/j.neuint.2006.03.016

Cited by 115 publications

(95 citation statements)

References 81 publications

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“…A protective effect of therapeutic hypothermia has also been reported after cardiac arrest in adults 165 , while hypothermia as rescue therapy after stroke and traumatic brain injury has so far shown disappointing results [166][167][168] . • Normal background activity with some electrical seizure activity…”

Section: History Of Therapeutic Hypothermiamentioning

confidence: 99%

Post-hypoxic hypothermia is protective in human NT2-N neurons regardless of oxygen concentration during reoxygenation

et al. 2009

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Section: History Of Therapeutic Hypothermiamentioning

confidence: 99%

Post-hypoxic hypothermia is protective in human NT2-N neurons regardless of oxygen concentration during reoxygenation

et al. 2009

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“…Hypothermia can also modify gene expression responses to ischemia/reperfusion of brain (Fukui et al 2006;Kobayashi et al 2008;Ohta et al 2007;Yenari and Han 2006) and liver (Niemann et al 2010). In the spleen, changes in cytokine and chemokine expression occur even after sympathetic denervation, suggesting that cold itself, and not the increase in sympathetic activity that occurs during hypothermic exposure, may be responsible for some of the changes seen (Ganta et al 2006).…”

Section: Introductionmentioning

confidence: 99%

A microarray analysis of the effects of moderate hypothermia and rewarming on gene expression by human hepatocytes (HepG2)

Sonna

Kuhlmeier

Khatri

et al. 2010

Cell Stress and Chaperones

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The gene expression changes produced by moderate hypothermia are not fully known, but appear to differ in important ways from those produced by heat shock. We examined the gene expression changes produced by moderate hypothermia and tested the hypothesis that rewarming after hypothermia approximates a heat-shock response. Six sets of human HepG2 hepatocytes were subjected to moderate hypothermia (31°C for 16 h), a conventional in vitro heat shock (43°C for 30 min) or control conditions (37°C), then harvested immediately or allowed to recover for 3 h at 37°C. Expression analysis was performed with Affymetrix U133A gene chips, using analysis of variance-based techniques. Moderate hypothermia led to distinct time-dependent expression changes, as did heat shock. Hypothermia initially caused statistically significant, greater than or equal to twofold changes in expression (relative to controls) of 409 sequences (143 increased and 266 decreased), whereas heat shock affected 71 (35 increased and 36 decreased). After 3 h of recovery, 192 sequences (83 increased, 109 decreased) were affected by hypothermia and 231 (146 increased, 85 decreased) by heat shock. Expression of many heat shock proteins was decreased by hypothermia but significantly increased after rewarming. A comparison of sequences affected by thermal stress without regard to the magnitude of change revealed that the overlap between heat and cold stress was greater after 3 h of recovery than immediately following thermal stress. Thus, while some overlap occurs (particularly after rewarming), moderate hypothermia produces extensive, timedependent gene expression changes in HepG2 cells that differ in important ways from those induced by heat shock.

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“…This should be investigated to confirm that there is also enhanced expression of the proinflammatory target genes that are regulated by NFκB and important in stroke pathophysiology. The latter include molecules such as intercellular cell adhesion molecule 1, inducible nitric oxide synthase, cyclooxygenase-2, interleukin-1β and tumor necrosis factor α [3,4]. A vicious cycle can ensue, as cytokines induced by NFκB activation can then act as stimuli for more NFκB activation [43].…”

Section: Discussionmentioning

confidence: 99%

“…Nuclear factor κB (NFκB) is a transcription factor that is key in amplifying the inflammatory response involved in stroke pathophysiology [3,4]. Increased NFκB activation has been demonstrated in human stroke [5,6] and experimental models of brain ischemia [5,[7][8][9][10][11][12][13][14].…”

Section: Introductionmentioning

confidence: 99%

Protein–energy malnutrition increases activation of the transcription factor, nuclear factor κB, in the gerbil hippocampus following global ischemia☆

Nazarali

Paterson

2008

The Journal of Nutritional Biochemistry

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Protein-energy malnutrition (PEM) exacerbates functional impairment caused by brain ischemia. This is correlated with reactive gliosis, which suggests an increased inflammatory response. The objective of the current study was to investigate if PEM increases hippocampal activation of nuclear factor κB (NFκB), a transcription factor that amplifies the inflammatory response involved in ischemic brain injury. Mongolian gerbils (11-12 weeks old) were randomly assigned to control diet (12.5% protein) or protein-deficient diet (2%) for 4 weeks. The 2% protein group had a 15% decrease in voluntary food intake (P<.001; unpaired t test), resulting in PEM. Body weight after 4 weeks was 20% lower in the PEM group (P<.001). Gerbils were then exposed to sham surgery or global ischemia induced by 5-min bilateral common carotid artery occlusion. PEM independently increased hippocampal NFκB activation detected by electrophoretic mobility shift assay at 6 h after surgery (P=.014; 2-factor ANOVA). Ischemia did not significantly affect NFκB activation nor was there interaction between diet and ischemia. Serum glucose and cortisol concentrations at 6 h postischemia were unaltered by diet or ischemia. A second experiment using gerbils of the same age and feeding paradigm demonstrated that PEM also increases hippocampal NFκB activation in the absence of surgery. These findings suggest that PEM, which exists in 16% of elderly patients at admission for stroke, may worsen outcome by increasing activation of NFκB. Since PEM increased NFκB activation independent of ischemia or surgery, the data also have implications for the inflammatory response of the many individuals affected globally by PEM.

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Influence of hypothermia on post-ischemic inflammation: Role of nuclear factor kappa B (NFκB)

Cited by 115 publications

References 81 publications

Post-hypoxic hypothermia is protective in human NT2-N neurons regardless of oxygen concentration during reoxygenation

Post-hypoxic hypothermia is protective in human NT2-N neurons regardless of oxygen concentration during reoxygenation

A microarray analysis of the effects of moderate hypothermia and rewarming on gene expression by human hepatocytes (HepG2)

Protein–energy malnutrition increases activation of the transcription factor, nuclear factor κB, in the gerbil hippocampus following global ischemia☆

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