Genomic response of the rat brain to global ischemia and reperfusion

Büttner, F; Cordes, Christian; Gerlach, Frank; Heimann, Axel; Alessandri, Beat; Luxemburger, Ulrich; Türeci, Özlem; Hankeln, Thomas; Kempski, Oliver; Burmester, Thorsten

doi:10.1016/j.brainres.2008.10.045

Cited by 28 publications

(25 citation statements)

References 63 publications

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“…Our study demonstrates that CYGB is significantly up-regulated at both transcriptional and translational levels in a time-dependent manner. However, it must be noted that two previous studies reported that the expression of CYGB was not significantly upregulated in the ischemic model of adult rats (44,45). A possible explanation for the paradoxical findings is that there were some limitations in these two studies, such that no detailed data were presented to illustrate the changes in CYGB expression during the first 36 h after ischemia, and different animal models that only suffered ischemic treatment were used.…”

Section: Discussionmentioning

confidence: 92%

Mechanisms of Neuroprotection from Hypoxia-Ischemia (HI) Brain Injury by Up-regulation of Cytoglobin (CYGB) in a Neonatal Rat Model

Tian

Yang

Xiao

et al. 2013

Journal of Biological Chemistry

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Background: Potential functions of cytoglobin (CYGB) in neonatal hypoxia-ischemia (HI) brain injury have not been reported. Results: Up-regulation of CYGB reduces HI injury and improves long term cognitive impairment after neonatal HI. Conclusion: CYGB exhibits neuroprotective effects, possibly through antioxidant and antiapoptotic functions as well as by stimulating angiogenesis. Significance: These results provide a novel target for developing a clinically relevant strategy for future studies.

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Section: Discussionmentioning

confidence: 92%

Mechanisms of Neuroprotection from Hypoxia-Ischemia (HI) Brain Injury by Up-regulation of Cytoglobin (CYGB) in a Neonatal Rat Model

Tian

Yang

Xiao

et al. 2013

Journal of Biological Chemistry

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“…By monitoring oligonucleotide microarrays of approximately 30,000 transcripts after global transient ischemia in rat brain, it was determined that the immediate response to transient ischemia is mediated by the induction of specific transcription factors and stress genes (2). Delayed gene expression was characterized by inflammation and a delayed response by immune-related genes.…”

Section: Discussionmentioning

confidence: 99%

Cluster analysis of mrna expression levels identifies multiple sequential patterns following focal cerebral ischemia

Kaido¹,

Kempski²,

Heimann³

et al. 2012

Turkish Neurosurgery

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AIM:The purpose of this study is to detect gene expression patterns following focal cerebral ischemia. MATeRIAL and MeTHods:25 male Wistar rats were divided into control (n = 8) and ischemic (n = 17) groups. In the ischemic group, slowly progressing focal ischemia was simulated by two-vein occlusion with spreading depression (SD) a cortical microinjection of KCl induced. Ischemic tissue was removed at 2, 8, 24, or 72 h postischemia. Using semiquantitative reverse transcription polymerase chain reaction, we investigated mRNA expression levels of 13 representative genes related to cerebral ischemia. Cluster analysis of the gene expression levels was done. ResULTs:In the ischemic group, the expression levels of c-fos, cyclin D1, and COX-2 were significantly higher at 2 h postischemia, and those of bcl-2, bcl-xL, and HO-1 at 72 h. Based on the cluster analysis, we statistically divided examined genes into three groups: group A, early expression (COX-2, c-fos, and bcl-2); group B, s expression (c-jun, SOD-1, bad, p53, SOD-2, bcl-xL, and bax); and group C, late expression (cyclin D1, c-myc, and HO-1). CoNCLUsIoN:We statistically classified the genes into three groups after focal ischemia. The genes of the early-and late-expression groups can be possible therapeutic targets for the treatment of cerebral ischemia.

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“…Microarray studies investigating the transcriptome of both focal and global ischemia showed that the differentially expressed genes involved immediate early genes, stress response genes, apoptosis, signal transduction, neurotransmission, ion channels, inflammation, cytoskeleton, ribosome, and neurotrophic factors, et al (Buttner et al 2009; Cox-Limpens et al 2014; Gilbert et al 2003; Hori et al 2012; Jin et al 2001b; Lu et al 2003; Lu et al 2004; Ramos-Cejudo et al 2012; Sarabi et al 2008; Schmidt-Kastner et al 2002; Soriano et al 2000; Sun et al 2007; Tang et al 2002; Wang et al 2011a; Yakubov et al 2004). …”

Section: Endogenous Protective Mechanisms and Secreted Help-me Sigmentioning

confidence: 99%

Help-me signaling: Non-cell autonomous mechanisms of neuroprotection and neurorecovery

Xing

2017

Progress in Neurobiology

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Self-preservation is required for life. At the cellular level, this fundamental principle is expressed in the form of molecular mechanisms for preconditioning and tolerance. When the cell is threatened, internal cascades of survival signaling become triggered to protect against cell death and defend against future insults. Recently, however, emerging findings suggest that this principle of self-preservation may involve not only intracellular signals; the release of extracellular signals may provide a way to recruit adjacent cells into an amplified protective program. In the central nervous system where multiple cell types co-exist, this mechanism would allow threatened neurons to “ask for help” from glial and vascular compartments. In this review, we describe this new concept of help-me signaling, wherein damaged or diseased neurons release signals that may shift glial and vascular cells into potentially beneficial phenotypes, and help remodel the neurovascular unit. Understanding and dissecting these non-cell autonomous mechanisms of self-preservation in the CNS may lead to novel opportunities for neuroprotection and neurorecovery.

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Genomic response of the rat brain to global ischemia and reperfusion

Cited by 28 publications

References 63 publications

Mechanisms of Neuroprotection from Hypoxia-Ischemia (HI) Brain Injury by Up-regulation of Cytoglobin (CYGB) in a Neonatal Rat Model

Mechanisms of Neuroprotection from Hypoxia-Ischemia (HI) Brain Injury by Up-regulation of Cytoglobin (CYGB) in a Neonatal Rat Model

Cluster analysis of mrna expression levels identifies multiple sequential patterns following focal cerebral ischemia

Help-me signaling: Non-cell autonomous mechanisms of neuroprotection and neurorecovery

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