Neuroglobin and cytoglobin in search of their role in the vertebrate globin family

Hankeln, Thomas; Ebner, Bettina; Fuchs, Christine; Gerlach, Frank; Haberkamp, Mark; Laufs, Tilmann; Roesner, Anja; Schmidt, Marc; Weich, Bettina; Wystub, Sylvia; Saaler-Reinhardt, Sigrid; Reuss, Stefan; Bolognesi, Martino; Sanctis, Daniele de; Marden, Michael C.; Kiger, Laurent; Moëns, Luc; Dewilde, Sylvia; Nevo, Eviatar; Avivi, Aaron; Weber, Roy E.; Fago, Angela; Burmester, Thorsten

doi:10.1016/j.jinorgbio.2004.11.009

Cited by 282 publications

(231 citation statements)

References 56 publications

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“…CYGB is a recently described, intracellular globin (Burmester et al, 2002(Burmester et al, , 2004 whose function was, until recently, unknown (Trent III and Hargrove, 2002). Phylogenetic principles suggest that it has a common ancestral origin with vertebrate myoglobins (Hankeln et al, 2005). TOC is a rare, autosomal dominantly inherited skin condition associated with an increased risk of squamous cell oesophageal cancer and oral lesions (Tyldesley, 1974;Ellis et al, 1994).…”

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confidence: 99%

“…The exact physiological role of Cygb is currently speculative, although intracellular oxygen storage, peroxidase function, oxygen sensing or binding and detoxification of nitric oxide have all been suggested (Burmester et al, 2002(Burmester et al, , 2004Trent III and Hargrove, 2002;Hankeln et al, 2005;Hodges et al, 2008). It has been recently shown that upregulation of CYGB in rat liver cells has a protective effect against damage-induced fibrosis (Xu et al, 2006) and this has led to the hypothesis that CYGB has a homoeostatic effect, inhibiting free radical-induced fibroblast activation and consequent fibrosis.…”

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confidence: 99%

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Cytoglobin is upregulated by tumour hypoxia and silenced by promoter hypermethylation in head and neck cancer

et al. 2009

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BACKGROUND: Cytoglobin (Cygb) was first described in 2002 as an intracellular globin of unknown function. We have previously shown the downregulation of cytoglobin as a key event in a familial cancer syndrome of the upper aerodigestive tract. METHOD: Cytoglobin expression and promoter methylation were investigated in sporadic head and neck squamous cell carcinoma (HNSCC) using a cross-section of clinical samples. Additionally, the putative mechanisms of Cygb expression in cancer were explored by subjecting HNSCC cell lines to hypoxic culture conditions and 5-aza-2-deoxycitidine treatment. RESULTS: In clinically derived HNSCC samples, CYGB mRNA expression showed a striking correlation with tumour hypoxia (measured by HIF1A mRNA expression P ¼ 0.013) and consistent associations with histopathological measures of tumour aggression. CYGB expression also showed a marked negative correlation with promoter methylation (P ¼ 0.018). In the HNSCC cell lines cultured under hypoxic conditions, a trend of increasing expression of both CYGB and HIF1A with progressive hypoxia was observed. Treatment with 5-aza-2-deoxycitidine dramatically increased CYGB expression in those cell lines with greater baseline promoter methylation. CONCLUSION: We conclude that the CYGB gene is regulated by both promoter methylation and tumour hypoxia in HNSCC and that increased expression of this gene correlates with clincopathological measures of a tumour's biological aggression.

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Cytoglobin is upregulated by tumour hypoxia and silenced by promoter hypermethylation in head and neck cancer

et al. 2009

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“…It was also closely associated with the mitochondria. 17 The induction of mitochondrial dysfunction can lead to the overproduction of superoxide anions, which is essential to promote enhanced apoptosis in neuronal cells. 18 Maintaining the mitochondrial function may be crucial for cell survival.…”

Section: Discussionmentioning

confidence: 99%

The protective effects of the lentivirus-mediated neuroglobin gene transfer on spinal cord injury in rabbits

et al. 2011

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Study design: We introduced a lentiviral vector containing the neuroglobin (Ngb) gene into the injured spinal cords to evaluate the therapeutic potential of Ngb in a rabbit model of spinal cord injury (SCI). Objectives: It is not clear whether Ngb has the neuroprotective role to SCI. The purpose of this study was to investigate the possible protective effects of the Ngb overexpression on traumatic SCI in rabbits. Setting: Department of Orthopedic Surgery, The First Affiliated Hospital, Fujian Medical University, Fuzhou, People's Republic of China. Methods: A lentiviral vector containing Ngb gene was constructed and injected at the SCI sites 24 h after SCI. The rabbits' motor functions were evaluated by the Basso-Beattie-Bresnahan rating scale. Quantitative real-time PCRs, western blots, malondialdehyde (MDA) tests and terminal deoxynucleotidyl transferase-mediated UTP end labeling assays were also performed. Results: The Ngb expression in the LV-Ngb group increased significantly at days 7, 14 and 21. A more significant functional improvement was observed in the LV-Ngb group compared with the improvements in all other groups at days 14 and 21. The traumatic SCI seemed to lead to an increase in the levels of MDA and in the number of the apoptotic cells, which could be prevented by the LV-Ngb treatment. Conclusion: This study demonstrated that the Ngb overexpression may have potential therapeutic benefits for both reducing secondary damages and improving the outcomes after traumatic SCI.

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“…Neuroglobin is not expressed at the same level in all cell types but is at significantly high levels only in some brain neurons and retinal rod cells (14). These cell types have some common characteristics.…”

Section: The Significance Of Resetting the Trigger Level For Apoptosismentioning

confidence: 94%

“…Phylogenetic analysis indicates a very ancient lineage for this protein, with the other vertebrate globins diverging from neuroglobin more than 600 M years ago (14).…”

Section: Introductionmentioning

confidence: 99%

A role for human neuroglobin in apoptosis

et al. 2010

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SummaryOver the past decade, following the discovery of the human heme protein neuroglobin, many studies have searched for evidence for this protein's mechanism of action. Much data has accrued showing that high levels of neuroglobin will protect cells from apoptotic cell death, following a wide range of challenges. Various explanations of its actions, based on measured reactivity with oxygen, nitric oxide, or free radicals, have been proposed, but none have, as yet, been substantiated in vivo. Following preliminary experiments, it was previously hypothesised that ''the central role of neuroglobin in highly metabolically active cells and retinal and brain neurons is to reset the trigger level of mitochondrial cytochrome c release necessary to commit the cells to apoptosis'' (I.U.M.B.M. Life (2008) 60, 398). In this article, we review the evidence, which has accumulated to support this hypothesised mechanism of action of neuroglobin and integrate this data, with other reported intracellular functions of neuroglobin, to suggest a plausible central role for neuroglobin in the control of apoptosis. IUBMBIUBMB Life, 62(12): 878-885, 2010

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Neuroglobin and cytoglobin in search of their role in the vertebrate globin family

Cited by 282 publications

References 56 publications

Cytoglobin is upregulated by tumour hypoxia and silenced by promoter hypermethylation in head and neck cancer

Cytoglobin is upregulated by tumour hypoxia and silenced by promoter hypermethylation in head and neck cancer

The protective effects of the lentivirus-mediated neuroglobin gene transfer on spinal cord injury in rabbits

A role for human neuroglobin in apoptosis

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