Bach2 is involved in neuronal differentiation of N1E-115 neuroblastoma cells

Shim, Ki Shuk; Rosner, Margit; Freilinger, Angelika; Lubec, Gert; Hengstschläger, Markus

doi:10.1016/j.yexcr.2006.03.018

Cited by 16 publications

(17 citation statements)

References 36 publications

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“…In fact, it has been reported that Bach2 contributes to the differentiation of a murine NB cell line which, however, does not express Bach1 49 . Moreover, in the work there is no evidence concerning cell response to oxidative stress.…”

Section: Discussionmentioning

confidence: 99%

Differentiation impairs Bach1 dependent HO-1 activation and increases sensitivity to oxidative stress in SH-SY5Y neuroblastoma cells

Piras

Furfaro

Brondolo

et al. 2017

Sci Rep

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Neuronal adaptation to oxidative stress is crucially important in order to prevent degenerative diseases. The role played by the Nrf2/HO-1 system in favoring cell survival of neuroblastoma (NB) cells exposed to hydrogen peroxide (H2O2) has been investigated using undifferentiated or all-trans retinoic acid (ATRA) differentiated SH-SY5Y cells. While undifferentiated cells were basically resistant to the oxidative stimulus, ATRA treatment progressively decreased cell viability in response to H2O2. HO-1 silencing decreased undifferentiated cell viability when exposed to H2O2, proving the role of HO-1 in cell survival. Conversely, ATRA differentiated cells exposed to H2O2 showed a significantly lower induction of HO-1, and only the supplementation with low doses of bilirubin (0,5–1 μM) restored viability. Moreover, the nuclear level of Bach1, repressor of HO-1 transcription, strongly decreased in undifferentiated cells exposed to oxidative stress, while did not change in ATRA differentiated cells. Furthermore, Bach1 was displaced from HO-1 promoter in undifferentiated cells exposed to H2O2, enabling the binding of Nrf2. On the contrary, in ATRA differentiated cells treated with H2O2, Bach1 displacement was impaired, preventing Nrf2 binding and limiting HO-1 transcription. In conclusion, our findings highlight the central role of Bach1 in HO-1-dependent neuronal response to oxidative stress.

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Section: Discussionmentioning

confidence: 99%

Differentiation impairs Bach1 dependent HO-1 activation and increases sensitivity to oxidative stress in SH-SY5Y neuroblastoma cells

Piras

Furfaro

Brondolo

et al. 2017

Sci Rep

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“…At least 5 TFBS sites were colocated with CpG46 in the human IDS promoter region which may contribute to the high expression of this gene in human nerve and brain tissues (Table 4). Of special interest among these transcription factor binding sites were the following: BACH1 and BACH2 have been recognized as members of the BTB-basic region leucine zipper transcription factor family which downregulate cell proliferation of neuroblastoma cells (Shim et al 2006); AP1 is constitutively upregulated in activated microglia and during the pathogenesis of Parkinson’s disease (Pal et al 2016); NFE2 has been shown to participate in the developmental regulation of the brain in zebrafish embryos (Williams et al 2013); and XBP1 has been identified as a risk factor for Alzheimer’s disease and bipolar disorders, contributing to impairment of contextual memory formation (Martinez et al 2016). …”

Section: Resultsmentioning

confidence: 99%

Comparative studies of vertebrate iduronate 2-sulfatase (IDS) genes and proteins: evolution of A mammalian X-linked gene

Holmes

2017

3 Biotech

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IDS is responsible for the lysosomal degradation of heparan sulfate and dermatan sulfate and linked to an X-linked lysosomal storage disease, mucopolysaccharidosis 2 (MPS2), resulting in neurological damage and early death. Comparative IDS amino acid sequences and structures and IDS gene locations were examined using data from several vertebrate genome projects. Vertebrate IDS sequences shared 60–99% identities with each other. Human IDS showed 47% sequence identity with fruit fly (Drosophila melanogaster) IDS. Sequence alignments, key amino acid residues, N-glycosylation sites and conserved predicted secondary and tertiary structures were also studied, including signal peptide, propeptide and active site residues. Mammalian IDS genes usually contained 9 coding exons. The human IDS gene promoter contained a large CpG island (CpG46) and 5 transcription factor binding sites, whereas the 3′-UTR region contained 5 miRNA target sites. These may contribute to IDS gene regulation of expression in the brain and other neural tissues of the body. An IDS pseudogene (IDSP1) was located proximally to the IDS gene on the X-chromosome in primate genomes. Phylogenetic analyses examined the relationships and potential evolutionary origins of the vertebrate IDS gene. These suggested that IDS has originated in an invertebrate ancestral genome and retained throughout vertebrate evolution and conserved on marsupial and eutherian X-chromosomes, with the exception of rat Ids on chromosome 8.Electronic supplementary materialThe online version of this article (doi:10.1007/s13205-016-0595-3) contains supplementary material, which is available to authorized users.

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“…BACH1 is more ubiquitously expressed whereas BACH2 expression is restricted to mononuclear and neuronal cells. (Shim et al, 2006;Hoshino and Igarashi, 2002;Muto et al, 1998;Oyake et al, 1996).…”

Section: Descriptionmentioning

confidence: 99%

“…P21 is a cdk inhibitor known to arrest the cell cycle. In N1E-115 cells regulation of differentiation involves a down regulation of cellular proliferation (Shim et al, 2006). Immune response: BACH2 is involved in the antiviral response triggered by dsRNA or dsDNA molecular patterns (Hong et al, 2008 …”

Section: Functionmentioning

confidence: 99%