Characterization of gene expression induced by RTN-1C in human neuroblastoma cells and in mouse brain

Fazi, Barbara; Biancolella, Michela; Mehdawy, Bisan; Corazzari, Marco; Minella, Daniela; Blandini, Fabio; Moreno, Sandra; Nardacci, Roberta; Nisticò, Robert; Sepe, Sara; Novelli, Giuseppe; Piacentini, Mauro; Sano, Federica Di

doi:10.1016/j.nbd.2010.08.007

Cited by 6 publications

(8 citation statements)

References 37 publications

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“…15 In contrast, RTN1C over-expression in cortical neurons caused the elevation of CHOP/GADD153 and Bip associated with apoptotic death in vivo. 19 RTN proteins may thus exert opposite effect on the expression of ER stress proteins and the survival of cells. Concerning Nogo-A, the protein was not detectable in apoptotic RGCs labelled with annexin V, and the downregulation of Nogo-A had no global effect on RGC survival.…”

Section: Discussionmentioning

confidence: 99%

“…15 Only few and contradictory observations are available on such a role of Nogo (reticulon 4 (RTN4)) or other RTN proteins, and they rely mostly on in vitro or overexpression experiments. 15,[17][18][19][20][21] We therefore investigated axonal regeneration and survival of RGCs after optic nerve crush in mice with systemic Nogo-A deletion (KO) or neuron-specific knock down using adeno-associated virus vector of serotype 2 (AAV2) that selectively infect RGCs in the retina. For the first time, our work demonstrates that the exogenous increase of neuronal Nogo-A driven by AAV2.Nogo-A, but not the endogenous upregulation of neuronal Nogo-A because of axonal damage enhanced RGC cell loss.…”

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confidence: 99%

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Neuronal Nogo-A upregulation does not contribute to ER stress-associated apoptosis but participates in the regenerative response in the axotomized adult retina

Pernet

Joly

Dalkara³

et al. 2011

Cell Death Differ

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Nogo-A, an axonal growth inhibitory protein known to be mostly present in CNS myelin, was upregulated in retinal ganglion cells (RGCs) after optic nerve injury in adult mice. Nogo-A increased concomitantly with the endoplasmic reticulum stress (ER stress) marker C/EBP homologous protein (CHOP), but CHOP immunostaining and the apoptosis marker annexin V did not co-localize with Nogo-A in individual RGC cell bodies, suggesting that injury-induced Nogo-A upregulation is not involved in axotomyinduced cell death. Silencing Nogo-A with an adeno-associated virus serotype 2 containing a short hairpin RNA (AAV2.shRNANogo-A) or Nogo-A gene ablation in knock-out (KO) animals had little effect on the lesion-induced cell stress or death. On the other hand, Nogo-A overexpression mediated by AAV2.Nogo-A exacerbated RGC cell death after injury. Strikingly, however, injury-induced sprouting of the cut axons and the expression of growth-associated molecules were markedly reduced by AAV2.shRNA-Nogo-A. The axonal growth in the optic nerve activated by the intraocular injection of the inflammatory molecule Pam3Cys tended to be lower in Nogo-A KO mice than in WT mice. Nogo-A overexpression in RGCs in vivo or in the neuronal cell line F11 in vitro promoted regeneration, demonstrating a positive, cell-autonomous role for neuronal Nogo-A in the modulation of axonal regeneration.

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Section: Discussionmentioning

confidence: 99%

mentioning

confidence: 99%

Neuronal Nogo-A upregulation does not contribute to ER stress-associated apoptosis but participates in the regenerative response in the axotomized adult retina

Pernet

Joly

Dalkara³

et al. 2011

Cell Death Differ

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“…By using microarray analysis of the whole human genome, we have recently demonstrated that RTN-1C is able to specifically regulate gene expression, modulating transcript clusters which have been implicated in the onset of neurodegenerative disorders. Interestingly, we show that some of the identified genes were also modulated in vivo in a brain-specific mouse model overexpressing RTN-1C [49].…”

Section: Discussionmentioning

confidence: 84%

The reticulons: Guardians of the structure and function of the endoplasmic reticulum

Sano

Bernardoni

Piacentini

2012

Experimental Cell Research

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The endoplasmic reticulum (ER) consists of the nuclear envelope and a peripheral network of tubules and membrane sheets. The tubules are shaped by a specific class of curvature stabilizing proteins, the reticulons and DP1; however it is still unclear how the sheets are assembled. The ER is the cellular compartment responsible for secretory and membrane protein synthesis. The reducing conditions of ER lead to the intra/inter-chain formation of new disulphide bonds into polypeptides during protein folding assessed by enzymatic or spontaneous reactions. Moreover, ER represents the main intracellular calcium storage site and it plays an important role in calcium signaling that impacts many cellular processes. Accordingly, the maintenance of ER function represents an essential condition for the cell, and ER morphology constitutes an important prerogative of it. Furthermore, it is well known that ER undergoes prominent shape transitions during events such as cell division and differentiation. Thus, maintaining the correct ER structure is an essential feature for cellular physiology. Now, it is known that proper ER-associated proteins play a fundamental role in ER tubules formation. Among these ER-shaping proteins are the reticulons (RTN), which are acquiring a relevant position. In fact, beyond the structural role of reticulons, in very recent years new and deeper functional implications of these proteins are emerging in relation to their involvement in several cellular processes.

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“…We have recently shown, by the use of microarray analysis of the whole human genome, that RTN-1C is able to specifically regulate gene expression, modulating transcript clusters implicated in the onset of neurodegenerative disorders [77]. …”

Section: Rtn-1c and Neurodegenerationmentioning

confidence: 99%

Reticulon Protein-1C: A New Hope in the Treatment of Different Neuronal Diseases

Sano

Piacentini

2012

International Journal of Cell Biology

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Reticulons (RTNs) are a group of membrane proteins localized on the ER and known to regulate ER structure and functions. Several studies have suggested that RTNs are involved in different important cellular functions such as changes in calcium homeostasis, ER-stress-mediated cell death, and autophagy. RTNs have been demonstrated to exert a cancer specific proapoptotic function via the interaction or the modulation of specific proteins. Reticulons have also been implicated in different signaling pathways which are at the basis of the pathogenesis of several neurodegenerative diseases. In this paper we discuss the accumulating evidence identifying RTN-1C protein as a promising target in the treatment of different pathologies such as cancer or neurodegenerative disorders.

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Characterization of gene expression induced by RTN-1C in human neuroblastoma cells and in mouse brain

Cited by 6 publications

References 37 publications

Neuronal Nogo-A upregulation does not contribute to ER stress-associated apoptosis but participates in the regenerative response in the axotomized adult retina

Neuronal Nogo-A upregulation does not contribute to ER stress-associated apoptosis but participates in the regenerative response in the axotomized adult retina

The reticulons: Guardians of the structure and function of the endoplasmic reticulum

Reticulon Protein-1C: A New Hope in the Treatment of Different Neuronal Diseases

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