Elevation of neuronal expression of NAIP reduces ischemic damage in the rat hippocampus

Xu, Daigen; Crocker, Stephen J.; Doucet, Jean‐Pierre; St-Jean, Martin; Tamai, Katsuyuki; Hakim, Antoine M.; Ikeda, Joh E.; Liston, Peter; Thompson, C. S.; Korneluk, Robert G.; MacKenzie, Alex; Robertson, Graham

doi:10.1038/nm0997-997

Cited by 238 publications

(140 citation statements)

References 26 publications

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“…Various IAPs are expressed in human [59,60], mouse [61], and rat [62,63] germ cells or their progenitors, and it has been reported that Naip expression plays a role in mouse oocyte viability [61]. Although nothing is known about a potential NAIP stress response in the germ line, it has been demonstrated that NAIP mRNA and protein is upregulated in neurons following ischemic stress [64]. It is also interesting that activity of the human NAIP HERV-P LTR promoter is highest in testis, and, in general, ERVs are transcribed highly in germ cells and early embryogenesis compared to most normal somatic cells [32,65].…”

Section: Discussionmentioning

confidence: 99%

Repeated Recruitment of LTR Retrotransposons as Promoters by the Anti-apoptotic Locus NAIP During Mammalian Evolution

Romanish¹,

Lock²,

Lagemaat³

et al. 2005

PLoS Genet

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Neuronal apoptosis inhibitory protein (NAIP, also known as BIRC1) is a member of the conserved inhibitor of apoptosis protein (IAP) family. Lineage-specific rearrangements and expansions of this locus have yielded different copy numbers among primates and rodents, with human retaining a single functional copy and mouse possessing several copies, depending on the strain. Roles for this gene in disease have been documented, but little is known about transcriptional regulation of NAIP. We show here that NAIP has multiple promoters sharing no similarity between human and rodents. Moreover, we demonstrate that multiple, domesticated long terminal repeats (LTRs) of endogenous retroviral elements provide NAIP promoter function in human, mouse, and rat. In human, an LTR serves as a tissue-specific promoter, active primarily in testis. However, in rodents, our evidence indicates that an ancestral LTR common to all rodent genes is the major, constitutive promoter for these genes, and that a second LTR found in two of the mouse genes is a minor promoter. Thus, independently acquired LTRs have assumed regulatory roles for orthologous genes, a remarkable evolutionary scenario. We also demonstrate that 59 flanking regions of IAP family genes as a group, in both human and mouse are enriched for LTR insertions compared to average genes. We propose several potential explanations for these findings, including a hypothesis that recruitment of LTRs near NAIP or other IAP genes may represent a host-cell adaptation to modulate apoptotic responses.

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Section: Discussionmentioning

confidence: 99%

Repeated Recruitment of LTR Retrotransposons as Promoters by the Anti-apoptotic Locus NAIP During Mammalian Evolution

Romanish¹,

Lock²,

Lagemaat³

et al. 2005

PLoS Genet

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show abstract

“…Therefore, to prevent brain injury, numerous studies have focused on the development of neuroprotective agents that effectively prevent delayed neuronal death following transient forebrain ischemia. [15][16][17][18][19][20][21][22][23] Recently, HGF has been the center of interest in neuroprotective substances, since HGF is both a chemoattractant and a survival factor for embryonic motor neurons. 8 In addition, sensory and sympathetic neurons and their precursors respond to HGF with increased differentiation, survival and axonal outgrowth.…”

Section: Discussionmentioning

confidence: 99%

Gene therapy for preventing neuronal death using hepatocyte growth factor: in vivo gene transfer of HGF to subarachnoid space prevents delayed neuronal death in gerbil hippocampal CA1 neurons

et al. 2001

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To develop a novel strategy to prevent delayed neuronal death (DND) following transient occlusion of arteries, the gene of hepatocyte growth factor (HGF), a novel neurotrophic factor, was transfected into the subarachnoid space of gerbils after transient forebrain ischemia. Importantly, transfection of HGF gene into the subarachnoid space prevented DND, accompanied by a significant increase in HGF

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“…Intracellular anti-apoptotic proteins (Bcl-2 and NAIP) have been used in models of ischemia. In these studies 32,33 vectors were injected in distinct brain areas, transducing glia as well as neurons, and neuroprotective effects were determined 2-5 days after lesion. Longer lasting neuroprotective effects have been observed so far only in axotomized motorneurons, which have been transduced by injection into the nerve stump with neurotrophin coding vectors.…”

Section: Discussionmentioning

confidence: 99%

Transduction of axotomized retinal ganglion cells by adenoviral vector administration at the optic nerve stump: an in vivo model system for the inhibition of neuronal apoptotic cell death

et al. 1999

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Axotomy of the rat optic nerve leads to apoptotic cell death present beyond the time-point of detectable transcription of retinal ganglion cells (RGCs). We have used adenoviral of the p35 transgene, we conclude that apoptosis has been vectors to transduce RGCs from the cut optic nerve stump, efficiently inhibited. In addition, we observed that transduca paradigm in which only those neurons are transduced tion with two control vectors without a transgene in E1 also which are directly affected by the axonal lesion. Transresulted in a minor but significant RGC rescue, implicating genes encoded by the vectors were p35 and CrmA, which neuroprotective effects due to adenoviral transduction are potent intracellular anti-apoptotic proteins. We found itself. This system will be useful in dissecting the pathways that p35, but not CrmA exerted significant rescue effects leading to neuronal cell death after axonal lesions and in on RGCs 14 days after axotomy. Expression of the transthe evaluation of the important question whether the genes was driven by the murine CMV (MCMV) promoter. cellular suicide program can be reverted to survival by The respective mRNAs were detectable 7 days but not 14 therapeutic gene delivery. days after transduction. Since surviving RGCs were

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Elevation of neuronal expression of NAIP reduces ischemic damage in the rat hippocampus

Cited by 238 publications

References 26 publications

Repeated Recruitment of LTR Retrotransposons as Promoters by the Anti-apoptotic Locus NAIP During Mammalian Evolution

Repeated Recruitment of LTR Retrotransposons as Promoters by the Anti-apoptotic Locus NAIP During Mammalian Evolution

Gene therapy for preventing neuronal death using hepatocyte growth factor: in vivo gene transfer of HGF to subarachnoid space prevents delayed neuronal death in gerbil hippocampal CA1 neurons

Transduction of axotomized retinal ganglion cells by adenoviral vector administration at the optic nerve stump: an in vivo model system for the inhibition of neuronal apoptotic cell death

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