Evidence map›Paper›PMID 18691073›Full record

ArticleCurrent neurovascular research2008

Enhanced tolerance against early and late apoptotic oxidative stress in mammalian neurons through nicotinamidase and sirtuin mediated pathways.

Zhao Zhong Chong, Kenneth Maiese

Open access · greenAbstract read
In one paragraph

Article in Current neurovascular research, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 53 papers.

0numbers the graph read from it
0cells of the map it votes in
53citing papers in PubMed
4.7field-weighted citation impact, top 6% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

53 citing papers in PubMed, 77 citations in OpenAlex.

  1. Article
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  7. New Insights for nicotinamide: Metabolic disease, autophagy, and mTOR.Frontiers in bioscience (Landmark edition) · 2020
    Review
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

2 authors at 2 institutions in 1 country.

Zhao Zhong ChongDivision of Cellular and Molecular Cerebral Ischemia, Wayne State University School of Medicine; Detroit, Michigan 48201, USA.
Kenneth Maiese
Detroit R&D (United States) · USWayne State University · US

Funding

RESEARCH CORE-- SIGNAL TRANSDUCTIONP30ES006639 · NIEHS · WAYNE STATE UNIVERSITY · PI DERESKI, MARY O · 1994 to 2008
$13.1M
Impacting Oxidative Stress and Cell Injury through Novel Pathways of the Wnt GeneR01NS053946 · NINDS · WAYNE STATE UNIVERSITY · PI MAIESE, KENNETH · 2007 to 2011
$2.4M
NIEHS NIH HHS P30 ES006639NIEHS NIH HHS P30 ES06639NINDS NIH HHS R01 NS053946
6 · The paper itself

Abstract

Focus upon therapeutic strategies that intersect between pathways that govern cellular metabolism and cellular survival may offer the greatest impact for the treatment of a number of neurodegenerative and metabolic disorders, such as diabetes mellitus. In this regard, we investigated the role of a Drosophila nicotinamidase (DN) in mammalian SH-SY5Y neuronal cells during oxidative stress. We demonstrate that during free radical exposure to nitric oxide generators DN neuronal expression significantly increased cell survival and blocked cellular membrane injury. Furthermore, DN neuronal expression prevented both apoptotic late DNA degradation and early phosphatidylserine exposure that may serve to modulate inflammatory cell activation in vivo. Nicotinamidase activity that limited nicotinamide cellular concentrations appeared to be necessary for DN neuroprotection, since application of progressive nicotinamide concentrations could abrogate the benefits of DN expression during oxidative stress. Pathways that involved sirtuin activation and SIRT1 were suggested to be vital, at least in part, for DN to confer protection through a series of studies. First, application of resveratrol increased cell survival during oxidative stress either alone or in conjunction with the expression of DN to a similar degree, suggesting that DN may rely upon SIRT1 activation to foster neuronal protection. Second, the overexpression of either SIRT1 or DN in neurons prevented apoptotic injury specifically in neurons expressing these proteins during oxidative stress, advancing the premise that DN and SIRT1 may employ similar pathways for neuronal protection. Third, inhibition of sirtuin activity with sirtinol was detrimental to neuronal survival during oxidative stress and prevented neuronal protection during overexpression of DN or SIRT1, further supporting that SIRT1 activity may be necessary for DN neuroprotection during oxidative stress. Implementation of further work to elucidate the cellular mechanisms that govern nicotinamidase activity in mammalian cells may offer novel avenues for the treatment of disorders tied to oxidative stress and cellular metabolic dysfunction.

Indexed as

ApoptosisBenzamidesBrain Diseases, MetabolicCell Line, TumorCytoprotectionFree RadicalsHumansNaphtholsNeurodegenerative DiseasesNeuronsNicotinamidaseNitric Oxide DonorsOxidative StressPhosphatidylserinesSignal TransductionSirtuin 1BenzamidesFree RadicalsNaphtholsNicotinamidaseNitric Oxide DonorsPhosphatidylserinesSIRT1 protein, humansirtinolSirtuin 1Sirtuins

Identifiers

PMID18691073
PMCPMC2615543
OpenAlexW1981299173

What OpenQuestion holds

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LicenceTDM
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.