Evidence map›Paper›PMID 25903517›Full record

ArticleJournal of neurochemistry2015

Phosphoinositide and Erk signaling pathways mediate activity-driven rodent olfactory sensory neuronal survival and stress mitigation.

So Yeun Kim, Alex Mammen, Seung-Jun Yoo, Bongki Cho, Eun-Kyoung Kim, Jong-In Park, Cheil Moon, Gabriele V Ronnett

Abstract read
In one paragraph

Article in Journal of neurochemistry, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
1.5field-weighted citation impact, top 21% 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

12 citing papers in PubMed, 14 citations in OpenAlex.

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  12. New paradigms in GPCR drug discovery.Biochemical pharmacology · 2015
    Review
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

8 authors at 4 institutions in 2 countries.

So Yeun KimDepartment of Brain & Cognitive Sciences, Graduate School, DaeguGyeungbuk Institute of Science and Technology, Daegu, Korea.
Alex MammenDepartments of Neuroscience, The Johns Hopkins University School of Medicine, Baltimore, Maryland, USA.
Seung-Jun YooDepartment of Brain & Cognitive Sciences, Graduate School, DaeguGyeungbuk Institute of Science and Technology, Daegu, Korea.
Bongki ChoDepartment of Brain & Cognitive Sciences, Graduate School, DaeguGyeungbuk Institute of Science and Technology, Daegu, Korea.
Eun-Kyoung KimDepartment of Brain & Cognitive Sciences, Graduate School, DaeguGyeungbuk Institute of Science and Technology, Daegu, Korea.
Jong-In ParkDepartment of Biochemistry, Medical College of Wisconsin, Milwaukee, Wisconsin, USA.
Cheil MoonDepartment of Brain & Cognitive Sciences, Graduate School, DaeguGyeungbuk Institute of Science and Technology, Daegu, Korea.
Gabriele V RonnettDepartment of Brain & Cognitive Sciences, Graduate School, DaeguGyeungbuk Institute of Science and Technology, Daegu, Korea.
Daegu Gyeongbuk Institute of Science and Technology · KRJohns Hopkins Medicine · USJohns Hopkins University · USMedical College of Wisconsin · US

Funding

REGULATION OF GUANYLYL CYCLASES IN THE OLFACTORY SYSTEMR01DC002979 · NIDCD · JOHNS HOPKINS UNIVERSITY · PI RONNETT, GABRIELE V · 1997 to 2012
$4.2M
OLFACTORY ABNORMALITIES IN THE MODELING OF RETT SYNDROMER01NS041079 · NINDS · JOHNS HOPKINS UNIVERSITY · PI RONNETT, GABRIELE V · 2000 to 2013
$3.5M
Stress and Survival of Olfactory Sensory NeuronsR01DC008643 · NIDCD · JOHNS HOPKINS UNIVERSITY · PI AJA, SUSAN M · 2010 to 2014
$1.7M
NIDCD NIH HHS R01 DC002979NIDCD NIH HHS R01 DC008643NINDS NIH HHS R01 NS041079
6 · The paper itself

Abstract

Olfactory sensory neurons (OSNs) are the initial site for olfactory signal transduction. Therefore, their survival is essential to olfactory function. In the current study, we demonstrated that while odorant stimulation promoted rodent OSN survival, it induced generation of reactive oxygen species in a dose- and time-dependent manner as well as loss of membrane potential and fragmentation of mitochondria. The MEK-Erk pathway played a critical role in mediating these events, as its inhibition decreased odorant stimulation-dependent OSN survival and exacerbated intracellular stress measured by reactive oxygen species generation and heat-shock protein 70 expression. The phosphoinositide pathway, rather than the cyclic AMP pathway, mediated the odorant-induced activation of the MEK-Erk pathway. These findings provide important insights into the mechanisms of activity-driven OSN survival, the role of the phosphoinositide pathway in odorant signaling, and demonstrate that odorant detection and odorant stimulation-mediated survival proceed via independent signaling pathways. This mechanism, which permits independent regulation of odorant detection from survival signaling, may be advantageous if not diminished by repeated or prolonged odor exposure. We investigated the role of odorant stimulation in generating cellular stress and the molecular mechanisms mitigating such stress and promoting neuronal survival. Odorant stimulation promoted olfactory sensory neuron (OSN) survival and also induced intracellular oxidative stress, which was exacerbated when MEK/Erks pathway was inhibited. Sensory stimulation simultaneously activated at least two parallel pathways, the AC/cAMP cascade responsible for odorant detection, and phosphoinositide hydrolysis to promote odorant stimulation-dependent neuronal survival odorants may activate parallel signaling cascades to mediate sensory detection and sensory stimulation-dependent survival. AC, adenylyl cyclase; cAMP, cyclic adenosine monophosphate; Erk, extracellular signal-regulated kinase; MEK, MAPK/ERK kinase.

Indexed as

AnimalsBlotting, NorthernCell SurvivalImmunoblottingImmunohistochemistryMAP Kinase Signaling SystemMiceMice, Inbred C57BLOlfactory Receptor NeuronsOxidative StressPhosphatidylinositolsRatsRats, Sprague-DawleySmellPhosphatidylinositolsactivity-driven survivalmitogen-activated protein kinaseolfactoryoxidative stressphosphoinositidesensory transduction

Identifiers

PMID25903517
PMCPMC4496289
OpenAlexW2047815408

What OpenQuestion holds

Textmetadata
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.