Evidence map›Paper›PMID 19816194›Full record

ArticleJournal of neuropathology and experimental neurology2009

Nerve growth factor mediates mechanical allodynia in a mouse model of type 2 diabetes.

Hsinlin T Cheng, Jacqueline R Dauch, John M Hayes, Yu Hong, Eva L Feldman

Open access · bronzeAbstract readComparative Study
In one paragraph

Article in Journal of neuropathology and experimental neurology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 57 papers.

0numbers the graph read from it
0cells of the map it votes in
57citing papers in PubMed
3.5field-weighted citation impact, top 8% 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

57 citing papers in PubMed, 94 citations in OpenAlex.

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  7. NGF and Its Role in Immunoendocrine Communication during Metabolic Syndrome.International journal of molecular sciences · 2023
    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

5 authors at 2 institutions in 1 country.

Hsinlin T ChengDepartment of Neurology, University of Michigan Medical Center, Ann Arbor, Michigan 48109-2200, USA. chengt@umich.edu
Jacqueline R Dauch
John M Hayes
Yu Hong
Eva L Feldman
University of Michigan–Ann Arbor · USMichigan Medicine · US

Funding

PUBLIC HEALTH DEMONSTRATIONP60DK020572 · NIDDK · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI MYERS, MARTIN G · 1985 to 2012
$26.5M
Mouse Models of Diabetic Nephropathy and NeuropathyU01DK060994 · NIDDK · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI BROSIUS, FRANK C · 2001 to 2005
$3.3M
Nerve Growth Factor Signaling in Painful Diabetic NeuropathyK08NS061039 · NINDS · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI CHENG, HSINLIN THOMAS · 2009 to 2013
$881k
NIDDK NIH HHS P60 DK020572NIDDK NIH HHS U01 DK060994NIDDK NIH HHS U01-DK60994NINDS NIH HHS 1K08NS061039NINDS NIH HHS K08 NS061039
6 · The paper itself

Abstract

C57BLKS db/db (db/db) mice develop a neuropathy with features of human type 2 diabetic neuropathy. Here, we demonstrate that these mice develop transient mechanical allodynia at the early stage of diabetes. We hypothesized that nerve growth factor (NGF), which enhances the expression of key mediators of nociception (i.e. substance P [SP] and calcitonin gene-related peptide), contributes to the development of mechanical allodynia in these mice. We found that NGF, SP, and calcitonin gene-related peptide gene expression is upregulated in the dorsal root ganglion (DRG) of db/db mice before or during the period that they develop mechanical allodynia. There were more small- to medium-sized NGF-immunopositive DRG neurons in db/db mice than in control db+ mice; these neurons also expressed SP, consistent with its role in nociception. Nerve growth factor expression in the hind paw skin was also increased in a variety of dermal cell types and nerve fibers, suggesting the contribution of a peripheral source of NGF to mechanical allodynia. The upregulation of NGF coincided with enhanced tropomyosin-related kinase A receptor phosphorylation in the DRG. Finally, an antibody against NGF inhibited mechanical allodynia and decreased the numbers of SP-positive DRG neurons in db/db mice. These results suggest that inhibition of NGF action is a potential strategy for treating painful diabetic neuropathy.

Indexed as

AnimalsDiabetes Mellitus, Type 2Disease Models, AnimalMaleMiceMice, Inbred C57BLNerve Growth FactorPainPain MeasurementPhysical StimulationNerve Growth Factor

Identifiers

PMID19816194
PMCPMC3163104
OpenAlexW1970472489

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.