Evidence map›Paper›PMID 22509106›Full record

ArticleMolecular vision2012

NGF promotes cell cycle progression by regulating D-type cyclins via PI3K/Akt and MAPK/Erk activation in human corneal epithelial cells.

Jiaxu Hong, Tingting Qian, Qihua Le, Xinghuai Sun, Jihong Wu, Junyi Chen, Xiaobo Yu, Jianjiang Xu

Open access · greenAbstract read
In one paragraph

Article in Molecular vision, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.

0numbers the graph read from it
0cells of the map it votes in
27citing papers in PubMed
1.0field-weighted citation impact, top 30% 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

27 citing papers in PubMed, 36 citations in OpenAlex.

  1. Review
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  12. Corneal alteration and pathogenesis in diabetes mellitus.International journal of ophthalmology · 2019
    Review
  13. Article
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  19. ROS and ROS-Mediated Cellular Signaling.Oxidative medicine and cellular longevity · 2016
    Review
  20. Human β-NGF gene transferred to cat corneal endothelial cells.International journal of ophthalmology · 2016
    Article
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 1 institution in 1 country.

Jiaxu HongDepartment of Ophthalmology, Eye, Ear, Nose, and Throat Hospital, School of Shanghai Medicine, Fudan University, Shanghai, China.
Tingting Qian
Qihua Le
Xinghuai Sun
Jihong Wu
Junyi Chen
Xiaobo Yu
Jianjiang Xu
Fudan University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

purposeNerve growth factor (NGF) plays an important role in promoting the healing of corneal wounds. However, the molecular mechanism by which NGF functions is unknown. We investigated the possible effects of NGF on phosphatidylinositol 3-kinase (PI3K)/protein kinase B (Akt) and mitogen activated protein kinase (MAPK)/extracellular signal-regulated kinase (Erk) pathways and cell growth in human corneal epithelial cells (HCECs).

methodsWe examined the effect of NGF on cell cycle and proliferation in HCECs by flow cytometry and cell proliferation assay, respectively. The levels of D-type cyclins in NGF-treated HCECs were determined by western blot. The tyrosine kinase A (TrkA), PI3K/Akt and MAPK/Erk pathways were then checked in cells stimulated with NGF for different time periods or cells undergoing a dose-dependent treatment. Furthermore, HCECs were treated with pathway inhibitors, LY294002 or PD98059, to confirm NGF-induced activations.

resultsWe found that NGF had a positive effect on the growth of HCECs, and D-type cyclins, and it was correlated with the percentage of the G(1) to S progression. We also observed a time-dependent and dose-dependent effect of NGF on the PI3K/Akt and MAPK/Erk pathways. Furthermore, NGF affected cell cycle progression of HCECs by regulating cyclin D through Akt and Erk activation upon treatment with the pathway inhibitors, LY294002 for Akt or PD98059 for Erk pathways.

conclusionsNGF stimulation could promote cell proliferation and cell cycle progression of HCECs by activation of cyclin D via the PI3K/Akt and MAPK/Erk signaling pathways.

Indexed as

Cell CycleCell ProliferationChromonesCorneaCyclin DDose-Response Relationship, DrugEnzyme InhibitorsEpithelial CellsExtracellular Signal-Regulated MAP KinasesFlavonoidsMitogen-Activated Protein Kinase KinasesMorpholinesNerve Growth FactorPhosphatidylinositol 3-KinasePhosphoinositide-3 Kinase InhibitorsPrimary Cell Culture2-(2-amino-3-methoxyphenyl)-4H-1-benzopyran-4-one2-(4-morpholinyl)-8-phenyl-4H-1-benzopyran-4-oneChromonesCyclin DEnzyme InhibitorsExtracellular Signal-Regulated MAP KinasesFlavonoidsMitogen-Activated Protein Kinase KinasesMorpholinesNerve Growth FactorNGF protein, humanPhosphatidylinositol 3-KinasePhosphoinositide-3 Kinase InhibitorsProto-Oncogene Proteins c-akt

Identifiers

PMID22509106
PMCPMC3324366
OpenAlexW1923276314

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.