Evidence map›Paper›PMID 19761823›Full record

ArticleHearing research2010

PTEN attenuates PIP3/Akt signaling in the cochlea of the aging CBA/J mouse.

Su-Hua Sha, Fu-Quan Chen, Jochen Schacht

Abstract read
In one paragraph

Article in Hearing research, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed
1.0field-weighted citation impact, top 24% 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

22 citing papers in PubMed, 40 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Review
  5. Article
  6. Article
  7. Article
  8. Review
  9. mTOR Signaling in the Inner Ear as Potential Target to Treat Hearing Loss.International journal of molecular sciences · 2021
    Review
  10. Review
  11. Article
  12. Article
  13. Increased Sensitivity to Noise-Induced Hearing Loss by Blockade of Endogenous PI3K/Akt Signaling.Journal of the Association for Research in Otolaryngology : JARO · 2015
    Article
  14. Article
  15. Article
  16. Review
  17. Article
  18. Inner ear symptoms and disease: pathophysiological understanding and therapeutic options.Medical science monitor : international medical journal of experimental and clinical research · 2013
    Review
  19. Review
  20. 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

3 authors at 2 institutions in 2 countries.

Su-Hua ShaKresge Hearing Research Institute, University of Michigan, Ann Arbor, MI 48109, USA. shasha@umich.edu
Fu-Quan Chen
Jochen Schacht
University of Michigan–Ann Arbor · USAir Force Medical University · CN

Funding

Scientific Synergy CoreP30DC005188 · NIDCD · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI DOLAN, DAVID FRANCIS · 2002 to 2016
$10.3M
STRESS PATHWAYS IN THE AGING COCHLEAP01AG025164 · NIA · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI SCHACHT, JOCHEN · 2005 to 2009
$6.6M
NIA NIH HHS AG-025164NIA NIH HHS P01 AG025164NIDCD NIH HHS P30 DC005188NIDCD NIH HHS P30 DC-05188
6 · The paper itself

Abstract

We have previously reported the activation of cell death pathways in the sensory cells of the aging cochlea. Here we investigate age-associated changes in survival mechanisms focusing on phosphatidylinositol 3,4,5-trisphosphate (PIP(3))/Akt signaling. The animal model is the CBA/J mouse of 18 months of age prior to the onset of major functional loss (ABR thresholds, 26+/-8 dB SPL) which is compared to young animals of 3 months of age (ABR thresholds, 19+/-7 dB SPL). Immunostaining on cochlear cryosections revealed a wide-spread distribution of PIP(3) in the cochlea which was markedly attenuated in old animals in inner and outer hair cells, Deiters cells and pillar cells. Protein levels of the lipid phosphatase PTEN which regulates PIP(3) increased in those cells with aging while its mRNA did not, suggesting an age-related reduction of PTEN degradation. Furthermore, staining intensity of phosphorylated PTEN (ser380) and its nuclear localization increased. Consistent with a reduction of PIP(3), the phosphorylation of the downstream target Akt at threonine 308 significantly decreased in outer hair cells. The results suggest a decline of the survival capacity of aging outer hair cells due to a decrease in PIP(3)/Akt signaling caused by an increase of PTEN.

Indexed as

Signal TransductionAcoustic StimulationAge FactorsAgingAnimalsAuditory ThresholdBlotting, WesternCell SurvivalCochleaHair Cells, Auditory, OuterImmunohistochemistryMaleMiceMice, Inbred CBAPhosphatidylinositol PhosphatesPhosphorylationphosphatidylinositol 3,4,5-triphosphatePhosphatidylinositol PhosphatesProto-Oncogene Proteins c-aktPTEN PhosphohydrolasePten protein, mouseRNA, MessengerThreonine

Identifiers

PMID19761823
PMCPMC2868099
OpenAlexW1966324250

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.