Evidence map›Paper›PMID 26241124›Full record

ArticleEndocrinology2015

Age-Related Hearing Loss and Degeneration of Cochlear Hair Cells in Mice Lacking Thyroid Hormone Receptor β1.

Lily Ng, Emily Cordas, Xuefeng Wu, Kristen R Vella, Anthony N Hollenberg, Douglas Forrest

Open access · bronzeAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Endocrinology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed
2.4field-weighted citation impact, top 12% 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

23 citing papers in PubMed, 43 citations in OpenAlex.

  1. Review
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  15. Review
  16. The Clinical Spectrum of Resistance to Thyroid Hormone Alpha in Children and AdultsJournal of clinical research in pediatric endocrinology · 2021
    Review
  17. Article
  18. Article
  19. Analysis of FGF20-regulated genes in organ of Corti progenitors by translating ribosome affinity purification.Developmental dynamics : an official publication of the American Association of Anatomists · 2020
    Article
  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

6 authors at 4 institutions in 1 country.

Lily NgLaboratory of Endocrinology and Receptor Biology (L.N., E.C., X.W., D.F.), National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Bethesda, Maryland 20892; and Division of Endocrinology, Diabetes and Metabolism (K.R.V., A.N.H.), Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, Massachusetts 02215.
Emily CordasLaboratory of Endocrinology and Receptor Biology (L.N., E.C., X.W., D.F.), National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Bethesda, Maryland 20892; and Division of Endocrinology, Diabetes and Metabolism (K.R.V., A.N.H.), Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, Massachusetts 02215.
Xuefeng WuLaboratory of Endocrinology and Receptor Biology (L.N., E.C., X.W., D.F.), National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Bethesda, Maryland 20892; and Division of Endocrinology, Diabetes and Metabolism (K.R.V., A.N.H.), Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, Massachusetts 02215.
Kristen R VellaLaboratory of Endocrinology and Receptor Biology (L.N., E.C., X.W., D.F.), National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Bethesda, Maryland 20892; and Division of Endocrinology, Diabetes and Metabolism (K.R.V., A.N.H.), Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, Massachusetts 02215.
Anthony N HollenbergLaboratory of Endocrinology and Receptor Biology (L.N., E.C., X.W., D.F.), National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Bethesda, Maryland 20892; and Division of Endocrinology, Diabetes and Metabolism (K.R.V., A.N.H.), Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, Massachusetts 02215.
Douglas ForrestLaboratory of Endocrinology and Receptor Biology (L.N., E.C., X.W., D.F.), National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Bethesda, Maryland 20892; and Division of Endocrinology, Diabetes and Metabolism (K.R.V., A.N.H.), Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, Massachusetts 02215.
National Institute of Diabetes and Digestive and Kidney Diseases · USNational Institutes of Health · USBeth Israel Deaconess Medical Center · USHarvard University · US

Funding

Tissue-specific functions of thyroid hormone receptorsZIADK047037 · NIDDK · NATIONAL INSTITUTE OF DIABETES AND DIGESTIVE AND KIDNEY DISEASES · PI FORREST, DOUGLAS · 2009 to 2025
$13.3M
COREPRESSOR REGULATION OF THYROID HORMONE ACTIONR01DK056123 · NIDDK · WEILL MEDICAL COLL OF CORNELL UNIV · PI HOLLENBERG, ANTHONY N · 2000 to 2023
$7.6M
INTEGRATED ENDOCRINE &METABOLIC RESEARCH TRAININGT32DK007516 · NIDDK · BETH ISRAEL DEACONESS MEDICAL CENTER · PI BARBARA B. KAHN · 1986 to 2026
$6.8M
Negative regulation by thyroid hormoneR01DK078090 · NIDDK · BETH ISRAEL DEACONESS MEDICAL CENTER · PI HOLLENBERG, ANTHONY N · 2007 to 2010
$1.4M
Corepressor Regulation of Nuclear Receptor ActionR56DK056123 · NIDDK · BETH ISRAEL DEACONESS MEDICAL CENTER · PI HOLLENBERG, ANTHONY N · 2009 to 2009
$425k
Intramural NIH HHSNIDDK NIH HHS DK056123NIDDK NIH HHS DK078090NIDDK NIH HHS R01 DK056123NIDDK NIH HHS R01 DK078090NIDDK NIH HHS R56 DK056123NIDDK NIH HHS T32 DK007516
6 · The paper itself

Abstract

A key function of the thyroid hormone receptor β (Thrb) gene is in the development of auditory function. However, the roles of the 2 receptor isoforms, TRβ1 and TRβ2, expressed by the Thrb gene are unclear, and it is unknown whether these isoforms promote the maintenance as well as development of hearing. We investigated the function of TRβ1 in mice with a Thrb(b1) reporter allele that expresses β-galactosidase instead of TRβ1. In the immature cochlea, β-galactosidase was detected in the greater epithelial ridge, sensory hair cells, spiral ligament, and spiral ganglion and in adulthood, at low levels in the hair cells, support cells and root cells of the outer sulcus. Although deletion of all TRβ isoforms causes severe, early-onset deafness, deletion of TRβ1 or TRβ2 individually caused no obvious hearing loss in juvenile mice. However, over subsequent months, TRβ1 deficiency resulted in progressive loss of hearing and loss of hair cells. TRβ1-deficient mice had minimal changes in serum thyroid hormone and thyrotropin levels, indicating that hormonal imbalances were unlikely to cause hearing loss. The results suggest mutually shared roles for TRβ1 and TRβ2 in cochlear development and an unexpected requirement for TRβ1 in the maintenance of hearing in adulthood.

Indexed as

AgingAnimalsbeta-GalactosidaseCochleaGene Expression Regulation, DevelopmentalHair Cells, AuditoryHearing LossImmunohistochemistryMice, Inbred C57BLMice, KnockoutMice, TransgenicOrgan of CortiProtein IsoformsReverse Transcriptase Polymerase Chain ReactionThyroid Hormone Receptors betaThyroid Hormonesbeta-GalactosidaseProtein IsoformsThyroid Hormone Receptors betaThyroid HormonesThyrotropin

Identifiers

PMID26241124
PMCPMC4588828
OpenAlexW2202029616

What OpenQuestion holds

Textmetadata
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.