Evidence map›Paper›PMID 22178950›Full record

ArticleCellular physiology and biochemistry : international journal of experimental cellular physiology, biochemistry, and pharmacology2011

Complete activation of thyroid hormone receptor β by T3 is essential for normal cochlear function and morphology in mice.

Claus-Peter Richter, Adrian Münscher, Danielle Santana Machado, Fredric E Wondisford, Tania M Ortiga-Carvalho

Abstract read
In one paragraph

Article in Cellular physiology and biochemistry : international journal of experimental cellular physiology, biochemistry, and pharmacology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
0.6field-weighted citation impact, top 40% 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

15 citing papers in PubMed, 22 citations in OpenAlex.

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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 4 institutions in 2 countries.

Claus-Peter RichterDepartment of Otolaryngology-Head and Neck Surgery, Northwestern University, Feinberg School of Medicine, Chicago, IL, USA.
Adrian Münscher
Danielle Santana Machado
Fredric E Wondisford
Tania M Ortiga-Carvalho
Northwestern University · USJohns Hopkins University · USJohnson University · USUniversidade Federal do Rio de Janeiro · BR

Funding

THYROID HORMONE ACTION IN THE PITUITARYR01DK049126 · NIDDK · UNIVERSITY OF CHICAGO · PI WONDISFORD, FREDRIC E. · 1995 to 2016
$3.8M
MOLECULAR MECHANISMS OF THYROID HORMONE RESISTANCER01DK053036 · NIDDK · UNIVERSITY OF CHICAGO · PI WONDISFORD, FREDRIC E. · 1999 to 2009
$2.7M
NIDDK NIH HHS DK49126NIDDK NIH HHS DK53036NIDDK NIH HHS R01 DK049126NIDDK NIH HHS R01 DK053036
6 · The paper itself

Abstract

BACKGROUND/

aimsThyroid hormones (THs) regulate many developmental processes, including the developmental onset of cochlear differentiation and function. TH action is mediated mostly by triiodothyronine (T3) bound to thyroid hormone nuclear receptors (TRs). At positive regulated genes and in the absence of THs, nuclear co-repressors are bound to TRs and decrease basal transcription rate. Ligand (T(3)) binding results in the dissociation of co-repressors and the recruitment of co-activators to the complex, which results in full transcriptional activation.

methodsWe measured cochlear function in two knock-in mouse models: TRβ(E457A/E457A), with the TRβ co-activator binding surface (AF-2) disrupted to prevent co-activator binding; and TRβ(Δ337T/Δ337T), which is unable to bind T(3). Cochlear morphology and function were analyzed in 10-week-old normal and mutated mice. Cochlear function was determined by measuring auditory brainstem responses, cochlear tuning and compound action potential (CAP) thresholds.

resultsAll TRβ(Δ337T/Δ337T) and 85% of the TRβ(E457A/E457A) mice presented elevated CAP thresholds (P < 0.05 or less). Five percent of the TRβ(E457A/E457A) mice presented normal CAP thresholds with broadened cochlear tuning. TRβ(E457A/E457A) and TRβ(Δ337T/Δ337T) presented developmental defects that led to a decreased width (P < 0.01) and an increased thickness (P<0.01) of the tectorial membrane. In addition, TRβ(Δ337T/Δ337T) animals showed an increased tectorial membrane area (P<0.01).

conclusionBoth mutations were deleterious to tectorial membrane development and led to important alterations in cochlear morphology and loss of cochlear function.

Indexed as

CochleaAmino Acid SubstitutionAnimalsAuditory ThresholdGene Knock-In TechniquesMiceMice, Inbred C57BLMice, Inbred CBAMutationProtein BindingThyroid Hormone Receptors betaTriiodothyronineThyroid Hormone Receptors betaTriiodothyronine

Identifiers

PMID22178950
PMCPMC3709180
OpenAlexW1980095188

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.