Evidence map›Paper›PMID 18280526›Full record

ReviewSteroids2008

Non-genomic actions of thyroid hormone in brain development.

Jack L Leonard

Open access · greenAbstract readReview
In one paragraph

Review in Steroids, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed
1.9field-weighted citation impact, top 17% 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

24 citing papers in PubMed, 81 citations in OpenAlex.

  1. Review
  2. Article
  3. Review
  4. Review
  5. Article
  6. Article
  7. Article
  8. Review
  9. Article
  10. Article
  11. Article
  12. Article
  13. Actions of Thyroid Hormone Analogues on Chemokines.Journal of immunology research · 2016
    Review
  14. Overlapping nongenomic and genomic actions of thyroid hormone and steroids.Best practice & research. Clinical endocrinology & metabolism · 2015
    Review
  15. Functional status of thyroid and cognitive functions after menopause.Medical science monitor : international medical journal of experimental and clinical research · 2015
    Article
  16. Pain and thyroid hormones.Neurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology · 2013
    Review
  17. Review
  18. Article
  19. Iodothyronine deiodinases and cancer.Journal of endocrinological investigation · 2011
    Review
  20. Review
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

1 author at 1 institution in 1 country.

Jack L LeonardDepartment of Cellular and Molecular Physiology, UMASS Medical School, 55 Lake Avenue North, Worcester, MA 01655, USA. jack.leonard@umassmed.edu
University of Massachusetts Chan Medical School · US

Funding

TH-Dependent, Actin-Based Vesicle TraffickingR01DK060051 · NIDDK · UNIV OF MASSACHUSETTS MED SCH WORCESTER · PI LEONARD, JACK L. · 2001 to 2005
$1.7M
NIDDK NIH HHS R01 DK060051
6 · The paper itself

Abstract

Thyroid hormone (TH) is essential for neuronal migration and synaptogenesis in the developing brain. Assembly of neuronal circuits depends on guidance cues provided by the extracellular matrix. These cues are interpreted by the migrating neuron and its growing neurites through transmembrane signaling proteins anchored in place by the actin cytoskeleton. One of the best examples of a non-genomic action of thyroid hormone is its dynamic regulation of the number and quantity of actin fibers in astrocytes. Thyroxine (T4) and its transcriptionally inactive metabolite, 3',5',3-triiodothyronine (reverse T3) are responsible for modulating microfilament organization, while the transcriptional activator, 3',3,5-triiodothyronine (T3) is inert. The biological consequence of the loss of the actin filaments in astrocytes is the inability of the cell to anchor laminin, to its cell surface, and the loss of this key guidance molecule interrupts neurite pathfinding and neuronal migration. These data provide the essentials to construct a physiological pathway where TH-dependent regulation of the polymerization state of actin in the astrocyte and the developing neuron modulates the production and recognition of guidance cues--cues that if disrupted lead to abnormal neuronal migration and neuronal process formation--and lead to the morphological deficits observed in the cretinous brain.

Indexed as

ActinsAnimalsAstrocytesBrainCell MovementCerebellumHumansModels, BiologicalNeuronsProtein BindingRatsThyroid HormonesTranscription, GeneticTriiodothyronineActinsThyroid HormonesTriiodothyronine

Identifiers

PMID18280526
PMCPMC2601565
OpenAlexW1978293152

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.