Jove
Visualize
Contact Us
JoVE
x logofacebook logolinkedin logoyoutube logo
ABOUT JoVE
OverviewLeadershipBlogJoVE Help Center
AUTHORS
Publishing ProcessEditorial BoardScope & PoliciesPeer ReviewFAQSubmit
LIBRARIANS
TestimonialsSubscriptionsAccessResourcesLibrary Advisory BoardFAQ
RESEARCH
JoVE JournalMethods CollectionsJoVE Encyclopedia of ExperimentsArchive
EDUCATION
JoVE CoreJoVE BusinessJoVE Science EducationJoVE Lab ManualFaculty Resource CenterFaculty Site
Terms & Conditions of Use
Privacy Policy
Policies

Related Experiment Videos

Growth factor expression in cold and hot thyroid nodules.

M Eszlinger1, K Krohn, J Kratzsch

  • 1III Medical Department, University of Leipzig, Germany.

Thyroid : Official Journal of the American Thyroid Association
|April 6, 2001
PubMed
Summary

Hot thyroid nodules (HTNs) and cold thyroid nodules (CTNs) show lower growth factor levels. While increased cyclic adenosine monophosphate (cAMP) drives HTN proliferation, the role of growth factors in CTNs requires further study.

Related Concept Videos

You might also read

Related Articles

Articles linked to this work by shared authors, journal, and citation graph.

Sort by
Same author

Bone quality relies on hyaluronan synthesis - Insights from mice with complete knockout of hyaluronan synthase expression.

Matrix biology plus·2024
Same author

Environmental drivers of increased ecosystem respiration in a warming tundra.

Nature·2024
Same author

On the Employment of Phosphate of Ammonia.

Medical examiner (Philadelphia, Pa.)·2023
Same author

Differential locomotor activity responses to day-time light intensity in juvenile and adult solitary Cape mole-rats, <i>Georychus capensis</i> (Rodentia: Bathyergidae).

Chronobiology international·2023
Same author

Thawing Yedoma permafrost is a neglected nitrous oxide source.

Nature communications·2021
Same author

Aviation Contrail Cirrus and Radiative Forcing Over Europe During 6 Months of COVID-19.

Geophysical research letters·2021

Area of Science:

  • Endocrinology and Molecular Biology
  • Thyroid Pathophysiology
  • Cell Proliferation Signaling

Background:

  • Hot thyroid nodules (HTNs) are often caused by thyrotropin receptor (TSHR) mutations activating the cyclic adenosine monophosphate (cAMP) cascade, promoting thyroid epithelial cell growth.
  • The molecular basis for cold thyroid nodules (CTNs) remains largely unknown, though iodine deficiency is linked to multinodular goiters and potential growth factor involvement.
  • Investigating growth factors is crucial to understand thyroid nodule proliferation in both hot and cold types.

Purpose of the Study:

  • To determine if specific growth factors modulate thyroid epithelial cell proliferation in late-stage CTNs and HTNs.
  • To compare concentrations of epidermal growth factor (EGF), transforming growth factor-alpha (TGF-alpha), TGF-beta1, and insulin-like growth factor-1 (IGF-1) in nodules and surrounding tissues.

Related Experiment Videos

Main Methods:

  • Enzyme-linked immunosorbent assay (ELISA) was used to measure EGF, TGF-alpha, and TGF-beta1 concentrations in CTNs (n=7), HTNs (n=9), and surrounding tissues (ST).
  • Radioimmunoassay (RIA) was employed to quantify IGF-1 levels in CTNs (n=5) and HTNs (n=10) and their corresponding STs.
  • Iodine concentrations were also assessed in nodule samples.

Main Results:

  • CTNs exhibited lower concentrations of all investigated growth factors and iodine compared to ST, with only iodine showing a significant difference.
  • HTNs displayed significantly lower concentrations of EGF and TGF-beta1 compared to ST; TGF-alpha and IGF-1 differences were not statistically significant.
  • Low growth factor levels in CTNs, despite low iodine, suggest they may not be the primary drivers in late stages.

Conclusions:

  • Low concentrations of EGF, TGF-alpha, and IGF-1 in CTNs argue against their significant pathophysiological role in late stages.
  • Reduced EGF, TGF-alpha, and IGF-1 levels in HTNs, irrespective of mutation status, support increased cAMP as the primary driver of proliferation.
  • The pathophysiological significance of low TGF-beta1 in both CTNs and HTNs warrants further investigation, with potential roles in early clonal expansion.