Go to JCI Insight
  • About
  • Editors
  • Consulting Editors
  • For authors
  • Publication ethics
  • Alerts
  • Advertising
  • Job board
  • Subscribe
  • Contact
  • Current issue
  • Past issues
  • By specialty
    • COVID-19
    • Cardiology
    • Gastroenterology
    • Immunology
    • Metabolism
    • Nephrology
    • Neuroscience
    • Oncology
    • Pulmonology
    • Vascular biology
    • All ...
  • Videos
    • Conversations with Giants in Medicine
    • Author's Takes
  • Reviews
    • View all reviews ...
    • Immune Environment in Glioblastoma (Feb 2023)
    • Korsmeyer Award 25th Anniversary Collection (Jan 2023)
    • Aging (Jul 2022)
    • Next-Generation Sequencing in Medicine (Jun 2022)
    • New Therapeutic Targets in Cardiovascular Diseases (Mar 2022)
    • Immunometabolism (Jan 2022)
    • Circadian Rhythm (Oct 2021)
    • View all review series ...
  • Viewpoint
  • Collections
    • In-Press Preview
    • Commentaries
    • Research letters
    • Letters to the editor
    • Editorials
    • Viewpoint
    • Top read articles
  • Clinical Medicine
  • JCI This Month
    • Current issue
    • Past issues

  • Current issue
  • Past issues
  • Specialties
  • Reviews
  • Review series
  • Conversations with Giants in Medicine
  • Author's Takes
  • In-Press Preview
  • Commentaries
  • Research letters
  • Letters to the editor
  • Editorials
  • Viewpoint
  • Top read articles
  • About
  • Editors
  • Consulting Editors
  • For authors
  • Publication ethics
  • Alerts
  • Advertising
  • Job board
  • Subscribe
  • Contact
Top
  • View PDF
  • Download citation information
  • Send a comment
  • Share this article
  • Terms of use
  • Standard abbreviations
  • Need help? Email the journal
  • Top
  • Abstract
  • Version history
  • Article usage
  • Citations to this article

Advertisement

Concise Publication Free access | 10.1172/JCI106864

Thyrotropin Increases Prostaglandin Levels in Isolated Thyroid Cells

S.-C. Yu, L. Chang, and G. Burke

Division of Endocrinology and Nuclear Medicine, Department of Medicine, Michael Reese Hospital, Chicago, Illinois 60616

University of Chicago Pritzker School of Medicine, Chicago, Illinois 60616

Find articles by Yu, S. in: JCI | PubMed | Google Scholar

Division of Endocrinology and Nuclear Medicine, Department of Medicine, Michael Reese Hospital, Chicago, Illinois 60616

University of Chicago Pritzker School of Medicine, Chicago, Illinois 60616

Find articles by Chang, L. in: JCI | PubMed | Google Scholar

Division of Endocrinology and Nuclear Medicine, Department of Medicine, Michael Reese Hospital, Chicago, Illinois 60616

University of Chicago Pritzker School of Medicine, Chicago, Illinois 60616

Find articles by Burke, G. in: JCI | PubMed | Google Scholar

Published April 1, 1972 - More info

Published in Volume 51, Issue 4 on April 1, 1972
J Clin Invest. 1972;51(4):1038–1042. https://doi.org/10.1172/JCI106864.
© 1972 The American Society for Clinical Investigation
Published April 1, 1972 - Version history
View PDF
Abstract

We have shown that two unrelated prostaglandin antagonists block both thyrotropin (TSH) and prostaglandins E (PGE1, PGE2) stimulation of thyroidal adenyl cyclase activation and cyclic 3′,5′-adenosine monophosphate (cAMP) formation, suggesting that prostaglandins play an important role in regulating thyroid function. To further explore this postulate, we measured prostaglandin content by radioimmunoassay in homogeneous bovine thyroid cell preparations in the presence and absence of TSH. Antibodies to albumin-conjugated PGE1 and PGF2α showed specificity for prostaglandins E and F, respectively, but reacted, albeit far less effectively, with heterologous prostaglandins. A double antibody system was used to separate free from antibody-bound PGE1-3H and PGF2α-3H. Thyroid cells were extracted with ethanol/ethyl acetate and the various prostaglandins separated on silicic acid columns. Recoveries of added PGE1-3H and PGF2α-3H through the extraction and separation procedures ranged from 50-80%. The sensitivity of the method was 10-50 pg. Basal thyroid cell content of PGE1 and PGF2α “equivalents” varied between cell preparations (range = 2-6 ng/0.2 ml cell suspension) but, in each instance, remained constant during 5-30-min incubations at 37°C. TSH, 10-100 mU/ml, increased the levels of cell PGE1 and PGF2α “equivalents” 30-80% above basal during 5-15-min incubations. The stimulatory effect was specific for TSH, no increase in PGE1 or PGF2α “equivalent” levels being seen with luteinizing hormone (LH), human growth hormone (HGH), adrenocorticotropic hormone (ACTH), or glucagon. These data support the thesis that prostaglandins may mediate TSH effects on thyroid.

Browse pages

Click on an image below to see the page. View PDF of the complete article

icon of scanned page 1038
page 1038
icon of scanned page 1039
page 1039
icon of scanned page 1040
page 1040
icon of scanned page 1041
page 1041
icon of scanned page 1042
page 1042
Version history
  • Version 1 (April 1, 1972): No description

Article tools

  • View PDF
  • Download citation information
  • Send a comment
  • Share this article
  • Terms of use
  • Standard abbreviations
  • Need help? Email the journal

Metrics

  • Article usage
  • Citations to this article

Go to

  • Top
  • Abstract
  • Version history
Advertisement
Advertisement

Copyright © 2023 American Society for Clinical Investigation
ISSN: 0021-9738 (print), 1558-8238 (online)

Sign up for email alerts