Evidence map›Paper›PMID 19955180›Full record

ArticleThe Journal of biological chemistry2010

Thyrostimulin, but not thyroid-stimulating hormone (TSH), acts as a paracrine regulator to activate the TSH receptor in mammalian ovary.

Su-Chin Sun, Pei-Jen Hsu, Fang-Ju Wu, Sheng-Hsiang Li, Chung-Hao Lu, Ching-Wei Luo

Open access · hybridAbstract read
In one paragraph

Article in The Journal of biological chemistry, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers.

0numbers the graph read from it
0cells of the map it votes in
36citing papers in PubMed
2.6field-weighted citation impact, top 10% 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

36 citing papers in PubMed, 89 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Review
  5. Article
  6. Article
  7. Review
  8. Review
  9. Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. Expression of Endogenous Putative TSH Binding Protein in Orbit.Current issues in molecular biology · 2021
    Article
  15. Review
  16. Article
  17. Review
  18. Article
  19. Review
  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 2 institutions in 1 country.

Su-Chin SunFrom the Department of Life Sciences and Institute of Genome Sciences, National Yang-Ming University, Taipei 112 and.
Pei-Jen HsuFrom the Department of Life Sciences and Institute of Genome Sciences, National Yang-Ming University, Taipei 112 and.
Fang-Ju WuFrom the Department of Life Sciences and Institute of Genome Sciences, National Yang-Ming University, Taipei 112 and.
Sheng-Hsiang Lithe Department of Medical Research, Mackay Memorial Hospital, Tamshui, Taipei Country 251, Taiwan.
Chung-Hao Luthe Department of Medical Research, Mackay Memorial Hospital, Tamshui, Taipei Country 251, Taiwan.
Ching-Wei LuoFrom the Department of Life Sciences and Institute of Genome Sciences, National Yang-Ming University, Taipei 112 and. Electronic address: cwluo@ym.edu.tw.
National Yang Ming Chiao Tung University · TWMackay Memorial Hospital · TW

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The thyroid-stimulating hormone receptor (TSHR), activated by either TSH or the newly discovered glycoprotein hormone thyrostimulin, plays a central role in the control of body metabolism. Interestingly, in addition to its thyroid expression, we discovered that the mRNA level of TSHR is periodically regulated in rat ovary by gonadotropins. Ovarian microdissection followed by real-time PCR analysis indicated that granulosa cells show the highest level of TSHR expression. Cultures of follicles and primary granulosa cells demonstrated that the level of TSHR is up-regulated and decreased by the gonadotropin-driven cAMP cascade and estradiol production, respectively. Furthermore, in contrast to the negligible expression of TSH in the ovary, we also found by real-time PCR and immunohistochemical analysis that thyrostimulin is expressed mainly in oocytes. Evolving before the appearance of gonadotropins, thyrostimulin is considered the most ancestral glycoprotein hormone. Therefore, the presence of thyrostimulin in the ovary suggests that it may have a primitive function in reproduction when it activates ovarian TSHR. Next, we generated recombinant thyrostimulin protein and characterized its non-covalent heterodimeric nature. Using purified recombinant thyrostimulin, we show that the human ovarian cell line NIH:OVCAR-3 also expresses endogenous and functional TSHR. Using cultured rat granulosa cells isolated from different ovarian stages, we found that treatments with thyrostimulin significantly increase cAMP production and the c-fos gene response in the presence of gonadotropins. Thus, this study demonstrates that oocyte-derived thyrostimulin and granulosa cell-expressed TSHR compose a novel paracrine system in the ovary, where the activity is tightly controlled by gonadotropins.

Indexed as

8-Bromo Cyclic Adenosine MonophosphateAnimalsCell LineCell Line, TumorCells, CulturedColforsinCyclic AMPEstradiolFemaleGene ExpressionGlycoproteinsGonadotropinsGranulosa CellsHumansImmunohistochemistryMale8-Bromo Cyclic Adenosine MonophosphateColforsinCyclic AMPEstradiolGlycoproteinsGonadotropinsProto-Oncogene Proteins c-fosReceptors, ThyrotropinthyrostimulinThyrotropin

Identifiers

PMID19955180
PMCPMC2823517
OpenAlexW2072966398

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.