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Absence of lutropin (LH) receptor mRNA in the rat thyroid: further evidence for specificity cross-over at the thyroid-stimulating hormone receptor level.

Authors
  • Graves, P N
  • Davies, T F
Type
Published Article
Journal
Molecular and Cellular Endocrinology
Publisher
Elsevier
Publication Date
Aug 01, 1991
Volume
79
Issue
1-3
Pages
21–28
Identifiers
PMID: 1936543
Source
Medline
License
Unknown

Abstract

Chorionic gonadotropin (CG) and purified lutropin (LH) activate intact thyroid tissue and isolated thyroid cells. A recent report has suggested that the presence of aberrant LH/CG receptors in human and rat thyroid tissue may interact with gonadotropin thus explaining the mechanisms of thyroid cell stimulation. To detect putative thyroidal LH receptor mRNA, a segment of the transmembrane region containing domains 3 through 6 of the rat (r) LH receptor was targeted for amplification using the polymerase chain reaction (PCR). cDNA prepared from a rLH receptor-positive control tissue (testis) was efficiently amplified under stringent annealing conditions giving a 486 bp product as predicted. However, cDNAs from thyroidal tissue and from the thyroid-stimulating hormone (TSH)- and hCG-responsive 1B-6 subclone of Fisher rat thyroid cells (FRTL-5) yielded no detectable 486 bp product. A smaller (non-LH) fragment amplified to similar extents from both testis and thyroidal cDNAs provided a useful internal control for amplification. This allowed the conclusion that specificity cross-over between LH/CG and TSH occurs at the TSH receptor and that the LH/CG receptor gene is transcriptionally silent in rat thyroidal cells.

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