DES action in the thymus

inhibition of cell proliferation and genetic variation

Karen A Gould, James D. Shull, Jack Gorski

Research output: Contribution to journalArticle

25 Citations (Scopus)

Abstract

Many tissues, including the thymus, represent direct targets of estrogen action. In contrast to many estrogen responsive tissues, the thymus undergoes a profound atrophy in response to elevated levels of estrogens. The mechanism of estrogen-induced atrophy in the thymus is unknown; however, it appears not to involve massive thymocyte apoptosis. Here, we demonstrate that the estrogen diethylstilbestrol (DES) inhibits cell proliferation within the thymic cortex, the primary site of thymocyte proliferation. Unlike glucocorticoid action, the effect of DES on thymocyte proliferation does not appear to be mediated by direct down regulation of cyclin D3. We also demonstrate for the first time that rat strains vary in their sensitivity to DES-induced thymic atrophy. This sensitivity correlates with the ability of DES to inhibit cell proliferation in the thymus. These data suggest that genetic factors may regulate estrogen action within this tissue by affecting estrogen responsive pathways that control cell proliferation.

Original languageEnglish (US)
Pages (from-to)31-39
Number of pages9
JournalMolecular and Cellular Endocrinology
Volume170
Issue number1-2
DOIs
StatePublished - Dec 22 2000

Fingerprint

Thymus
Diethylstilbestrol
Cell proliferation
Thymus Gland
Estrogens
Cell Proliferation
Thymocytes
Atrophy
Tissue
Cyclin D3
Glucocorticoids
Rats
Down-Regulation
Apoptosis

Keywords

  • Atrophy
  • Estrogens
  • Genetics
  • Proliferation
  • T-cell
  • Thymus gland

ASJC Scopus subject areas

  • Biochemistry
  • Molecular Biology
  • Endocrinology

Cite this

DES action in the thymus : inhibition of cell proliferation and genetic variation. / Gould, Karen A; Shull, James D.; Gorski, Jack.

In: Molecular and Cellular Endocrinology, Vol. 170, No. 1-2, 22.12.2000, p. 31-39.

Research output: Contribution to journalArticle

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