Regulation of luteal regression: The ewe as a model

Research output: Contribution to journalArticle

25 Citations (Scopus)

Abstract

This article focuses on mechanisms that regulate functional and structural regression of the corpus luteum (CL) with special emphasis on the role of prostaglandin F(2α) (PGF2α) in mediating these events in large luteal cells in the ewe. Progesterone produced by the CL is absolutely required in all mammals for implantation and early maintenance of pregnancy. Luteal regression at the end of the nonpregnant cycle involves loss of progesterone production and tissue destruction via physiologic cell death, apoptosis. These are distinct events termed functional and structural regression, respectively. In many mammals, including ewes, luteal regression is initiated by prostaglandin F(2α) (PGF(2α)) of uterine origin. However, the exact mechanisms of this regulation are not well understood. Functional regression appears to be directly stimulated by PGF(2α) via activation of its membrane receptor. Whether structural regression is also initiated directly by PGF(2α) is not known. The ovine CL contains two morphologically and functionally distinct steroidogenic cell types, designated small and large. Receptors for PGF(2α) are exclusively located on large cells. Thus, the signal for regression is received in those cells. These data provide strong evidence that the intracellular determinant of regression resides within the large cell.

Original languageEnglish (US)
Pages (from-to)49-57
Number of pages9
JournalJournal of the Society for Gynecologic Investigation
Volume5
Issue number2
DOIs
StatePublished - Mar 1998

Fingerprint

Luteolysis
Prostaglandins F
Corpus Luteum
Progesterone
Mammals
Pregnancy Maintenance
Luteal Cells
Sheep
Cell Death
Apoptosis
Membranes

Keywords

  • Luteal regression
  • Ovine corpus luteum
  • Prostaglandin F(2α)

ASJC Scopus subject areas

  • Obstetrics and Gynecology

Cite this

Regulation of luteal regression : The ewe as a model. / Hoyer, Patricia B.

In: Journal of the Society for Gynecologic Investigation, Vol. 5, No. 2, 03.1998, p. 49-57.

Research output: Contribution to journalArticle

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