The molecular control of corpus luteum formation, function, and regression

Endocr Rev. 2007 Feb;28(1):117-49. doi: 10.1210/er.2006-0022. Epub 2006 Oct 31.

Abstract

The corpus luteum (CL) is one of the few endocrine glands that forms from the remains of another organ and whose function and survival are limited in scope and time. The CL is the site of rapid remodeling, growth, differentiation, and death of cells originating from granulosa, theca, capillaries, and fibroblasts. The apparent raison d'etre of the CL is the production of progesterone, and all the structural and functional features of this gland are geared toward this end. Because of its unique importance for successful pregnancies, the mammals have evolved a complex series of checks and balances that maintains progesterone at appropriate levels throughout gestation. The formation, maintenance, regression, and steroidogenesis of the CL are among the most significant and closely regulated events in mammalian reproduction. During pregnancy, the fate of the CL depends on the interplay of ovarian, pituitary, and placental regulators. At the end of its life span, the CL undergoes a process of regression leading to its disappearance from the ovary and allowing the initiation of a new cycle. The generation of transgenic, knockout and knockin mice and the development of innovative technologies have revealed a novel role of several molecules in the reprogramming of granulosa cells into luteal cells and in the hormonal and molecular control of the function and demise of the CL. The current review highlights our knowledge on these key molecular events in rodents.

Publication types

  • Research Support, N.I.H., Extramural
  • Review

MeSH terms

  • Animals
  • Corpus Luteum / metabolism*
  • Corpus Luteum / physiology*
  • Corpus Luteum Maintenance / physiology
  • Female
  • Humans
  • Luteolysis / physiology*
  • Menstrual Cycle
  • Models, Biological
  • Ovarian Follicle / cytology
  • Ovarian Follicle / physiology
  • Ovulation / physiology
  • Pregnancy
  • Signal Transduction