# REGULATION OF THE PRIMATE CORPUS LUTEUM

> **NIH NIH R01** · MAGEE-WOMEN'S HOSPITAL OF UPMC · 1993 · $79,195

## Abstract

The long-term objective of this research is to elucidate the mechanisms
responsible for the regression of the corpus luteum at the termination
of non-fertile menstrual cycles as well as to understand the mechanisms
by which chorionic gonadotropin rescues the corpus luteum during early
pregnancy.  In previous years of support we investigated the role of
pituitary LH secretion on the maintenance of luteal function and
lifespan.  While our results provided unequivocal evidence that LH
secretion is absolutely required for progesterone production by the
corpus luteum, our data also demonstrated that spontaneous luteal
regression at the termination of non-fertile cycles in not due to changes
in the pattern of LH secretion.  Therefore, the overall goal of the
current proposal is to investigate mechanisms intrinsic to the corpus
luteum that may be responsible for luteal regression.

The overall hypothesis we wil test is that the specialized functions of
the corpus luteum  (steroid and protein synthesis and release) are
independently superimposed on a cellular timing mechanism that results
in a highly reproducible 14-16 day lifespan of the tissue.  The
foundation for this hypothesis is a direct result of our previous studies
in which we demonstrated that a three day interruption of LH support to
the corpus luteum caused a total cessation of luteal progesterone
secretion but did not interfere with the lifespan of the tissue.

In pursuit of testing this hypothesis, we will determine if luteal
regression is due to a type of programmed cell death in which the
degradation of genomic DNA with the concomitant loss in the fidelity of
transcriptional processes is an early event in the process of luteal
regression.  For this purpose, we wil examine the integrity of genomic
DNA during the period of luteal regression as well as steady state levels
of mRNAs for major luteal cell proteins.  Our hypothesis would be
supported by the observation that degradation of genomic DNA precedes
reductions in steady state mRNA levels during luteal regression.

In addition, we will determine if the rescue of the corpus luteum by hCG
is due to a delay in the degradation of DNA and/or increases in either
the concentration and/or the duration of expression of mRNAs for major
luteal cell proteins. Lastly, we will use our GnRH-pulsed animal model
to determine whether LH is involved in the moment to moment regulation
of gene expression in the corpus luteum or whether LH serves solely to
regulate pre-existing pathways for steroidogenesis.

These studies, in addition to providing basic information on the
regulation of the corpus luteum, may also shed new information on the
cellular mechanisms involved in the pathological conditions of the
inadequate luteal phase and the short luteal phase, both of which are
associated with infertility in humans.

## Key facts

- **NIH application ID:** 2197368
- **Project number:** 5R01HD016842-09
- **Recipient organization:** MAGEE-WOMEN'S HOSPITAL OF UPMC
- **Principal Investigator:** Anthony J Zeleznik
- **Activity code:** R01 (R01, R21, SBIR, etc.)
- **Funding institute:** NIH
- **Fiscal year:** 1993
- **Award amount:** $79,195
- **Award type:** 5
- **Project period:** 1982-09-01 → 1994-12-31

## Primary source

NIH RePORTER: https://reporter.nih.gov/project-details/2197368

## Citation

> US National Institutes of Health, RePORTER application 2197368, REGULATION OF THE PRIMATE CORPUS LUTEUM (5R01HD016842-09). Retrieved via MORVS 2026-10-25 from https://api.morvs.ai/grant/nih/2197368. Licensed CC0.

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