# REGULATION OF LUTEAL FUNCTION

> **NIH NIH R37** · UNIVERSITY OF ILLINOIS AT CHICAGO · 1994 · $152,096

## Abstract

The maintenance of corpus luteum vascularization, growth and
steroidogenesis in the pregnant rat is a complex process involving
pituitary, placental and ovarian hormones.  Estradiol, formed in
the luteal cell from either endogenous or placental androgen
substrates. acts locally to stimulate blood supply, cell
hypertrophy and steroidogenesis of the corpus luteum previously
exposed to prolactin from either pituitary or placenta.  The first
aim of this study is to investigate the molecular mechanism by
which estradiol affects vascularization and growth of the corpus
luteum.  We will investigate the possibility that estradiol
enhances blood supply to the corpus luteum by increasing the
content and mRNA for basic fibroblast growth factor, the luteal
angiogenic factor.  Whether the requirement for prolactin and
estradiol for the optimal growth of the rat corpus luteum reflects
interaction of these two hormones on the production and action of
insulin-like growth factor-I will be determined.  We will examine
the possibility that estradiol enhances cholesterol availability
for progesterone biosynthesis by increasing the formation of both
HMG-CoA reductase, the key enzyme in cholesterol biosynthesis, and
Sterol Carrier Protein 2, the molecule responsible for cholesterol
transport to the mitochondria.  The significance and the role of
estrogen induced changes in calcium-calmodulin and calcium-
phospholipid-dependent phosphorylation of specific proteins in
subcellular fractions will be investigated.  Since estradiol
biosynthesis by the corpus luteum depends upon placental androgens
from mid-pregnancy, we will determine the reason why the placenta
does not synthesize androgen early in pregnancy and determine,
throughout placental development, the content and mRNA levels of
cytochrome P450scc and P45017 alpha, the enzymes responsible for
progesterone and androgen biosynthesis.  Finally, we will
investigate the mechanism by which LH, estradiol and calcium-
calmodulin controls placental steroidogenesis in the rat.

## Key facts

- **NIH application ID:** 2196782
- **Project number:** 5R37HD011119-17
- **Recipient organization:** UNIVERSITY OF ILLINOIS AT CHICAGO
- **SAM.gov UEI:** W8XEAJDKMXH3
- **Principal Investigator:** GEULA GIBORI
- **Activity code:** R37 (R01, R21, SBIR, etc.)
- **Funding institute:** NIH
- **Fiscal year:** 1994
- **Award amount:** $152,096
- **Award type:** 5
- **Project period:** 1978-01-01 → 1998-03-31

## Primary source

NIH RePORTER: https://reporter.nih.gov/project-details/2196782

## Citation

> US National Institutes of Health, RePORTER application 2196782, REGULATION OF LUTEAL FUNCTION (5R37HD011119-17). Retrieved via MORVS 2026-10-25 from https://api.morvs.ai/grant/nih/2196782. Licensed CC0.

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