# PEROXIDASE AND EOSINOPHILS IN UTERINE ESTROGEN ACTION

> **NIH NIH R01** · UNIVERSITY OF PENNSYLVANIA · 1994 · $146,388

## Abstract

Estradiol, has been shown to interact with specific receptors in target
cells resulting in the stimulation of gene expression.  Cell culture
models (eg. human breast cancer cell lines) have made valued
contributions to the understanding of the molecular mechanisms involved
in this process.  However, in vivo responses are more complicated since
responsive tissues such as the uterus are composed of at least three
resident cell types (epithelial, stromal and myometrial) each of which
can express different responses to steroids.  Furthermore, the
administration of estradiol to rats results in a specific, estrogen
dependent influx of leukocytes, especially eosinophils into the uterus.
There is approximately a 50 - fold increase in the number of eosinophils
in the uterus following stimulation with estradiol.  This increase has
been shown to be regulated through the normal estrous cycle of the rat
reaching a maximum of 8,000,000 eosinophils at estrus from a low of
150,000 at diestrus.  Similar increases have been seen in the post-partum
uterus.  The presence of an eosinophil chemotactic factor has been
documented in the uterus (ECF-U).  This factor is stimulated by estrogens
through a receptor mediated mechanism and further regulated through the
interaction of progestins and glucocorticoids.  The proposed research
will focus on two aspects regarding this chemotactic factor.  Firstly,
the nature of ECF-U will be examined, this will be accomplished through
the isolation and characterization of the factor and cloning of ECF-U
cDNA.  Secondly, the cellular origin and molecular mechanisms of
regulation of ECF-U expression will be examined.  The infiltration of
eosinophils, as in the case of lungs of patients with asthma, has been
associated with epithelial cell damage or death.  In the reproductive
tract eosinophils or eosinophil homologous proteins have been associated
with tissue remodeling during; the normal rat estrous cycle,
implantation, and regression of the post-partum uterus.  We hypothesize
that uterine eosinophils play a role in tissue remodeling. This
hypothesis will be tested by examining uterine growth and function in the
absence of eosinophil infiltration.  The infiltration of eosinophils will
be prevented by treatment of rats with neutralization antibodies against
ECF-U which prevent chemotaxis.  These studies will result in a sound
understanding of the nature of ECF-U and the mechanisms which control
eosinophil infiltration.  They will also provide new information as to
the regulation of uterine function and mechanisms of steroid regulation
in an integrated system.

## Key facts

- **NIH application ID:** 2197934
- **Project number:** 5R01HD020025-10
- **Recipient organization:** UNIVERSITY OF PENNSYLVANIA
- **SAM.gov UEI:** GM1XX56LEP58
- **Principal Investigator:** GREGORY S. KOPF
- **Activity code:** R01 (R01, R21, SBIR, etc.)
- **Funding institute:** NIH
- **Fiscal year:** 1994
- **Award amount:** $146,388
- **Award type:** 5
- **Project period:** 1985-04-01 → 1996-03-31

## Primary source

NIH RePORTER: https://reporter.nih.gov/project-details/2197934

## Citation

> US National Institutes of Health, RePORTER application 2197934, PEROXIDASE AND EOSINOPHILS IN UTERINE ESTROGEN ACTION (5R01HD020025-10). Retrieved via MORVS 2026-10-25 from https://api.morvs.ai/grant/nih/2197934. Licensed CC0.

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