# HORMONAL REGULATION OF BONE COLLAGEN METABOLISM

> **NIH NIH R01** · UNIVERSITY OF CONNECTICUT SCH OF MED/DNT · 1988 · $119,081

## Abstract

The goals of this grant are to further investigate the mechanisms
by which hormones alter collagen synthesis and gene expression in
bone.  The first goal of this grant is to study the effects of
insulin-like growth factor I, protein kinase C agonists and
glucocorticoids on collagen synthesis and steady state levels of
procollagen mRNA in 21-day fetal rat calvaria, rat osteoblast-like
cells and rat osteosarcoma cells.  If changes in procollagen mRNA
levels are found, the effect of these hormones on transcription
and stability of procollagen mRNA will be measured.  A second
goal is to use in situ hybridization to examine the effects of
glucocorticoids on procollagen mRNA levels in osteoblasts of 21-
day fetal rat calvaria.  Calvaria will be treated with
glucocorticoids for 24 and 96 hours and tissue sections hybridized
with RNA or cDNA probes for procollagen mRNA.  This study
should show whether glucocorticoids inhibit bone collagen
synthesis by decreasing procollagen mRNA levels per cell or by
decreasing the number of osteoblasts on the bone matrix.  A third
research goal is to transfect bone cells with recombinant plasmids
containing type I collagen gene promoters linked to the
chloramphenicol gene to examine the hormonal regulation of
promoter activity.  Site-directed mutagenesis and enzyme
cleavage will be used to produce mutations or deletions in
collagen gene promoters.  Recombinant plasmids containing
altered collagen promoters will be transfected into bone cells and
the effect of mutations on hormonal regulation of promoter
activity will be determined.  A gel-migration assay will be used to
study proteins in crude nuclear extracts from hormone-treated
bone cells which bind and presumably regulate collagen promoter
activity.  These studies should give a better understanding of the
mechanisms by which hormones regulate type I collagen synthesis
in bone and identify sequences within type I collagen gene
promoters which are modulated by hormones.  Knowledge of the
hormonal regulation of bone collagen synthesis and gene
expression is primary to understanding the pathologic basis of
metabolic bone disease.

## Key facts

- **NIH application ID:** 3155715
- **Project number:** 5R01AR029850-08
- **Recipient organization:** UNIVERSITY OF CONNECTICUT SCH OF MED/DNT
- **SAM.gov UEI:** H6D6JMXJXDE6
- **Principal Investigator:** BARBARA E KREAM
- **Activity code:** R01 (R01, R21, SBIR, etc.)
- **Funding institute:** NIH
- **Fiscal year:** 1988
- **Award amount:** $119,081
- **Award type:** 5
- **Project period:** 1981-07-01 → 1992-06-30

## Primary source

NIH RePORTER: https://reporter.nih.gov/project-details/3155715

## Citation

> US National Institutes of Health, RePORTER application 3155715, HORMONAL REGULATION OF BONE COLLAGEN METABOLISM (5R01AR029850-08). Retrieved via MORVS 2026-10-25 from https://api.morvs.ai/grant/nih/3155715. Licensed CC0.

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