# REGULATION OF FIBRONECTIN MATRIX ASSEMBLY

> **NIH NIH R01** · ALBANY MEDICAL COLLEGE · 1987 · $104,721

## Abstract

Plasma fibronectin has previously been shown to bind to cell surface
receptors which may mediate the assembly of soluble fibronectin into the
extracellular matrix.  Preliminary data suggest that the mechanism for
incorporation of soluble fibronectin into the extracellular matrix is not
functional in the transformed cell line, HT-1080.  However, the mechanism
can be induced when HT-1080 cells are treated with the glucocorticoid
dexamethasone.  The hypothesis that will be tested in these studies is that
the elaboration of a fibronectin matrix requires the participation of
specific receptors and that these receptors are no longer functional in
transformed and differentiating cells which do not incorporate fibronectin
into the extracellular matrix.  Identification of the fibronectin receptor
will be made using monoclonal antibodies which have been prepared against
fibronectin-binding proteins present in detergent extracts of human
fibroblasts.  After identification of receptor(s), experiments will be done
to determine whether this molecule(s) functions in the assembly of
endogenous (cell synthesized) fibronectin in the extracellular matrix or in
the attachment of cells to fibronectin matrices.  Immunofluorescent
colocalization studies will be done on both normal and transformed cell
lines to analyze the distribution of fibronectin and its receptor in the
cell layer.  Fibronectin receptor expression will be studied in two
transformed cell lines:  a human fibrosarcoma, HT-1080, and a rat cell
line, 2-R, which contain a temperature-sensitive transforming virus.
Receptor expression also will be monitored during in vitro chondrogenesis
of limb mesenchymal cells.  HT-1080 cells will be used to study the
potential role of the fibronectin receptor during dexamethasone induction
of fibronectin matrix deposition.  The 2-R cells will be used to determine
whether the loss of a functional fibronectin receptor can be correlated
with the loss of the pericellular matrix during transformation at the
permissive temperature.  Differentiating chondrocytes will be used to
correlate fibronectin receptor loss with overt chondrogenesis and to
determine whether the modulation of chondrocyte phenotype by Vitamin A is
mediated by the fibronectin receptor.  (A)

## Key facts

- **NIH application ID:** 3175610
- **Project number:** 7R01CA037785-04
- **Recipient organization:** ALBANY MEDICAL COLLEGE
- **SAM.gov UEI:** G6VVMPNK4Y48
- **Principal Investigator:** PAULA J MC KEOWN-LONGO
- **Activity code:** R01 (R01, R21, SBIR, etc.)
- **Funding institute:** NIH
- **Fiscal year:** 1987
- **Award amount:** $104,721
- **Award type:** 7
- **Project period:** 1987-03-01 → 1988-06-30

## Primary source

NIH RePORTER: https://reporter.nih.gov/project-details/3175610

## Citation

> US National Institutes of Health, RePORTER application 3175610, REGULATION OF FIBRONECTIN MATRIX ASSEMBLY (7R01CA037785-04). Retrieved via MORVS 2026-10-25 from https://api.morvs.ai/grant/nih/3175610. Licensed CC0.

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