# FETAL WOUND HEALING--ROLE OF THE EXTRACELLULAR MATRIX

> **NIH NIH R01** · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · 1994 · $199,727

## Abstract

Recent clinical and experimental evidence suggests that the fetus
responds to surgical injury in a fashion fundamentally different from the
adult: the fetus heals rapidly without the scarring and inflammation that
accompany adult wounds.  The mechanisms that underlie these differences
are unknown.  We have established scarless repair models in both the
long-gestation fetal sheep model and in an adult athymic mouse model of
human fetal skin repair.  We determined that scarless fetal repair
appears to be intrinsic to fetal tissue and is not secondary to extrinsic
fetal environmental factors (e.g., amniotic fluid exposure).  We
hypothesize that scarless fetal repair is a consequence of a unique
extracellular matrix (ECM) produced by the fetal fibroblast in
conjunction with the absence of an adult-like inflammatory response to
injury.  Our general strategy  is to delineate the crucial ECM (collagen
and proteoglycan) and cellular (fibroblast, myofibroblast, inflammatory
cell) components that differentiate fetal from adult healing using these
established fetal repair models.  The first aim of this proposal is to
use established morphologic techniques to investigate the ECM
(proteoglycan) and cellular (myofibroblast, inflammatory cell) components
that distinguish fetal from adult repair in sheep, particularly during
the in utero transition from scarless fetal wound healing to "adult"
healing with scar formation.  Related studies will determine the relative
contributions of fetal/adult ECM and fetal/adult cells at the healing
interface of adult sheep skin transplanted onto fetal lambs, since
scarring occurs only within the adult skin at this adult-fetal tissue
interface.  The second objective is to define the biochemical (collagen
types, glycosaminoglycan profile) and biomechanical (wound breaking
strength) differences between fetal and adult sheep wound repair.  The
third aim is to characterize a unique model of scarless human fetal skin
healing using human fetal skin grafts that are wounded after
transplantation onto adult athymic mice.  Experiments are planned to
elucidate the role of species-specific ECM, adult mouse vs. fetal human
fibroblasts, inflammatory cells, growth factor profile, differentiation,
and the air-tissue interface in this model of scarless human fetal wound
healing.  Our long-term objective is to apply this knowledge clinically
to avoid scarring (keloids, intra-peritoneal adhesions, strictures, etc.)
by altering the ECM and cellular response of adult wounds so that healing
occurs in a more fetal-like manner.

## Key facts

- **NIH application ID:** 2199615
- **Project number:** 5R01HD025505-05
- **Recipient organization:** UNIVERSITY OF CALIFORNIA, SAN FRANCISCO
- **SAM.gov UEI:** KMH5K9V7S518
- **Principal Investigator:** N SCOTT ADZICK
- **Activity code:** R01 (R01, R21, SBIR, etc.)
- **Funding institute:** NIH
- **Fiscal year:** 1994
- **Award amount:** $199,727
- **Award type:** 5
- **Project period:** 1989-12-01 → 1997-02-28

## Primary source

NIH RePORTER: https://reporter.nih.gov/project-details/2199615

## Citation

> US National Institutes of Health, RePORTER application 2199615, FETAL WOUND HEALING--ROLE OF THE EXTRACELLULAR MATRIX (5R01HD025505-05). Retrieved via MORVS 2026-10-25 from https://api.morvs.ai/grant/nih/2199615. Licensed CC0.

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