Hr. Higley et al., DISTRIBUTION OF TYPE-II TGF-BETA RECEPTOR IMMUNOREACTIVITY IN NORMAL AND IMPAIRED MURINE AND HUMAN WOUNDS, Wounds, 7(1), 1995, pp. 2-10
Cloning and sequencing of the Type II transforming growth factor-beta
receptor (TGF-beta IIR) gene has permitted the preparation of a polycl
onal anti-receptor antiserum. We have used this antiserum in an immuno
cytochemical survey of normal-healing, human skin wounds and chronic v
enous ulcers. In addition, the TGF-beta IIR distribution in a murine m
odel of full-thickness dermal wounds whose healing is impaired by appl
ication of a semi-occlusive, vapor-permeable dressing was compared to
that seen in control wounds treated with recombinant transforming grow
th factor-beta 2 (rTGF-beta 2). In unwounded human and murine skin, sp
ecific staining for the Type II TGF-beta receptor was seen in normal h
air follicle and appendageal epithelia, with minimal epidermal and der
mal immunoreactivity. Shortly after wounding, keratinocytes of the mig
rating epidermal tongue expressed TGF-beta IIR while increased stainin
g was only noted several days later in dermal fibroblasts, inflammator
y cells, and the neovasculature. Application of rTGF-beta 2 to dressin
g-inhibited mouse wounds increased the TGF-beta IIR staining in these
same cells in the areas of TGF-beta 2 augmented granulation tissue. Ve
nous ulcer biopsies exhibited TGF-beta IIR staining in the suprabasal
keratinocytes at the wound margins as well as in a variety of cells in
the non-healing wound bed. Using PCNA and procollagen immunostains, t
here appeared to be an inverse correlation between the expression of T
GF-beta IIR immunoreactivity and PCNA labeling density in human wound
epithelial cells, while fibroblasts with a proliferative or synthetic
phenotype expressed increased TGF-beta IIR immunoreactivity.