4 research outputs found
Differential expression of tissue kallikrein in the skin of systemic sclerosis
Systemic sclerosis (SSc) is characterised by
ischemic damage, impaired angiogenesis and skin
fibrosis. Tissue kallikrein (t-kallikrein) is involved
through kinins in inflammation, vasorelaxation and
angiogenesis. T-kallikrein is synthetised by endothelial,
smooth muscle, and inflammatory cells and, in skin, also
by dark cells of the sweat glands, where it is involved in
sweat formation.
Our aim was to analyse, by immunohistochemistry
and RT-PCR, the expression of t-kallikrein in the skin of
patients with different SSc subsets, limited (lSSc) and
diffuse (dSSc), and phases, early and advanced.
Skin biopsies were taken from 18 SSc patients and
10 controls. Immunohistochemistry was performed on
paraffin sections with an antibody against human urinary
t-kallikrein.
For RT-PCR, cDNA from skin biopsies was
amplified using primers specific for human t-kallikrein.
In the control skin, dark cells of the secretory units
of sweat glands showed immunopositivity for tkallikrein
as well as blood vessels. In the lSSc skin,
immunoreactivity was observed only in some glands,
with weak staining in the advanced phase. In early lSSc
skin, immunoreactivity was observed in microvessel
walls and in the inflammatory infiltrate. In dSSc skin,
dark cells of the glandular fundus units, and the few
remaining vessels showed scarcity (early phase) or lack
(advanced phase) of immunoreactivity for t-kallikrein. RT-PCR confirmed a decrease of t-kallikrein mRNA
levels from early to advanced phase in SSc subsets,
reaching its lowest level in advanced dSSc.
In conclusion, immunohistochemical and
biomolecular results indicate that t-kallikrein is
decreased in the skin of SSc patients and decreases
progressively from the early to advanced phase of lSSc
and dSSc. The decreased expression of t-kallikrein may be involved in the impairment of the sweating process,
vessel functionality and angiogenesis