Publication: Potential role of a new anti-03 integrin antibody
in the development of intimal hyperplasia after
vascular surgery: an in vitro smooth muscle cell model
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Date
2001
Authors
Gimeno, M.J. ; González, J. ; Rodríguez, M. ; Corrales, C. ; Bellón, J.M. ; Buján, J.
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Publisher
Murcia : F. Hernández
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DOI
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info:eu-repo/semantics/article
Description
Abstract
The occurrence of intimal hyperplasia after
vascular surgery is an ongoing concern in current
clinical practice. Arnong the many factors involved in
the development of this pathology, platelet adhesion and
myointimal proliferation play a major role. Both these
processes are mediated by integrins (mainly avP3
integrins). Over the past years, severa1 substances have
been designed to delay or inhibit the cell proliferation
that leads to hyperplasia and mainly include monoclonal
antibodies directed against integrins. The aim of the
present study was to evaluate the effects of an antibody
denoted P37 (anti B3 integrin) on human smooth muscle
cells (SMC) and its role in blocking the 83 subunit. To
this end, SMC from human umbilical artery were
cultured in the presence or absence of the cell substrate
vitronectin (VN) and incubated with P37. After 4 days of
treatment, determination was made of cell proliferation
and migration. Smooth muscle cells grown on VN
showed increased proliferation and migration compared
to control VN-free cultures. However, the presence of
P37 in the culture medium inhibited proliferation and
reduced migration. Combined treatment with VN and
P37 led to improved proliferation but VN was unable to
reverse the effects on migration observed in the former
cultures. Results suggest that in vitro, P37 is capable of
blocking human SMC 83 integrins and thus impedes cell
proliferation and migration These findings may have
clinical implications related to modulation of the
development of hyperplasia.
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