Publication: Role of macrophages in myocardial apoptosis following cardiac transplant. Influence of immunosuppressive treatment
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Date
1999
Authors
Jurado, F. ; Bellón, J.M. ; Golittsin, A. ; Gimeno, M.J. ; Pascual, G. ; 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
Cytotoxic T cells may induce myocardial
apoptosis by histiocyte activation during rejection
following allogenic heart transplant. The aim of the
present investigation was to evaluate the macrophage
response and its relationship to the programmed death of
cardiomyocytes in rejection and during cyclosporin-A
(CsA) treatment.
An abdominal, heterotopic heart transplant rat model
was used establishing two groups: singenic (ST) and
allogenic QAL 'tran splant. 5mglkglday (s.c.) CsA (Sandimun ) was administered to half of the animals in
each group. Morphological and structural analysis was
performed 7, 14,21,30,50 and 100 days post-transplant.
Macrophages were detected using the monoclonal
antibody (ED1). The TUNEL method was used to
visualise apoptotic cells.
Two weeks after ST in animals without immunosuppressive
treatment, the transplanted myocardium had
been extensively infiltrated by inflammatory cells, many
of which were ED1-positive. At 21 days follow-up, the
number of labelled cells had fallen. In animals treated
with CsA the amount of ED1-positive cells was lower
than that seen in the anterior group. Only a few isolated
cells of the infiltrate were TUNEL-positive. In the AT
group, rejection took place between 9-15 days in the
untreated animals. The myocardium was highly
infiltrated by mononuclear cells. Some were ED1-
positive. Small groups of apoptotic cells were visible in
the infiltrate and in some vessel lumens. Rejection was
resolved in animals treated with CsA. The macrophage
response diminished during follow-up in a similar way
to that occurring in the ST. Few cells showed TUNEL
positivity. It may be concluded that: a) CsA treatment
diminishes the amount of infiltrated macrophages; b)
animals receiving ST or AT, show a low level of
Offprint requests to: Prof. Julia BujAn, PhD., Department of
Morphological Sciences and Surgery, Faculty of Medicine, University of
AlcalA de Henares, Crta. Madrid-Barcelona Km. 33,600. 28871- AlcalA
de Henares (Madrid). Spain. Fax: 34.91885-48-85. e-mail: cmmjb@
cirug.alcala.es
apoptosis; c) in the present model, the apoptosis of
cardiomyocytes does not appear to be induced by
macrophages; and d) in this model it is not possible to
relate apoptosis and rejection.
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