Complement Deposition and Cell Death after Myoblast Transplantation
One of the problems limiting myoblast transplantation (MT) is the early death of the transplanted cells. Because complement can be fixed by myoblasts in vitro, and because it has the capacity to induce cell lysis, its possible role in the early death of transplanted myoblasts was investigated. CD1 m...
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doaj-ba9d66e758d14c25a0b6dd3f6b119cb12020-11-25T03:32:21ZengSAGE PublishingCell Transplantation0963-68971555-38921998-09-01710.1177/096368979800700501Complement Deposition and Cell Death after Myoblast TransplantationDaniel Skuk0Jacques P. Tremblay Ph.D.1Unité de Recherche en Génétique Humaine, Centre Hospitalier de l'Université Laval, Ste-Foy, Québec, G1V 4G2, CanadaUnité de Recherche en Génétique Humaine, Centre Hospitalier de l'Université Laval, Ste-Foy, Québec, G1V 4G2, CanadaOne of the problems limiting myoblast transplantation (MT) is the early death of the transplanted cells. Because complement can be fixed by myoblasts in vitro, and because it has the capacity to induce cell lysis, its possible role in the early death of transplanted myoblasts was investigated. CD1 mice and Macaca mulata monkeys were used as recipients for MT. In some mice, C3 was depleted before MT using Cobra Venom Factor. Mice were sacrificed during the first hour and up to 3 days after MT. Monkeys were biopsied 1 to 4 h after MT. Myoblast necrosis was assessed by the presence of intracellular calcium. Complement deposition was demonstrated by immunohistochemistry with anti-C3 and anti-C5b-9 neoantigen antibodies. In mice, C3 deposition was observed in damaged muscle fibers and in regions containing necrosed myoblasts. Complement depletion did not diminish the proportion of necrosed cells. In monkeys, only a small percentage of transplanted myoblasts showed C3 or C5b-9 deposition, mostly intracellular. Complement activation seems not to be implicated in directly damaging the transplanted cells, but seems secondary to cellular death. Taking into account its chemotactic functions, complement could be implicated in the migration of neutrophils and macrophages into the clusters of transplanted cells. © 1998 Elsevier Science Inc.https://doi.org/10.1177/096368979800700501 |
collection |
DOAJ |
language |
English |
format |
Article |
sources |
DOAJ |
author |
Daniel Skuk Jacques P. Tremblay Ph.D. |
spellingShingle |
Daniel Skuk Jacques P. Tremblay Ph.D. Complement Deposition and Cell Death after Myoblast Transplantation Cell Transplantation |
author_facet |
Daniel Skuk Jacques P. Tremblay Ph.D. |
author_sort |
Daniel Skuk |
title |
Complement Deposition and Cell Death after Myoblast Transplantation |
title_short |
Complement Deposition and Cell Death after Myoblast Transplantation |
title_full |
Complement Deposition and Cell Death after Myoblast Transplantation |
title_fullStr |
Complement Deposition and Cell Death after Myoblast Transplantation |
title_full_unstemmed |
Complement Deposition and Cell Death after Myoblast Transplantation |
title_sort |
complement deposition and cell death after myoblast transplantation |
publisher |
SAGE Publishing |
series |
Cell Transplantation |
issn |
0963-6897 1555-3892 |
publishDate |
1998-09-01 |
description |
One of the problems limiting myoblast transplantation (MT) is the early death of the transplanted cells. Because complement can be fixed by myoblasts in vitro, and because it has the capacity to induce cell lysis, its possible role in the early death of transplanted myoblasts was investigated. CD1 mice and Macaca mulata monkeys were used as recipients for MT. In some mice, C3 was depleted before MT using Cobra Venom Factor. Mice were sacrificed during the first hour and up to 3 days after MT. Monkeys were biopsied 1 to 4 h after MT. Myoblast necrosis was assessed by the presence of intracellular calcium. Complement deposition was demonstrated by immunohistochemistry with anti-C3 and anti-C5b-9 neoantigen antibodies. In mice, C3 deposition was observed in damaged muscle fibers and in regions containing necrosed myoblasts. Complement depletion did not diminish the proportion of necrosed cells. In monkeys, only a small percentage of transplanted myoblasts showed C3 or C5b-9 deposition, mostly intracellular. Complement activation seems not to be implicated in directly damaging the transplanted cells, but seems secondary to cellular death. Taking into account its chemotactic functions, complement could be implicated in the migration of neutrophils and macrophages into the clusters of transplanted cells. © 1998 Elsevier Science Inc. |
url |
https://doi.org/10.1177/096368979800700501 |
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