Please use this identifier to cite or link to this item: https://repositorio.unifesp.br/handle/11600/36274
Title: Cyclooxygenase-2 expression in skeletal muscle of knockout mice suffering Duchenne muscular dystrophy
Authors: Flavia, De Oliveira [UNIFESP]
Quintana, Hananiah Tardivo [UNIFESP]
Bortolin, Jeferson Andre [UNIFESP]
Gomes, Odair Alfredo
Liberti, Edson Aparecido
Ribeiro, Daniel Araki [UNIFESP]
Universidade Federal de São Paulo (UNIFESP)
Univ Ribeirao Preto
Universidade de São Paulo (USP)
Keywords: Skeletal muscle
Duchenne muscular dystrophy
Connective Tissue
Cyclooxygenase-2
Collagen
Issue Date: 1-May-2013
Publisher: Springer
Citation: Histochemistry and Cell Biology. New York: Springer, v. 139, n. 5, p. 685-689, 2013.
Abstract: The purpose of the present study was to investigate the role of cyclooxygenase-2 (COX-2) expression in fibrotic lesion in mdx mice. A total of six male C57BL/10 mice and six C57BL/10-DMD/mdx were distributed into two groups: control and animals with Duchenne muscular dystrophy (DMD). the medial part of gastrocnemius muscle was evaluated being the specimens stained with hematoxylin and eosin (H&E) and Sirius Red under normal and polarized light to differentiate type I (red and yellow) and III (green) collagen. COX-2 expression was assessed by immunohistochemistry. the results revealed histopathological changes in C57BL/10-DMD/mdx as depicted by regenerating fibers. Sirius Red stain showed a substantial increase in the amount of type I collagen of mdx mice. DMD induced a strong COX-2 immunoexpression in intercellular space. Taken together, our results are consistent with the notion that necrotic and fibrotic lesions are able to increase COX-2 expression in DMD.
URI: http://repositorio.unifesp.br/handle/11600/36274
ISSN: 0948-6143
Other Identifiers: http://dx.doi.org/10.1007/s00418-012-1056-7
Appears in Collections:Em verificação - Geral

Files in This Item:
There are no files associated with this item.


Items in DSpace are protected by copyright, with all rights reserved, unless otherwise indicated.