Increased neointimal thickening in dystrophin-deficient mdx mice.

<h4>Background</h4>The dystrophin gene, which is mutated in Duchenne muscular dystrophy (DMD), encodes a large cytoskeletal protein present in muscle fibers. While dystrophin in skeletal muscle has been extensively studied, the function of dystrophin in vascular smooth muscle is less cle...

Descripción completa

Guardado en:

Detalles Bibliográficos
Autores principales:	Uwe Rauch, Annelie Shami, Feng Zhang, Virginie Carmignac, Madeleine Durbeej, Anna Hultgårdh-Nilsson
Formato:	article
Lenguaje:	EN
Publicado:	Public Library of Science (PLoS) 2012
Materias:	Medicine R Science Q
Acceso en línea:	https://doaj.org/article/c74fb0fcae3f48cbb9d370ae464a43d0
Etiquetas:	Agregar Etiqueta Sin Etiquetas, Sea el primero en etiquetar este registro!

id	oai:doaj.org-article:c74fb0fcae3f48cbb9d370ae464a43d0
record_format	dspace
spelling	oai:doaj.org-article:c74fb0fcae3f48cbb9d370ae464a43d02021-11-18T07:30:55ZIncreased neointimal thickening in dystrophin-deficient mdx mice.1932-620310.1371/journal.pone.0029904https://doaj.org/article/c74fb0fcae3f48cbb9d370ae464a43d02012-01-01T00:00:00Zhttps://www.ncbi.nlm.nih.gov/pmc/articles/pmid/22238670/?tool=EBIhttps://doaj.org/toc/1932-6203<h4>Background</h4>The dystrophin gene, which is mutated in Duchenne muscular dystrophy (DMD), encodes a large cytoskeletal protein present in muscle fibers. While dystrophin in skeletal muscle has been extensively studied, the function of dystrophin in vascular smooth muscle is less clear. Here, we have analyzed the role of dystrophin in injury-induced arterial neointima formation.<h4>Methodology/principal findings</h4>We detected a down-regulation of dystrophin, dystroglycan and β-sarcoglycan mRNA expression when vascular smooth muscle cells de-differentiate in vitro. To further mimic development of intimal lesions, we performed a collar-induced injury of the carotid artery in the mdx mouse, a model for DMD. As compared with control mice, mdx mice develop larger lesions with increased numbers of proliferating cells. In vitro experiments demonstrate increased migration of vascular smooth muscle cells from mdx mice whereas the rate of proliferation was similar in cells isolated from wild-type and mdx mice.<h4>Conclusions/significance</h4>These results show that dystrophin deficiency stimulates neointima formation and suggest that expression of dystrophin in vascular smooth muscle cells may protect the artery wall against injury-induced intimal thickening.Uwe RauchAnnelie ShamiFeng ZhangVirginie CarmignacMadeleine DurbeejAnna Hultgårdh-NilssonPublic Library of Science (PLoS)articleMedicineRScienceQENPLoS ONE, Vol 7, Iss 1, p e29904 (2012)
institution	DOAJ
collection	DOAJ
language	EN
topic	Medicine R Science Q
spellingShingle	Medicine R Science Q Uwe Rauch Annelie Shami Feng Zhang Virginie Carmignac Madeleine Durbeej Anna Hultgårdh-Nilsson Increased neointimal thickening in dystrophin-deficient mdx mice.
description	<h4>Background</h4>The dystrophin gene, which is mutated in Duchenne muscular dystrophy (DMD), encodes a large cytoskeletal protein present in muscle fibers. While dystrophin in skeletal muscle has been extensively studied, the function of dystrophin in vascular smooth muscle is less clear. Here, we have analyzed the role of dystrophin in injury-induced arterial neointima formation.<h4>Methodology/principal findings</h4>We detected a down-regulation of dystrophin, dystroglycan and β-sarcoglycan mRNA expression when vascular smooth muscle cells de-differentiate in vitro. To further mimic development of intimal lesions, we performed a collar-induced injury of the carotid artery in the mdx mouse, a model for DMD. As compared with control mice, mdx mice develop larger lesions with increased numbers of proliferating cells. In vitro experiments demonstrate increased migration of vascular smooth muscle cells from mdx mice whereas the rate of proliferation was similar in cells isolated from wild-type and mdx mice.<h4>Conclusions/significance</h4>These results show that dystrophin deficiency stimulates neointima formation and suggest that expression of dystrophin in vascular smooth muscle cells may protect the artery wall against injury-induced intimal thickening.
format	article
author	Uwe Rauch Annelie Shami Feng Zhang Virginie Carmignac Madeleine Durbeej Anna Hultgårdh-Nilsson
author_facet	Uwe Rauch Annelie Shami Feng Zhang Virginie Carmignac Madeleine Durbeej Anna Hultgårdh-Nilsson
author_sort	Uwe Rauch
title	Increased neointimal thickening in dystrophin-deficient mdx mice.
title_short	Increased neointimal thickening in dystrophin-deficient mdx mice.
title_full	Increased neointimal thickening in dystrophin-deficient mdx mice.
title_fullStr	Increased neointimal thickening in dystrophin-deficient mdx mice.
title_full_unstemmed	Increased neointimal thickening in dystrophin-deficient mdx mice.
title_sort	increased neointimal thickening in dystrophin-deficient mdx mice.
publisher	Public Library of Science (PLoS)
publishDate	2012
url	https://doaj.org/article/c74fb0fcae3f48cbb9d370ae464a43d0
work_keys_str_mv	AT uwerauch increasedneointimalthickeningindystrophindeficientmdxmice AT annelieshami increasedneointimalthickeningindystrophindeficientmdxmice AT fengzhang increasedneointimalthickeningindystrophindeficientmdxmice AT virginiecarmignac increasedneointimalthickeningindystrophindeficientmdxmice AT madeleinedurbeej increasedneointimalthickeningindystrophindeficientmdxmice AT annahultgardhnilsson increasedneointimalthickeningindystrophindeficientmdxmice
_version_	1718423375211134976

Increased neointimal thickening in dystrophin-deficient mdx mice.

Ejemplares similares