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Extraocular muscle is spared upon complete laminin alpha2 chain deficiency: comparative expression of laminin and integrin isoforms.
Department of Experimental Medical Science, Division for Cell and Matrix Biology, Lund University.
Department of Experimental Medical Science, Division for Cell and Matrix Biology, Lund University.
Umeå University, Faculty of Medicine, Department of Clinical Sciences, Ophthalmology. Umeå University, Faculty of Medicine, Department of Integrative Medical Biology (IMB), Anatomy.
Max-Planck-Institut für Biochemie, Martinsried, Germany.
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2006 (English)In: Matrix Biology, ISSN 0945-053X, E-ISSN 1569-1802, Vol. 25, no 6, 382-385 p.Article in journal (Refereed) Published
Abstract [en]

Mutations in the gene encoding laminin (LM) alpha2 chain cause congenital muscular dystrophy. Here, we show that extraocular muscle (EOM) is spared upon complete LMalpha2 chain absence. The major LM chains in limb muscle basement membranes are alpha2, beta1, beta2 and gamma1 whereas alpha2, alpha4, beta1, beta2 and gamma1 chains are expressed in EOM. Expression of LMalpha4 chain mRNA is further increased in LMalpha2 chain deficient EOM. Mainly integrin alpha7X1 subunit, which binds to laminin-411, is expressed in EOM and in contrast to dystrophic limb muscle, sustained integrin alpha7B expression is seen in LMalpha2 chain deficient EOM. We propose that LMalpha4 chain, possibly by binding to integrin alpha7BX1beta1D, protects EOM in LMalpha2 chain deficient muscular dystrophy.

Place, publisher, year, edition, pages
Elsevier , 2006. Vol. 25, no 6, 382-385 p.
Keyword [en]
extraocularn muscle, laminin alpha2
National Category
Ophthalmology Cell and Molecular Biology
Research subject
Human Anatomy; Ophtalmology
Identifiers
URN: urn:nbn:se:umu:diva-35479DOI: 10.1016/j.matbio.2006.05.001PubMedID: 16782317Local ID: 744OAI: oai:DiVA.org:umu-35479DiVA: diva2:344480
Available from: 2010-08-19 Created: 2010-08-19 Last updated: 2017-12-12Bibliographically approved

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CiteExportLink to record
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