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Overexpression of myofibrillar proteins and metallothionein 3 genes in transgenic mice overexpressing myostatin prodomain
Author(s) -
Kim Yong soo,
Kim Kyung Ho,
Yang Jinzeng
Publication year - 2008
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.22.2_supplement.143
Subject(s) - myostatin , skeletal muscle , transgene , biology , genetically modified mouse , gene , muscle hypertrophy , microbiology and biotechnology , gene expression , microarray analysis techniques , medicine , endocrinology , genetics
Myostatin, a member of the transforming growth factor‐beta superfamily, is a potent negative regulator of skeletal muscle growth. In our previous study, transgenic mice overexpressing myostatin prodomain exhibited a remarkable increase in skeletal muscle mass. To gain insights into the molecular mechanisms by which myostatin regulates skeletal muscle growth, we examined genes differentially expressed between the transgenic mice and wild type. Three pooled RNA samples of the gastrocnemius muscle in each group were subjected to microarray analysis using the Affymetrix GeneChip Mouse 430‐2.0 platform, and microarray data were analyzed using the GeneSifter program. 247 genes were found to be significantly (t‐test) differentially expressed when a fold change cutoff of 1.5 was applied. Overexpression of many myofibrillar protein genes as well as changes in genes involved in various cellular processes were observed in the transgenic mice. The most significant change in gene expression was the 32‐fold overexpression of metallothionein 3 gene in transgenic mice. The results indicate that various gene groups contribute to the skeletal muscle hypertrophy observed in the prodomain transgenic mice.