Denervation-induced alterations in gene expression in mouse skeletal muscle
Motoneurons are important for regulating the function and properties of skeletal muscle. In the present study high‐density oligonucleotide arrays have been used to compare gene expression in innervated and six‐days denervated NMRI mouse skeletal muscle. To avoid looking at genes mainly participating...
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Veröffentlicht in: | The European journal of neuroscience 2005-01, Vol.21 (2), p.577-580 |
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Sprache: | eng |
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Zusammenfassung: | Motoneurons are important for regulating the function and properties of skeletal muscle. In the present study high‐density oligonucleotide arrays have been used to compare gene expression in innervated and six‐days denervated NMRI mouse skeletal muscle. To avoid looking at genes mainly participating in the process of atrophy, both hind‐limb muscles (atrophic after denervation) and hemidiaphragm muscle (transiently hypertrophic after denervation) were used. Only genes previously not known to respond to denervation and with potential roles in DNA/RNA interactions/transcription and/or cellular communication/signalling are presented. Data for additional genes are provided as supplementary material. Thirty‐two genes, up‐regulated by a factor of two or down‐regulated to the same extent after denervation, are presented. These include genes that may act through chromatin remodelling and/or as transcription factors/regulators (Cdkn1a, Cdr2, Hrmt1l2, Idb2, Myc/c‐myc, L‐myc1, Rb1, Sap30 and Tgif), genes possibly involved in the regulation of muscle membrane properties and/or excitation‐contraction coupling (Cacng1, Camk2d, Hrmt1l2, Kcnj12, Kcna7 and Rrad) and genes potentially involved in neuromuscular interactions and/or receptor signalling (Acvr2b, Adam19, D0H4S114, Kai1, Maged1, Mt2, Prkcabp, Ptp4a3, Ramp1, Rras, Timp1, Vegfa and Zfp145). A set of five genes with altered expression after denervation (Fzd9, Nr4a1, Frat2, Ctgf and Cyr61) indicate that Wnt signalling may be reduced in denervated skeletal muscle. |
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ISSN: | 0953-816X 1460-9568 |
DOI: | 10.1111/j.1460-9568.2005.03855.x |