Metabolomics,Unknown,Transcriptomics,Genomics,Proteomics

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Signaling pathways in skeletal muscle of Amyotrophic Lateral Sclerosis mouse model


ABSTRACT: Gene expression analyses through cDNA microarray of fifteen gastrocnemius muscles from transgenic and wild-type SOD1G93A mouse model by the ages of 40 and 80 days old were performed. We used a customized cDNA array containing the cDNA platform comprised of 2352 spots, 326 of them orthologous to mouse, 1384 additional human cDNA sequences, 496 negative controls (DMSO) and 48 positive controls (the Q gene from M-NM-;-phage). Gene expression results for SOD1G93A and WT age matched mice pointed to eight up- (LOXL2, PIK4CA, FZD9, CUL1, CTNND1, SNF1LK, PRKX, DNER) and nine down-regulated genes (PIK3C2A, RIPK4, ID2, C1QDC1, EIF2AK2, RAC3, CDS1, INPPL1, TBL1X) at 40 days and also to one up- (PIK3CA) and five down-regulated genes (CD44, EEF2K, FZD2, CREBBP, PIKI3R1) at 80 days. Based on differentially expressed genes, analyses for gene priorization were performed and used to construct a network of protein-protein interaction. The network based on the genes of 40 and 80 days old mice was composed by 251 and 531 genes, respectively. GRB2 and SRC were identified as central genes of both networks. In conclusion, changes in gene expression of skeletal muscle from transgenic ALS mice in pre-symptomatic periods give further evidence of early neuromuscular abnormalities that precede motor neuron death. We performed gene expression analyses by customized cDNA array, using reference design, of fifteen gastrocnemius muscles from transgenic and wild-type SOD1G93A mouse model by the ages of 40 and 80 days old. These differentially expressed lists were submitted to analyses for gene priorization and used to construct a network of protein-protein interaction.

ORGANISM(S): Mus musculus

SUBMITTER: Renato Puga 

PROVIDER: E-GEOD-40328 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Publications

Early gene expression changes in skeletal muscle from SOD1(G93A) amyotrophic lateral sclerosis animal model.

de Oliveira Gabriela P GP   Maximino Jessica R JR   Maschietto Mariana M   Zanoteli Edmar E   Puga Renato D RD   Lima Leandro L   Carraro Dirce M DM   Chadi Gerson G  

Cellular and molecular neurobiology 20140118 3


Amyotrophic lateral sclerosis (ALS) is a neurodegenerative disease characterized by loss of motor neurons. Familial ALS is strongly associated to dominant mutations in the gene for Cu/Zn superoxide dismutase (SOD1). Recent evidences point to skeletal muscle as a primary target in the ALS mouse model. Wnt/PI3 K signaling pathways and epithelial-mesenchymal transition (EMT) have important roles in maintenance and repair of skeletal muscle. Wnt/PI3 K pathways and EMT gene expression profile were in  ...[more]

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