Research Paper Volume 14, Issue 24 pp 9832—9859

Transcriptomic analysis of human ALS skeletal muscle reveals a disease-specific pattern of dysregulated circRNAs

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Figure 5. Tracking circRNA levels in skeletal muscle and spinal cord tissue from the SOD1G93A ALS mouse model. (A) Schematic of disease progression in a genetic ALS mouse model (SOD1G93A), from which the gastrocnemius muscle was harvested. Based on rotarod performance and weight measurements, mice are presymptomatic by day 60, early symptomatic by day 125, and late symptomatic by day 150. (BD) Shown are the predicted mouse orthologs of circRNAs differentially expressed in human ALS muscle that were found differentially abundant in mouse skeletal muscle at the presymptomatic (B), early symptomatic (C), and late symptomatic (D) stages. (E) Schematic of disease progression in a genetic ALS mouse model (SOD1G93A), from which spinal cord tissue was harvested. (FH) Shown are the predicted mouse orthologs of circRNAs differentially expressed in human ALS muscle that were found differentially abundant in spinal cord at the early (F) and late symptomatic (G) stage; one circRNA did not change significantly (H). The circRNAs are represented in red (upregulated) or blue (downregulated) following their patterns of abundance in human ALS muscle biopsies (Figure 2). Data were normalized to Rps9 mRNA levels; p-values *p < 0.05, **p < 0.01, ***p < 0.001.