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Mineralocorticoid Receptor Antagonists and Glucocorticoids Differentially Affect Skeletal Muscle Inflammation and Pathology in Muscular Dystrophy

ABSTRACT: We report the RNA Sequencing of myleoid cells isolated from 4.5-week-old mdx mice that were administered spironolactone, prednisolone, or vehicle for 7 days. We find that both spironolactone and prednisolone downregulated expression of genes involved in inflammation and fibrosis, while prednisolone further perturbed cell cycle genes.

ORGANISM(S): Mus musculus

PROVIDER: GSE197553 | GEO | 2022/11/23

REPOSITORIES: GEO

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Mineralocorticoid receptor antagonists and glucocorticoids differentially affect skeletal muscle inflammation and pathology in muscular dystrophy.

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Mineralocorticoid Receptor Antagonists and Glucocorticoids Differentially Affect Skeletal Muscle Inflammation and Pathology in Muscular Dystrophy

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2020-08-10 | GSE150302 | GEO

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Project description:The mdx mouse (C57BL/10ScSn-DMDmdx/J), like Duchenne muscular dystrophy (DMD) patients, lacks the protein dystrophin. However, the mdx mouse has a normal lifespan and mild pathology while DMD remains a severe, fatal disease. New mouse models have been developed that are more severely affected but they have not replaced the mdx mouse in DMD research. A few years ago RNA-sequencing (RNA-seq) results of biopsies from DMD and normal human muscle were published but we could not find equivalent data for the mouse. We now report RNA-sequencing of three wild-type and mdx mouse muscles: the flexor digitorum brevis (FDB), the extensor digitorum longus (EDL), and the soleus (SOL). The FDB, a plantar foot muscle is often used for in vivo and ex vivo experiments but may be less affected by the lack of dystrophy than the hindlimb muscles. We compared muscles from 2- and 5-month old mice to investigate the time-course of the mdx pathology. The results show a muscle- and age-dependent parallel between mdx and DMD muscles. Although the FDB is less affected than EDL and SOL at 2 months, the three muscles show, at both ages, activation of close to 100 genes from 7 pathways that are affected in presymptomatic DMD patients and have been called "DMD disease signature".

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