Identification of potential target genes associated with the reversion of androgen-dependent skeletal muscle atrophy

Muscle wasting or atrophy is extensively associated with human systemic diseases including diabetes, cancer, and kidney failure. Accumulating evidence from transcriptional profiles has noted that a common set of genes, termed atrogenes, is modulated in atrophying muscles. However, the transcriptiona...

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Published inArchives of biochemistry and biophysics Vol. 663; pp. 173 - 182
Main Authors de O. Coelho, Priscila, Guarnier, Flavia A., Figueiredo, Leonardo Bruno, Zaramela, Livia S., Pacini, Enio S.A., Godinho, Rosely O., Gomes, Marcelo D.
Format Journal Article
LanguageEnglish
Published United States Elsevier Inc 15.03.2019
Subjects
And atrophy reversion
Androgens - metabolism
Animals
Atrogenes
Fasting
FBXO32
Gene Expression Profiling
Hormone Replacement Therapy
Male
Mice
Models, Biological
Muscle atrophy
Muscle, Skeletal - metabolism
Muscle, Skeletal - pathology
Muscular Atrophy - metabolism
Oligonucleotide Array Sequence Analysis
Orchiectomy
Rats
Rats, Wistar
Testosterone - administration & dosage
Muscle atrophy
FBXO32
Atrogenes
And atrophy reversion
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Summary:Muscle wasting or atrophy is extensively associated with human systemic diseases including diabetes, cancer, and kidney failure. Accumulating evidence from transcriptional profiles has noted that a common set of genes, termed atrogenes, is modulated in atrophying muscles. However, the transcriptional changes that trigger the reversion or attenuation of muscle atrophy have not been characterized at the molecular level until now. Here, we applied cDNA microarrays to investigate the transcriptional response of androgen-sensitive Levator ani muscle (LA) during atrophy reversion. Most of the differentially expressed genes behaved as atrogenes and responded to castration-induced atrophy. However, seven genes (APLN, DUSP5, IGF1, PIK3IP1, KLHL38, PI15, and MKL1) did not respond to castration but instead responded exclusively to testosterone replacement. Considering that almost all proteins encoded by these genes are associated with the reversion of atrophy and may function as regulators of cell proliferation/growth, our results provide new perspectives on the existence of anti-atrogenes.
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ISSN:0003-9861
1096-0384
DOI:10.1016/j.abb.2019.01.009