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

Autor(es)

Coelho, Priscila de O. ^[1] ; Guarnier, Flavia A. ^[2] ; Figueiredo, Leonardo Bruno ^[3] ; Zaramela, Livia S. ^{[1, 4]} ; Pacini, Enio S. A. ^[3] ; Godinho, Rosely O. ^[3] ; Gomes, Marcelo D. ^[1]

Afiliação do(s) autor(es)

^[1] Univ Sao Paulo, Ribeirao Preto Med Sch, Dept Biochem & Immunol, Ave Bandeirantes 39000, BR-14049900 Ribeirao Preto, SP - Brazil

^[2] Univ Estadual Londrina, Lab Pathophysiol & Muscle Adaptat, Londrina - Brazil

^[3] Univ Fed Sao Paulo, Escola Paulista Med, Dept Pharmacol, Sao Paulo - Brazil

^[4] Univ Calif San Diego, Dept Pediat, La Jolla, CA 92093 - USA

• Tipo de documento: Artigo Científico
• Fonte: Archives of Biochemistry and Biophysics; v. 663, p. 173-182, MAR 15 2019.
• Citações Web of Science: 0

Resumo

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. (AU)

• Processo FAPESP: 15/07019-4 - Papel da via extracelular AMP cíclico-adenosina na fisiopatologia do sistema respiratório e do sistema neuromuscular esquelético
• Beneficiário: Rosely Oliveira Godinho
• Modalidade de apoio: Auxílio à Pesquisa - Regular
• Processo FAPESP: 14/10898-7 - Triagem do tipo high-throughput de bibliotecas de RNAi para identificar novos reguladores das ERKs
• Beneficiário: Marcelo Damário Gomes
• Modalidade de apoio: Auxílio à Pesquisa - Regular
• Processo FAPESP: 11/07487-7 - Identificação e caracterização de RNAs não codificantes ligantes a Lsm no extremófilo Halobacterium salinarum
• Beneficiário: Lívia Soares Zaramela
• Modalidade de apoio: Bolsas no Brasil - Doutorado