Osteoglycin post-transcriptional regulation by miR-155 induces cellular architecture changes in H9c2 cardiomyoblasts

Autor(es)

de Oliveira, Grasieli ^[1] ; Freire, Paula Paccielli ^[1] ; Mieko Omoto, Ana Carolina ^[1] ; Cury, Sarah Santiloni ^[1] ; Fuziwara, Cesar Seigi ^[2] ; Kimura, Edna Teruko ^[2] ; Dal-Pai-Silva, Maeli ^[1] ; Carvalho, Robson Francisco ^[1]

Afiliação do(s) autor(es)

^[1] Sao Paulo State Univ, Inst Biosci Botucatu, Dept Morphol, Botucatu, SP - Brazil

^[2] Univ Sao Paulo, Inst Biomed Sci, Dept Cell & Dev Biol, Sao Paulo - Brazil

• Tipo de documento: Artigo Científico
• Fonte: Gene; v. 676, p. 9-15, NOV 15 2018.
• Citações Web of Science: 0

Resumo

Several studies have demonstrated dysregulated cardiac microRNAs (miRNAs) following cardiac stress and development of cardiac hypertrophy and failure. miRNAs are also differentially expressed in the inflammation that occurs in heart failure and, among these inflammatory-related miRNAs, the miR-155 has been implicated in the regulation of cardiac hypertrophy. Despite these data showing the role of miRNA-155 in cardiomyocyte hypertrophy under a hypertrophic stimulus, it is also important to understand the endogenous regulation of this miRNA without a hypertrophic stimulus to fully appreciate its function in this cell type. The first aim of the present study was to determine whether, without a hypertrophic stimulus, miR-155 overexpression induces H9c2 cardiac cells hypertrophy in vitro. The second objective was to determine whether osteoglycin (Ogn), a key regulator of heart mass in rats, mice, and humans, is post-transcriptionally regulated by miR-155 with a potential role in inducing H9c2 cells hypertrophy. Here, we show that, without a hypertrophic stimulus, miR-155 significantly repressed Ogn protein levels, but induce neither alteration in morphological phenotype nor in the expression of the molecular markers that fully characterize pathological hypertrophy of H9c2 cells. However, most importantly, Ogn silencing in H9c2 cells mimicked the effects of miR-155 overexpression in inducing cellular architecture changes that were characterized by a transition of the cell shape from fusiform to rounded. This is a new role of the post-transcriptional regulation of Ogn by miR-155 in the maintenance of the cardiac cell morphology in physiological and pathological conditions. (AU)

• Processo FAPESP: 14/14340-0 - Regulação pós-transcricional da osteoglicina pelo microRNA miR-155 em cardiomiócitos
• Beneficiário: Grasieli de Oliveira
• Linha de fomento: Bolsas no Brasil - Mestrado
• Processo FAPESP: 12/13961-6 - Perfil genômico de RNAs mensageiros e microRNAs em células musculares esqueléticas tratadas in vitro com TNF-alfa e IFN-gama
• Beneficiário: Robson Francisco Carvalho
• Linha de fomento: Auxílio à Pesquisa - Regular