Abstracts 2018
DOI: 10.1136/heartjnl-2018-bscr.15
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P10 MIR-133a overexpression impairs endothelial cell migration and tube formation in vitro

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“…For example, overexpression of miR-133a significantly reduced cardiac fibrosis and disrupted the phosphorylation of ERK1/2 and SMAD-2 [152]. miR-133a also has an anti-angiogenic effect, as expression of this miRNA reduced VEGF-induced proliferation of endothelial cells in HUVEC by also targeting ERK1/2 phosphorylation [153]. In addition, miR-103-3p was found to play an important role in preventing apoptosis and autophagy of cardiomyocytes under hypoxia/reoxygenation, as inhibition of miR-103a-3p leads to Atg5 being able to promote apoptosis and autophagy in cells [118].…”
Section: Limitations and Future Directionsmentioning
confidence: 99%
“…For example, overexpression of miR-133a significantly reduced cardiac fibrosis and disrupted the phosphorylation of ERK1/2 and SMAD-2 [152]. miR-133a also has an anti-angiogenic effect, as expression of this miRNA reduced VEGF-induced proliferation of endothelial cells in HUVEC by also targeting ERK1/2 phosphorylation [153]. In addition, miR-103-3p was found to play an important role in preventing apoptosis and autophagy of cardiomyocytes under hypoxia/reoxygenation, as inhibition of miR-103a-3p leads to Atg5 being able to promote apoptosis and autophagy in cells [118].…”
Section: Limitations and Future Directionsmentioning
confidence: 99%