MicroRNA-92a Controls Angiogenesis and Functional Recovery of Ischemic Tissues in Mice

Bonauer, Angelika; Carmona, Guillaume; Iwasaki, Masanori; Mione, Marina; Koyanagi, Masamichi; Fischer, Ariane; Burchfield, Jana; Fox, Henrik; Doebele, Carmen; Ohtani, Kisho; Chavakis, Emmanouil; Potente, Michael; Tjwa, Marc; Urbich, Carmen; Zeiher, Andreas M.; Dimmeler, Stefanie

doi:10.1126/science.1174381

Cited by 1,127 publications

(1,011 citation statements)

References 28 publications

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“…However, the research of Bonauer et al showed that miR-92a inhibited angiogenesis via integrin-α5 in an ischemic model. 9 We speculated that miR92a regulates angiogenesis via different pathways under different conditions. So we determined the integrin-α5 expression level in both the control group and HUA group.…”

Section: Hua Inhibits Angiogenesis In Vitromentioning

confidence: 99%

High Concentrations of Uric Acid Inhibit Angiogenesis via Regulation of the Krüppel-Like Factor 2-Vascular Endothelial Growth Factor-A Axis by miR-92a

Hong

Wang

et al. 2015

Circ J

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Section: Hua Inhibits Angiogenesis In Vitromentioning

confidence: 99%

High Concentrations of Uric Acid Inhibit Angiogenesis via Regulation of the Krüppel-Like Factor 2-Vascular Endothelial Growth Factor-A Axis by miR-92a

Hong

Wang

et al. 2015

Circ J

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“…MicroRNAs (miRNAs) act as negative regulators of gene expression [23][24][25][26][27][28][29] . Strikingly, a single miRNA is even able to modulate complex physiological or disease phenotypes by regulating the entire functional networks 26,30,31 .…”

mentioning

confidence: 99%

miR-484 regulates mitochondrial network through targeting Fis1

et al. 2012

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mitochondria constantly undergo fusion and fission, two necessary processes for the maintenance of organelle fidelity. The abnormal mitochondrial fission participates in the pathogenesis of many diseases, but its regulation remains poorly understood. Here we show that miR-484 can suppress translation of mitochondrial fission protein Fis1, and inhibit Fis1-mediated fission and apoptosis in cardiomyocytes and in the adrenocortical cancer cells. We demonstrate that Fis1 is necessary for mitochondrial fission and apoptosis, and is upregulated during anoxia, whereas miR-484 is downregulated. miR-484 is able to attenuate Fis1 upregulation and mitochondrial fission, by binding to the amino acid coding sequence of Fis1 and inhibiting its translation. In exploring the underlying mechanism of miR-484 downregulation upon apoptosis, we observe that Foxo3a transactivates miR-484 expression. Foxo3a transgenic or knockout mice exhibit, respectively, a high or low level of miR-484 and a reduced or enhanced mitochondrial fission, apoptosis and myocardial infarction. our data reveal a model of mitochondrial fission regulation by a microRnA.

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“…The upstream transcriptional start site of the cluster is highly conserved across vertebrates, contains an extensive CpG island, a core putative promoter regulated by epigenetic modifications 50, 69. Notably, forced‐expression of miR‐92a alone, in ECs was found to block angiogenesis in ischaemia mouse model which has been corresponded to targeting pro‐angiogenic integrin subunit alpha5 24.…”

Section: Some Mirna Key Mechanisms In Reparative Angiogenesismentioning

confidence: 99%

MicroRNAs; easy and potent targets in optimizing therapeutic methods in reparative angiogenesis

Pourrajab

Zarch

Hekmatimoghaddam

et al. 2015

J Cellular Molecular Medi

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The age‐related senescence of adult tissues is associated with the decreased level of angiogenic capability and with the development of a degenerative disease such as atherosclerosis which thereafter result in the deteriorating function of multiple systems. Findings indicate that tissue senescence not only diminishes repair processes but also promotes atherogenesis, serving as a double‐edged sword in the development and prognosis of ischaemia‐associated diseases. Evidence evokes microRNAs (miRNAs) as molecular switchers that underlie cellular events in different tissues. Here, miRNAs would promote new potential targets for optimizing therapeutic methods in blood flow recovery to the ischaemic area. Effectively beginning an ischaemia therapy, a more characteristic of miRNA changes in adult tissues is prerequisite and in the forefront. It may also be a preliminary phase in treatment strategies by stem cell‐based therapy.

show abstract

MicroRNA-92a Controls Angiogenesis and Functional Recovery of Ischemic Tissues in Mice

Cited by 1,127 publications

References 28 publications

High Concentrations of Uric Acid Inhibit Angiogenesis via Regulation of the Krüppel-Like Factor 2-Vascular Endothelial Growth Factor-A Axis by miR-92a

High Concentrations of Uric Acid Inhibit Angiogenesis via Regulation of the Krüppel-Like Factor 2-Vascular Endothelial Growth Factor-A Axis by miR-92a

miR-484 regulates mitochondrial network through targeting Fis1

MicroRNAs; easy and potent targets in optimizing therapeutic methods in reparative angiogenesis

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