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MiRNA-210[edit]

MiRNA-210 as Therapy for Myocardial Infarction[edit]

MicroRNAs (miRNA for short) are single strands of non-coding RNA that typically consist of 20 – 22 nucleotides. MiRNAs are involved in many cellular functions such as regulation of differentiation, proliferation, angiogenesis (new blood vessel formation) and apoptosis (programmed cell death). MiRNA-210 in particular, has been studied for its effects in rescuing cardiac function after myocardial infarcts via the up-regulation of angiogenesis and inhibition of cardiomyocyte apoptosis.^[1]

Myocardial infarction[edit]

Myocardial infarction is cardiac tissue necrosis that results from occlusion of blood supply via coronary arteries, thereby starving cells of oxygen and nutrients (termed ischemia). Prolong ischemia will eventually kill the cells and the destruction of cardiac cells leads to tissue death, which can lead to heart failure.

MiRNA-210 in myocardial infarction recovery[edit]

Delivery of miRNA-210 to an ischemic heart improves heart function, possibly by promoting the release of angiogenic factors like interleukin-1α (IL-1α), tumor necrosis factor-α (TNF-α) and leptin, as seen in HL-1 cardiomyocytes injected with miRNA-210.^[1] However, miRNA-210 also targets the Efna3 and Ptp1b genes, which are genes which endogenously regulate angiogenesis and apoptosis, respectively.^[1]

Ephrin-A3 (Efna3) is a gene that is involved in the inhibition of angiogenesis. Although it is known that Efna3 inhibits the formation of new blood vessels, its specific role is still unknown ^[2]. MiRNA-210 suppresses Efna3 at the mRNA level, thereby allowing angiogenesis to occur in cardiac tissue post-infarct.^[1]

The second target gene, protein tyrosine phosphatase-1B (Ptp1b) is involved in the induction of apoptosis. Ptp1b gene protein has been known to regulate apoptosis by regulating the phosphorylation status of apoptotic proteins such as caspase-3 and caspase-8.^[3] MiRNA-210 inhibits the effects of Ptp1b protein, which suppresses its pro-apoptotic functions.^[1] Therefore, suppression of these two particular genes may contribute to the improvement of cardiac tissue and function by up-regulating angiogenesis and inhibiting apoptosis of cardiomyocytes after myocardial infarct.

References[edit]

^ ^a ^b ^c ^d ^e Hu et al. “MicroRNA-210 as a Novel Therapy for treatment of Ischemic Heart Disease.” Journal of the American Heart Association. (2010) 122: S124 – S131
^ Fasanaro et al. “MicroRNA-210 Modulates Endothelial Cell Response to Hypoxia and Inhibits the Receptor Tyrosine Kinase Ligand Ephrin-A3.” The Journal of Biological Chemistry. (2008) 283.23: 15878 – 15883
^ Song et al. “Small interference RNA against PTP-1B reduces hypoxia/reoxygenation induced apoptosis of rat cardiomyocytes.” Apoptosis. (2008) 13: 383 – 393

[Hu-1] Hu et al. “MicroRNA-210 as a Novel Therapy for treatment of Ischemic Heart Disease.” Journal of the American Heart Association. (2010) 122: S124 – S131

[Fas-2] Fasanaro et al. “MicroRNA-210 Modulates Endothelial Cell Response to Hypoxia and Inhibits the Receptor Tyrosine Kinase Ligand Ephrin-A3.” The Journal of Biological Chemistry. (2008) 283.23: 15878 – 15883

[Song-3] Song et al. “Small interference RNA against PTP-1B reduces hypoxia/reoxygenation induced apoptosis of rat cardiomyocytes.” Apoptosis. (2008) 13: 383 – 393

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