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We began analyzing https://link.springer.com/article/10.1007/s10495-013-0899-2, but it redirected us to https://link.springer.com/article/10.1007/s10495-013-0899-2. The analysis below is for the second page.

Title[redir]:
MicroRNA-15b enhances hypoxia/reoxygenation-induced apoptosis of cardiomyocytes via a mitochondrial apoptotic pathway | Apoptosis
Description:
Myocardial ischemia reperfusion (I/R) can induce altered expression of microRNAs (miRNAs). The miRNAs—miR-15a, miR-15b and miR-16 have been shown to play a role in apoptosis, although not in cardiac-related models. We investigated the roles of miR-15b in hypoxia/reoxygenation (H/R)-induced apoptosis of cardiomyocytes. Quantitative real time polymerase chain reaction results showed that the expression of miR-15a and miR-15b were up-regulated in Sprague–Dawley rat hearts subjected to I/R. Expression levels of miR-15b increased more than four fold above basal levels. Similar results were obtained for cardiomyocytes exposed to H/R. Recombinant adenoviral vectors were generated to explore the functional role of miR-15b in cultured cardiomyocytes exposed to H/R. Overexpression of miR-15b enhanced cell apoptosis and the loss of mitochondrial membrane potential, as determined by flow cytometric analysis. Conversely, down-regulated expression was cytoprotective. The effects of miR-15b can by mimicked by Bcl-2 short-interfering RNAs. The inhibition of miR-15b increased expression levels of the Bcl-2 protein without affecting Bcl-2 mRNA levels, suppressed the release of mitochondrial cytochrome c to the cytosol and decreased the activities of caspase-3 and 9. It is possible that miR-15b is the upstream regulator of a mitochondrial signaling pathway for H/R induced apoptosis.

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Keywords {🔍}

article, pubmed, google, scholar, cas, apoptosis, liu, myocardial, mirb, micrornas, injury, cell, bcl, central, mitochondrial, wang, role, heart, cardiomyocytes, zhang, reperfusion, expression, protein, access, beijing, privacy, cookies, content, pathway, levels, infarction, cardiac, china, data, information, publish, research, search, apoptotic, liang, fan, induced, ischemiareperfusion, targeting, cardiology, res, olson, usa, department, general,

Topics {✒️}

month download article/chapter bcl-2 short-interfering rnas myocardial ischemia/reperfusion injury cardiac ischemia/reperfusion injury cardiomyocyte apoptosis induced hypoxia/reoxygenation ischemia–reperfusion injury article apoptosis aims p53-mediated bcl-2 myocardial reperfusion injury mitochondrial apoptotic pathway full article pdf privacy choices/manage cookies mir-15b increased mitochondrial signaling pathway induced apoptosis induced apoptosis cardiac-related models related subjects stress-responsive micrornas bartel dp van rooij mirnas—mir-15a mir-16 induce apoptosis mir-15b/16-2 clusters cardiac ischemic injury mitochondrion-dependent apoptosis acute myocardial infarction myocardial infarction reveals murine myocardial infarction mitochondrial membrane potential latronico mv article liu myocardial ischemia reperfusion injury evoke cardiac hypertrophy european economic area recombinant adenoviral vectors stroke statistics–2012 update double-edged sword myocardial reperfusion conditions privacy policy induce altered expression flow cytometric analysis lloyd-jones dm article log american heart association accepting optional cookies yu wang check access

Questions {❓}

Braunwald E, Kloner RA (1985) Myocardial reperfusion: a double-edged sword?
Condorelli G, Latronico MV, Dorn GN (2010) MicroRNAs in heart disease: putative novel therapeutic targets?

Schema {🗺️}

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         description:Myocardial ischemia reperfusion (I/R) can induce altered expression of microRNAs (miRNAs). The miRNAs—miR-15a, miR-15b and miR-16 have been shown to play a role in apoptosis, although not in cardiac-related models. We investigated the roles of miR-15b in hypoxia/reoxygenation (H/R)-induced apoptosis of cardiomyocytes. Quantitative real time polymerase chain reaction results showed that the expression of miR-15a and miR-15b were up-regulated in Sprague–Dawley rat hearts subjected to I/R. Expression levels of miR-15b increased more than four fold above basal levels. Similar results were obtained for cardiomyocytes exposed to H/R. Recombinant adenoviral vectors were generated to explore the functional role of miR-15b in cultured cardiomyocytes exposed to H/R. Overexpression of miR-15b enhanced cell apoptosis and the loss of mitochondrial membrane potential, as determined by flow cytometric analysis. Conversely, down-regulated expression was cytoprotective. The effects of miR-15b can by mimicked by Bcl-2 short-interfering RNAs. The inhibition of miR-15b increased expression levels of the Bcl-2 protein without affecting Bcl-2 mRNA levels, suppressed the release of mitochondrial cytochrome c to the cytosol and decreased the activities of caspase-3 and 9. It is possible that miR-15b is the upstream regulator of a mitochondrial signaling pathway for H/R induced apoptosis.
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