Control of Stress-Dependent Cardiac Growth and Gene Expression by a MicroRNA

By Eva van Rooij, L. Sutherland, X. Qi, J. Richardson, Joseph A. Hill, E. Olson. Science, 2007

1,689 citations recorded by the source corpus.

Subfields: Cancer Research, Molecular Biology

View Paper: https://www.semanticscholar.org/paper/08fbefbb286253a8069b626ff865098fdba1e38c

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Citations in the corpus

Small non-coding RNAs in animal development (2008, background): “These data hint at a role for miR-208 in setting the threshold of induction of βMHC in response to stress and hypothyroidis”
microRNA-133a regulates cardiomyocyte proliferation and suppresses smooth muscle gene expression in the heart. (2008, methodology): “Mutagenesis of the miR-133a-binding site, cell culture, and luciferase assay were performed as described previously (van Rooij et al. 2007).”
MicroRNAs in stress signaling and human disease (2012, background): “For example, deletion of miR-208a has no effect on cardiovascular development or baseline function but abrogates stress-responsive cardiac remodeling (van Rooij et al., 2007).”
Metazoan MicroRNAs (2018, background): “…Abnormal atrial cardiac conduction (Callis et al., 2009); reduced cardiac pathology in response to stress and in model of hypothyroidism (van Rooij et al., 2007) miR-214 (1) miR-214 Increased pathology in heart disease model (Aurora et al., 2012) miR-218 (2) miR-218-1, miR-218-2 Neonatal…”
Development of microRNA therapeutics is coming of age (2014, background): “…inflammation, cardiovascular diseases and metabolic disorders, suggesting that miRNAs could serve as targets for therapeutic intervention (van Rooij et al, 2007; Gottwein & Cullen, 2008; Ventura & Jacks, 2009; Najafi-Shoushtari et al, 2010; Rayner et al, 2010; Grueter et al, 2012; van…”
miR-375 maintains normal pancreatic α- and β-cell mass (2009, background): “For instance, tissue-enriched miRNAs in the heart, such as miR-1, miR-208, and miR-133, have been shown to regulate the hypertrophic proliferative activity in response to a variety of stresses, and miR-126 affects survival after induction of a myocardial infarction (7, 12, 33).”
An Endothelial-specific microRNA Governs Vascular Integrity and Angiogenesis (2008, background): “As another example of this form of coregulation, we showed previously that miR-208, which is encoded by an intron of the a-myosin heavy chain (MHC) gene, functions within a regulatory network to control cardiac stress response (van Rooij et al., 2007).”
A family of microRNAs encoded by myosin genes governs myosin expression and muscle performance. (2009, background): “Although miR-208a is required for upregulation of b-MHC in the adult heart in response to stress and hypothyroidism ( van Rooij et al., 2007; Callis et al., 2009), expression of b-MHC and miR-208b during the neonatal period is independent of miR- 208a (Figure 2C).”
Circulating microRNA: a novel potential biomarker for early diagnosis of acute myocardial infarction in humans. (2010, result): “As expected, miR-499 and miR-208a were detected only in heart, whereas miR-1 and miR-133a were highly expressed both in skeletal muscle and heart (see Supplementary material online, Figure S1), which is in agreement with previous reports.(11,19,20) Then, realtime PCR analysis, a more sensitive metho”
Therapeutic miRNA and siRNA: Moving from Bench to Clinic as Next Generation Medicine (2017, background): “It is a heartspecific miRNA that is required for cardiac hypertrophy, fibrosis, and myosin switching.(63,65)”
MicroRNA Functions in Stress Responses (2010, positive): “…temperatures (Li et al., 2009), miR-14 mutant flies are sensitive to high salinity (Xu et al., 2003), mice deficient in miR-208 cannot cope with cardiac overload (van Rooij et al., 2007), and inactivation of miR-8 renders zebrafish incapable of responding to osmotic stress (Flynt et al., 2009).”
Transcriptional mechanisms regulating skeletal muscle differentiation, growth and homeostasis (2011, background): “Whereas miR-133 and miR-206 are expressed as independent transcriptional units, miR-208 is encoded by an intron of its host gene, α-myosin heavy chain (αMHC”