MiR-483-5p controls angiogenesis in vitro and targets serum response factor

Qiao, Yu; Ma, Ning; Wang, Xidi; Yang, Hui; Li, Fuyuan; Xiang, Ying; Zhou, Jianying; Zou, Chaoxia; Jin, Jianfeng; Lv, Guixiang; Jin, Hongbo; Gao, Xu

doi:10.1016/j.febslet.2011.08.039

Cited by 64 publications

(57 citation statements)

References 23 publications

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“…MiR‐483‐5p is down‐regulated under hypoxia condition and can inhibit the growth of HUVECs by targeting serum response factor (SRF), which recedes wound healing and tube formation 110. Consistent with this, Kong et al111 found miR‐483‐3p can inhibit angiogenesis, up‐regulated in EPCs of DVT patients, which can inhibit EPC migration and tube formation and enhance apoptosis in vitro by targeting SRF, thus, reducing EPC homing and thrombus organization and recanalization in rat inferior vena cava thrombosis model.…”

Section: Mirnas Regulated By Pro‐or Anti‐angiogenesis Factors or Hypomentioning

confidence: 99%

The regulatory role of microRNAs in angiogenesis‐related diseases

Sun

Lei

et al. 2018

J Cellular Molecular Medi

116

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MicroRNAs (miRNAs) are small non‐coding RNAs that regulate gene expression at a post‐transcriptional level via either the degradation or translational repression of a target mRNA. They play an irreplaceable role in angiogenesis by regulating the proliferation, differentiation, apoptosis, migration and tube formation of angiogenesis‐related cells, which are indispensable for multitudinous physiological and pathological processes, especially for the occurrence and development of vascular diseases. Imbalance between the regulation of miRNAs and angiogenesis may cause many diseases such as cancer, cardiovascular disease, aneurysm, Kawasaki disease, aortic dissection, phlebothrombosis and diabetic microvascular complication. Therefore, it is important to explore the essential role of miRNAs in angiogenesis, which might help to uncover new and effective therapeutic strategies for vascular diseases. This review focuses on the interactions between miRNAs and angiogenesis, and miRNA‐based biomarkers in the diagnosis, treatment and prognosis of angiogenesis‐related diseases, providing an update on the understanding of the clinical value of miRNAs in targeting angiogenesis.

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Section: Mirnas Regulated By Pro‐or Anti‐angiogenesis Factors or Hypomentioning

confidence: 99%

The regulatory role of microRNAs in angiogenesis‐related diseases

Sun

Lei

et al. 2018

J Cellular Molecular Medi

116

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“…It is also known that Igf2 enables Myod to activate its target genes by acting on the recruitment of Myod co-activators (Polesskaya et al, 2001). More recently, the Srf transcription factor has been shown to be a direct target of miR-483-5p, the gene for which is embedded in intron 2 of Igf2 (Qiao et al, 2011). Srf is one of the factors responsible for the activation of Myod expression.…”

Section: Myodmentioning

confidence: 99%

“…Development 140 (6) Srf was recently shown to be a direct target of miR-483 (Qiao et al, 2011) and is known to be a direct regulator of Myod expression. We confirmed by ChIP assay on whole limb muscle tissue that Srf binds to the Myod CArG box (Fig.…”

Section: Research Articlementioning

confidence: 99%

“…Further studies suggested that Igf2, through binding to the Igf1 receptor (Igf1r), activates the Akt pathway and Myod downstream targets, although the exact mechanism has not been elucidated (Wilson and Rotwein, 2006;Woelfle et al, 2005). Recently, a microRNA, miR-483-5p, the gene for which is embedded in intron 2 of Igf2, has been shown to target the 3ЈUTR of serum response factor (Srf) (Qiao et al, 2011). The transcription factor Srf is one of the factors responsible for the activation of Myod expression (Gauthier-Rouviere et al, 1996;L'honore et al, 2003).…”

Section: Introductionmentioning

confidence: 99%

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Myod and H19-Igf2 locus interactions are required for diaphragm formation in the mouse

et al. 2013

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SUMMARYThe myogenic regulatory factor Myod and insulin-like growth factor 2 (Igf2) have been shown to interact in vitro during myogenic differentiation. In order to understand how they interact in vivo, we produced double-mutant mice lacking both the Myod and Igf2 genes. Surprisingly, these mice display neonatal lethality due to severe diaphragm atrophy. Alteration of diaphragm muscle development occurs as early as 15.5 days post-coitum in the double-mutant embryos and leads to a defect in the terminal differentiation of muscle progenitor cells. A negative-feedback loop was detected between Myod and Igf2 in embryonic muscles. Igf2 belongs to the imprinted H19-Igf2 locus. Molecular analyses show binding of Myod on a mesodermal enhancer (CS9) of the H19 gene. Chromatin conformation capture experiments reveal direct interaction of CS9 with the H19 promoter, leading to increased H19 expression in the presence of Myod. In turn, the non-coding H19 RNA represses Igf2 expression in trans. In addition, Igf2 also negatively regulates Myod expression, possibly by reducing the expression of the Srf transcription factor, a known Myod activator. In conclusion, Igf2 and Myod are tightly co-regulated in skeletal muscles and act in parallel pathways in the diaphragm, where they affect the progression of myogenic differentiation. Igf2 is therefore an essential player in the formation of a functional diaphragm in the absence of Myod.

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“…32 miR483-5p, miR500 and miR576-3p are involved in the processes of angiogenesis, cell cycle and immune response. 33 Our data raise the questions of whether the sustained over-expression of these miRNA induced by G-CSF could lead to modifications in any of these biological processes and whether or not this has any clinical implication.On the other hand, G-CSF produced changes in proteinencoding gene expression levels at all time-points analyzed during the follow up. In our study we identified 617 genes with a greater modification in their expression levels after treatment.…”

mentioning

confidence: 99%

Granulocyte colony-stimulating factor produces long-term changes in gene and microRNA expression profiles in CD34+ cells from healthy donors

et al. 2013

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© F e r r a t a S t o r t i F o u n d a t i o ngene and miRNA expression profiles in HPC from healthy donors, and to determine whether any changes in expression signatures persist in the long-term or return to the original status. Methods SamplesCD34 + progenitor cells from peripheral blood of six healthy donors were collected before and at 5, 30 and 365 days after the mobilization with G-CSF (mobilization regimen: 10-15 mg/kg of G-CSF daily for 5 days). All donors were included in the transplant program of the Hematology Department of the University Hospital Virgen del Rocío (Seville, Spain). The local ethics committee of the same hospital provided institutional review boardapproval for this study, and informed consent was obtained from all donors in accordance with the Declaration of Helsinki. Isolation of hematopoietic progenitor cellsMononuclear cells were collected from all samples by density gradient centrifugation with Ficoll-Paque solution (Amersham Biosciences, Uppsala, Sweden). The CD34 + cells were isolated in an AutoMACS pro separator (Miltenyi Biotec, Bergisch Gladbach, Germany) by positive immunomagnetic selection using the CD34 MACS microbead Human Kit (Miltenyi Biotec, Bergisch Gladbach, Germany) and, after magnetic enrichment, CD34 + cells were sorted by flow cytometry. The purity of the isolated CD34 + cells was greater than 95% in all cases. RNA extractionTotal RNA was extracted by TRIsure (Bioline, Luckenwalde, Germany) in all samples. The quality and integrity of the RNA were verified by a Bioanalyzer 2100 (Agilent Technologies, Santa Clara, CA, USA). MicroRNA and gene expressionThe expression profiles of 384 miRNA were analyzed in all samples using TaqMan Human MicroRNA v2.0 Arrays (Applied Biosystems, Foster City, CA. USA) which were analyzed on a 7900 HT Fast Real Time Polymerase Chain Reaction (PCR) System (Applied Biosystems, Foster City, CA, USA). The SDS 2.3 and RQ Manager 1.2 software (both Applied Biosystems, Foster City, CA, USA) were used for the analysis. Data were normalized using the average of the endogenous small-nucleolar RNU48 and the noncoding small nuclear U6, both included in the array.The expression profile of 45,000 genes was analyzed in the same samples using the Whole Human Genome Oligo microarray kit 4x44K (Agilent Technologies, Santa Clara, CA, USA). The microarrays were scanned in a GenePix reader (Molecular Devices, Sunnyvale, CA, USA). Samples from non-mobilized CD34 + cells were used as the reference group in both types of expression analysis.The expression of significant genes was validated by quantitative real-time PCR using Quantitec Primer Assays and the Quantitec SYBR Green Kit (both from Qiagen, Hilden, Germany) in a 7900 HT Fast Real Time PCR System (Applied Biosystems, Foster City, CA, USA). Data were normalized to the housekeeping gene ACTB and the group of samples from non-mobilized CD34 + cells was used as a control. The relative gene expression levels were calculated by the 2 -ΔΔCT method. Statistical analysisUnsupervised hierarchical clust...

show abstract

MiR-483-5p controls angiogenesis in vitro and targets serum response factor

Cited by 64 publications

References 23 publications

The regulatory role of microRNAs in angiogenesis‐related diseases

The regulatory role of microRNAs in angiogenesis‐related diseases

Myod and H19-Igf2 locus interactions are required for diaphragm formation in the mouse

Granulocyte colony-stimulating factor produces long-term changes in gene and microRNA expression profiles in CD34+ cells from healthy donors

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