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7 publications mentioning dre-mir-218a-2

Open access articles that are associated with the species Danio rerio and mention the gene name mir-218a-2. Click the [+] symbols to view sentences that include the gene name, or the word cloud on the right for a summary.

1
[+] score: 384
Although we do not know whether the slit2 is expressed in proepicardial cells, it is tempting to speculate that the up regulation of the Tbx5- miR-218 circuit might also impact the proepicardial cell migration by targeting robo1 or other cell migration regulators such as Semaphorins, some members of this large class of molecules being predicted targets of miR-218 (not shown). [score:9]
Tbx5 over -expression tripled slit2 expression, almost doubled miR-218 expression and had no effect on slit3 expression (Fig. 1C). [score:9]
To verify whether miR-218 over -expression can affect cardiac valve development, we analyzed the expression of the tie-2 gene, a member of the Tie family of tyrosine kinase receptors, which is expressed mainly in endothelial cells [31] and is up regulated during atrio-ventricular canal differentiation [32], [33]. [score:9]
Moreover, the transfection of a siRNA mix against Slit2 cut the level of Slit2 by half without affecting miR-218 expression, supporting the idea that miR-218 expression depends on the regulation of Slit2 transcription rather than on its translation. [score:8]
In line with data showing robo1 as target of miR-218a, over -expression of miR-218a significantly reduces the translational rate of a reporter construct (sensor), carrying GFP coding sequence upstream of robo1 3′UTR (Fig. S7). [score:7]
Interestingly, down-regulation of miR-218 is able to rescue most of the defects generated by Tbx5 over -expression, demonstrating the pivotal role of miR-218 in mediating the effects of Tbx5 dosage on heart development. [score:7]
To show that the slit/ miR-218 increase was at least partially dependent on Tbx5, tbx5 was up- or down-regulated by transfecting P19CL6 cells with a tbx5-carrying expression vector (CMV-Tbx5), or with a siRNA mix directed against tbx5, respectively. [score:7]
slit3 expression was also analyzed since its host miRNA, miR-218-2, cannot be separately quantified because it is identical to miR-218-1. In agreement with the literature [19], we observed tight co -expression of slit2 and miR-218, and a general correlation among tbx5, slit2, slit3 and miR-218 expression (Fig. S2). [score:7]
The knockdown efficiency of these morpholinos was confirmed by their ability to down-regulate mature miR-218 (Fig. S4A), and to rescue the phenotype caused by miR-218a over -expression (Fig. S4B). [score:7]
Fish et al [16] showed that robo1 is a miR-218a direct target and that early robo1 down-regulation by morpholino injection in zebrafish embryos induces severe pericardial edema and heart defects caused by reduced migration rate of endocardial cells. [score:7]
miR-218 and Robo1 are supposed to be upregulated and downregulated, respectively, when myocardial cell migration is about to end. [score:7]
Since Tbx5 and Slit2 are both expressed in myocardial cells [16] we hypothesized that early Tbx5 over -expression might cause heart malformation through early activation of miR-218a and silencing of the target genes of this miRNA. [score:7]
Therefore it is likely that modulation of Tbx5 in general, and over -expression of miR-218 as a consequence of Tbx5 up-regulation in particular, might have a higher impact on CHD population than previously hypothesized. [score:6]
In this view, Tbx5 mis -expression by mRNA microinjection at the one-cell stage might speed up the up-regulation of miR-218 and reduce the migration of myocardial cells precociously, which in turn might affect heart morphogenesis by impairing the correct interaction between myocardial and endocardial cells. [score:6]
To down regulate miR-218a, we injected either a morpholino targeting the mature form of miR-218a (MO [M]-218), or a longer morpholino also targeting the Drosha cleavage site of pre- miR-218a (MO [D]-218, see and [16]). [score:6]
Tbx5 Over -expression can be Rescued by Down-regulation of miR-218. [score:6]
Therefore our data showing a migration delay of cmlc2 -positive cardiac precursors in embryos over -expressing miR-218 (Fig. 4), but not in embryos in which miR-218 was down-regulated by MO-218 injection (Fig. 4C), are in line with these findings. [score:6]
We confirmed a correlation between tbx5 and miR-218 expression and showed that alterations of miR-218 expression have a significant impact on zebrafish heart development. [score:6]
Down-regulation of miR-218 can rescue the defects generated by tbx5 over -expression. [score:6]
This hypothesis is supported by the observation that miR-218 down-regulation by MO-218a injection rescues the effects of Tbx5 over -expression (Fig. 6). [score:6]
miR-218a over -expressing hearts were not able to complete the looping process, showed marked alteration of the cardiac chamber morphology and mis -expression of a marker of valve cardiac tissues. [score:5]
We reasoned that if the phenotype induced by Tbx5 over -expression was due, at least in part, to increased expression of miR-218, the co-injection of MO-218 should rescue the Tbx5 gain of function phenotype. [score:5]
miR-218a relative expression was calculated as the ratio between the expression of injected and the expression of non injected embryos. [score:5]
We speculate that the timing of miR-218a upregulation during heart development is crucial for heart morphogenesis. [score:5]
Despite the strong cardiac morphological alterations, miR-218a over -expressing embryos showed normal expression of the ventricular myosin heavy chain and the atrial myosin heavy chain (Fig. S6), as previously described in Tbx5 (hst) mutants [10]. [score:5]
miR-218a over -expression leads to the expansion of tie-2 expression. [score:5]
The apparent lack of phenotype that we observed after MO-218a injection (Fig. 2D,I) and the very low expression of miR-218 at early developmental stages, suggest that decreased miR-218a should not contribute to the phenotype generated by Tbx5 knockdown. [score:5]
Finally, we analyzed the expression of some cardiac markers in embryos over -expressing miR-218a. [score:5]
Figure S6 tbx5 and miR-218a misexpression does not alter amhc and vmhc cardiac marker expression in zebrafish embryos. [score:5]
This result strengthened our hypothesis that the effect of Tbx5 over -expression on heart development might, at least in part, be be mediated by miR-218. [score:4]
miR-218a Over -expression Affects Zebrafish Heart Development. [score:4]
Overall, these observations suggest that Tbx5 over -expression affects heart and eye development and that this might be at least partially mediated by miR-218. [score:4]
Increased miR-218a expression was observed as a consequence of Tbx5 up regulation (Fig. 5B). [score:4]
miR-218 over -expression affects cardiac development. [score:4]
All together these data indicate that correct expression of miR-218 is crucial for proper cardiac development. [score:4]
Injection of miR-218a mimic or MOs-218 in Tg(flk1:eGFP), which express GFP driven by the endothelial-specific enhancer of flk1, allowed a direct visualization of vascular integrity. [score:4]
Moreover, we showed that Tbx5 deregulation affects miR-218 expression. [score:4]
org); ii) the miR-218-1 host gene, slit2, is highly sensitive to Tbx5 mis -expression [8]; iii) the secreted Slit ligands, together with their Robo receptors, contribute to the control of oriented cell tissue growth during chamber morphogenesis of the mammalian heart [18]; iv) Slit/ miR-218/Robo are part of a regulatory loop required during heart tube formation in zebrafish [16]. [score:4]
As in zebrafish the expression level of miR-218a is extremely low during the first stages of development (our observation is supported also by the data of Fish et al. [16] and by data regarding miRNA microarray of Thatcher et al. [29], the introduction of very low amounts of miR-218a mimic into embryos at the one- or two-cell stage generated a severe cardiac phenotype. [score:4]
This is inconsistent with both our data and with the results of Fish et al. [16] who observed that Robo1 knock-down generates the same phenotype, because the same authors also showed that Robo1 is targeted by miR-218. [score:4]
Thus, robo1 is a candidate gene through which Tbx5 and miR-218a early over -expression affects heart development. [score:4]
tbx5 and miR-218 are Co-expressed in Mouse Tissues and in Cardiomyocyte Differentiation of P19CL6 Cells. [score:3]
Even after injection of high miR-218 doses, cardia bifida was never observed, suggesting that miR-218 over -expression slows down but does not arrest the migration of cardiomyocytes to the midline. [score:3]
miR-218 has also been shown to affect cancer progression by inhibiting tumor cell migration and metastasis via the repression of the Slit2/Robo1 pathway in gastric [40] and in nasopharyngeal [39] tumors, respectively. [score:3]
Hemizygous Tg(tie-2:GFP) embryos injected with miR-218a showed an increase in Tie-2 expressing cells in the ventricle and atrium (Fig. 3A, b,b′ and Fig. 3B,C). [score:3]
Conversely, miR-218a down regulation, even through injection of high doses of two different morpholinos, did not affect heart development. [score:3]
It is interesting to know that Pax2, that is negatively controlled by Tbx5 [45], is a predicted target of miR-218. [score:3]
Figure S4 Rescue of cardiac defects induced by miR-218a over -expression was accomplished by co-injecting MO-218a. [score:3]
To over-express miR-218a1/2, we injected double stranded RNA oligonucleotide with a miR-218a sequence (miR-218a mimic) in Tg(cmlc2:eGFP) embryos. [score:3]
robo1 has been identified as a target of miR-218 in many different organs and tissues [19], [39], [41]. [score:3]
miR-218 over -expression causes a delay in early heart field migration. [score:3]
On the other hand, tbx5 silencing, the effect of which was highest 2 days after silencing (6th day in culture, see ), caused significant reduction of slit2 and miR-218 expression 4 days after transfection (8th day in culture, Fig. 1D). [score:3]
tbx5 and miR-218 are co-expressed in cardiomyocyte differentiation of P19CL6 cells. [score:3]
miR-218 Over -expression Decreases the Migration of Myocardial Precursors. [score:3]
Pre-miRNA 218-1 expression paralleled the increase in miR-218 level during cardiomyocyte differentiation (Fig. S3A) and after Tbx5 modulation (Fig. S3B). [score:3]
Figure S7 miR-218 targets the 3′ UTR of robo1 in zebrafish embryos. [score:3]
B, qRT-PCR analysis of t bx5, slit2, slit3 and miR-218 relative expression in either expanding (GM) or differentiating (8,10,12 days) P19CL6 cells. [score:3]
Figure S2 tbx5 and miR-218 are co-expressed in mouse tissues. [score:3]
We showed a functional relation between Tbx5, Slit2 and miR-218 in P19CL6 cells in which a progressive increase of Tbx5, Slit2 and miR-218 expression was observed during cardiomyocyte differentiation. [score:3]
However miR-218b, an intergenic miRNA, has very low expression, suggesting that its contribution to the global miR-218 level might be irrelevant [16]. [score:3]
miR-218a mimic was injected in Tg(cmlc2:eGFP) embryos and the migration of the GFP -expressing cells was followed by confocal analysis. [score:3]
Conversely, in miR-218a over -expressing embryos we found different cardiac defects accounting for the ratios shown in Fig. 2C: hearts failing to complete looping, ventricles showing very irregular walls, and atria that were strongly reduced and sometimes stretched to a thin “string-like” morphology (Fig. 2F,G). [score:3]
miR-218a over -expression did not affect vessel morphology either (Fig. S5B), supporting the idea that in zebrafish miR-218a does not overtly influence the organization of blood vessels during embryogenesis. [score:3]
These data show that the cardiac defects observed in miR-218a over -expressing embryos might be at least in part related to defects in heart field migration. [score:3]
Figure S3 Expression of pre-miR-218-1 parallels that of mature miR-218 during mouse differentiation and tbx5 modulation. [score:3]
Recent data have shown that, in zebrafish, delayed heart field migration was caused by either miR-218a reduction or by silencing of Robo1, an established target of miR-218a [16], [19]. [score:3]
A, qRT-PCR analysis of miR-218a relative expression in 24 hpf embryos microinjected with 12 ng of control morpholino (MO-Ct) or MO [D]-218a and with 260 pg of miR-Ct or miR-218a mimic. [score:3]
Therefore, we decided to verify whether miR-218a over -expression might modify the migration of bilateral heart field cells to the midline. [score:3]
To demonstrate that the Tbx5/ miR-218 regulatory circuit is also functional during development, we used the zebrafish as a mo del system. [score:3]
In fact, an effect of miR-218a on the migration of endocardial and myocardial cells is not expected, as miR-218a seems not to be substantially expressed before 24 hpf [16], [29], when the fusion of migrating cardiac cells is about to be completed. [score:3]
A progressive increase in tbx5 expression was also observed (Fig. 1B), which was paralleled by an increase in slit2, slit3 and miR-218 transcripts. [score:3]
Figure S5 miR-218 dysregulation does not affect vascular integrity. [score:2]
To assess whether there are functional regulatory interactions among Tbx5, Slit2 and miR-218, we first examined these genes in an in vitro mo del for cardiomyocyte differentiation. [score:2]
0050536.g004 Figure 4A,B, images of Tg(cmlc2:eGFP) embryos injected with 260 pg of miR-Ct (A) or with 260 pg of miR-218a mimic (B) at different times of development. [score:2]
In mice, it has been shown that miR-218 regulates vascular patterning by modulating Slit-Robo signaling [19]. [score:2]
Fish et al [16]reported that miR-218a down regulation, performed by the microinjection of one of the two morpholinos that we used in our study, causes severe cardiac defects and cardiac edema through reduced migration of endocardial and myocardial cells. [score:2]
B, qRT-PCR analysis of miR-218a relative expression in 24 and 34 hpf embryos injected with 100 pg of tbx5a mRNA compared with embryos injected with 100 pg of GFP mRNA. [score:2]
As previously reported [16], MO-218 microinjection did not cause gross alteration in vascular structures (Fig. S5C) nor the hemorrhagic events described in mice after miR-218a knock down [19]. [score:2]
In line with the hypothesis that miR-218 might be a Tbx5 effector, we demonstrated that miR-218a deregulation generates cardiac defects (Fig. 2A). [score:2]
E-H, phenotypic analysis of miR-218a misregulation in Tg(cmlc2:eGFP) embryos. [score:2]
A,B, images of Tg(cmlc2:eGFP) embryos injected with 260 pg of miR-Ct (A) or with 260 pg of miR-218a mimic (B) at different times of development. [score:2]
Our data suggest that the haplo-insufficiency of the Tbx5 gene, at the moment the most significant cause of HOS, does not impact heart and upper limb formation through miR-218 misregulation. [score:2]
The simplest explanation for this might be that other key RNAs controlled by Tbx5 than miR-218 might be necessary for heart morphogenesis by regulating mechanisms other than myocardial cell migration. [score:2]
Our data show that miR-218 is part of a regulatory circuit through which Tbx5 controls heart morphogenesis. [score:2]
This is consistent with the extremely low level of miR-218a during early stages of development (data not shown and [16], [29]). [score:2]
To analyze the role of miR-218 in heart development, we decided to use zebrafish since this mo del is particularly informative for studying cardiac early patterning networks due to its relatively simple two-chambered heart coupled with its ability to develop even in the absence of a functioning heart. [score:2]
B, FACS analysis of cells dissociated from 72 hpf Tg(tie-2:GFP-cmlc2:eRFP) embryos injected as described in A. C, confocal images of 72 hpf Tg(tie-2:GFP-cmlc2:eRFP) embryos injected with 260 ng of miR-Ct (top) or with miR-218a mimic (bottom). [score:1]
We focused our attention on miR-218 since: i) it is conserved from human to zebrafish (www. [score:1]
0050536.g003 Figure 3A, confocal images of 72 hpf Tg(tie-2:GFP) embryos injected with 260 ng of control miRNA (a,a′), 260 ng of miR-218a mimic (b,b′), 2 ng of MO-Tbx5a (c,c′) or 100 pg of mRNA Tbx5a (d,d′). [score:1]
The total numbers of embryos analyzed were as follows: Ct miRNA (1 ng) n = 293; miR-214 mimic (1 ng) n = 104; miR-492 mimic (1 ng) n = 103; miR-218 mimic (35 pg) n = 107; miR-218 mimic (135 pg) n = 180; miR-218 mimic (260 pg) n = 318; miR-218 mimic (2 ng) n = 180; MO-Ct (8 ng) n = 207; MO [D]-218 (12 ng) n = 323; MO [M]-218 (2 ng) n = 112; MO [M]-218 (4 ng) n = 165; MO [M]-218 (8 ng) n = 182. [score:1]
In zebrafish, as in mammals, two isoforms of miR-218, miR-218a-1 and miR-218a-2, are embedded in slit3 and slit2 genes, respectively. [score:1]
As a whole, these data support a functional interaction between Tbx5 and miR-218a in heart morphogenesis. [score:1]
The authors showed that miR-218 -driven repression of Robo1/2 and of heparan sulfate proteoglycans (HSPGs), which are proteins essential for Slit/Robo signaling, negatively affects endothelial cell (EC) migration. [score:1]
To further investigate the functional interaction between Tbx5 and miR-218a, we assessed whether the morphological alterations generated by Tbx5 misexpression might be compensated for the modulation of miR-218a. [score:1]
ReagentsMature miRNA mimics (mmu- miR-218a, mmu-miR-492, mmu-miR-214 and miR-Ct) were synthesized by GenePharma (Shanghai, China), morpholinos (Gene Tools, LLC USA. [score:1]
At the moment we do not know how miR-218 might also partially rescue eye defects. [score:1]
This synergism was further demonstrated by MO-Tbx5a and miR-218a mimic co-injection in sub-phenotypic doses. [score:1]
Confocal images of representative 72 hpf Tg(flk1:eGFP) embryos injected with 260 pg of miR-Ct (A), 260 pg of miR-218 mimic (B) or 8 ng MO [D]-218 (C). [score:1]
Bottom: examples of 24 hpf embryos microinjected with 40 pg of RFP mRNA, 400 pg of 3′UTR robo 1 sensor and 160 pg of miR-Ct (a,c,e) or miR-218a (b,d,f). [score:1]
A, phenotypic analysis of Tbx5a morphants co -injected with 1 ng of MO-Tbx5a and either 130 pg of miR-218a mimic or 130 pg of miR-Ct. [score:1]
Figure S9 Injection of miR-218a in Tbx5a morphants increases the severity of heartstring phenotype. [score:1]
B, representative images of 48 hpf embryos showing the edema expansion caused by the co-injection of miR-218a mimic. [score:1]
Co-injection of mimic miR-218a did not rescue the cardiac edema and looping defects generated by MO-Tbx5a (Fig. S9A). [score:1]
A negative role of miR-218 on cell migration has been highlighted in different biological contexts. [score:1]
C, Q-RT-PCR detection of slit2 and mature miR-218 in P19CL6 cells transfected with a mix of two siRNAs against slit2 or with a siRNA-Ct. [score:1]
The morpholino antisense oligonucleotide MO [M]-218 (5′-GCACATGGTTAGATCAAGCACAACA-3′) and MO [D]-218 (5′-TGCATGGTTAGATCAAGCACAAGGG-3′) were designed against the mature form of miR-218a and the Drosha cleavage site of pre- miR-218a respectively. [score:1]
0050536.g002 Figure 2A, miR-218a ISH of 72 hpf embryos. [score:1]
Injection of 260, 135 and 35 pg of miR-218a mimic generated embryos with cardiac defects in a dose -dependent way (Fig. 2C). [score:1]
A, miR-218a ISH of 72 hpf embryos. [score:1]
C, phenotypic analysis of embryos co -injected with sub-phenotypic doses of both MO-Tbx5a(0.5 ng) and miR-218a mimic (35 pg). [score:1]
C,D, phenotypes induced at 72 hpf by increasing doses of miR-218 mimic (C) or MO [M]/MO [D]-218 (D) injection. [score:1]
The anti-DIG antibody-alkaline phosphatase Fab fragment was diluted 1∶4.000 in MABlock buffer (2% Blocking reagent in 100 mM Maleic acid and 150 mM NaCl) and incubation was performed at +4°C for gene probes and at room temperature for miR-218 probe. [score:1]
Myocardial cells migrated more slowly in miR-218a than in miR-Ct injected embryos (Fig. 4). [score:1]
B, representative transgenic Tg(cmlc2:eGFP) embryos at 72 hpf showing heart morphological defects induced by the injection of 260 pg of miR-218a mimic in the absence (a,b) or in the presence (c,d) of MO [D]-218a (12 ng). [score:1]
Whole mount in situ hybridization was performed as previously described [53] with some modification: pre-hybridization temperature was 62°C; hybridization temperature was 62°C for gene probes and 52°C for miR-218 probe. [score:1]
A-D, relative expression of tbx5, slit2, slit3 and miR-218 as evaluated by q-RT-PCR in different newborn mouse tissues. [score:1]
However, the injection of both MO-Tbx5a and miR-218a mimic at these doses dramatically increased the number of embryos with looping defects (Fig. S9C,E). [score:1]
A, confocal images of 72 hpf Tg(tie-2:GFP) embryos injected with 260 ng of control miRNA (a,a′), 260 ng of miR-218a mimic (b,b′), 2 ng of MO-Tbx5a (c,c′) or 100 pg of mRNA Tbx5a (d,d′). [score:1]
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2
[+] score: 42
Other miRNAs from this paper: dre-mir-7b, dre-mir-7a-1, dre-mir-7a-2, dre-mir-34a, dre-mir-181b-1, dre-mir-181b-2, dre-mir-182, dre-mir-183, dre-mir-181a-1, dre-mir-219-1, dre-mir-219-2, dre-mir-221, dre-mir-222a, dre-mir-430a-1, dre-mir-430b-1, dre-mir-430c-1, dre-let-7a-1, dre-let-7a-2, dre-let-7a-3, dre-let-7a-4, dre-let-7a-5, dre-let-7a-6, dre-let-7b, dre-let-7c-1, dre-let-7c-2, dre-let-7d-1, dre-let-7d-2, dre-let-7e, dre-let-7f, dre-let-7g-1, dre-let-7g-2, dre-let-7h, dre-let-7i, dre-mir-7a-3, dre-mir-9-1, dre-mir-9-2, dre-mir-9-4, dre-mir-9-3, dre-mir-9-5, dre-mir-9-6, dre-mir-9-7, dre-mir-92b, dre-mir-96, dre-mir-100-1, dre-mir-100-2, dre-mir-124-1, dre-mir-124-2, dre-mir-124-3, dre-mir-124-4, dre-mir-124-5, dre-mir-124-6, dre-mir-125b-1, dre-mir-125b-2, dre-mir-125b-3, dre-mir-128-1, dre-mir-128-2, dre-mir-132-1, dre-mir-132-2, dre-mir-135c-1, dre-mir-135c-2, dre-mir-137-1, dre-mir-137-2, dre-mir-138-1, dre-mir-153a, dre-mir-181c, dre-mir-200a, dre-mir-218a-1, dre-mir-219-3, dre-mir-375-1, dre-mir-375-2, dre-mir-454a, dre-mir-430c-2, dre-mir-430c-3, dre-mir-430c-4, dre-mir-430c-5, dre-mir-430c-6, dre-mir-430c-7, dre-mir-430c-8, dre-mir-430c-9, dre-mir-430c-10, dre-mir-430c-11, dre-mir-430c-12, dre-mir-430c-13, dre-mir-430c-14, dre-mir-430c-15, dre-mir-430c-16, dre-mir-430c-17, dre-mir-430c-18, dre-mir-430a-2, dre-mir-430a-3, dre-mir-430a-4, dre-mir-430a-5, dre-mir-430a-6, dre-mir-430a-7, dre-mir-430a-8, dre-mir-430a-9, dre-mir-430a-10, dre-mir-430a-11, dre-mir-430a-12, dre-mir-430a-13, dre-mir-430a-14, dre-mir-430a-15, dre-mir-430a-16, dre-mir-430a-17, dre-mir-430a-18, dre-mir-430i-1, dre-mir-430i-2, dre-mir-430i-3, dre-mir-430b-2, dre-mir-430b-3, dre-mir-430b-4, dre-mir-430b-6, dre-mir-430b-7, dre-mir-430b-8, dre-mir-430b-9, dre-mir-430b-10, dre-mir-430b-11, dre-mir-430b-12, dre-mir-430b-13, dre-mir-430b-14, dre-mir-430b-15, dre-mir-430b-16, dre-mir-430b-17, dre-mir-430b-18, dre-mir-430b-5, dre-mir-430b-19, dre-mir-430b-20, dre-let-7j, dre-mir-181a-2, dre-mir-34b, dre-mir-34c, dre-mir-222b, dre-mir-138-2, dre-mir-181a-4, dre-mir-181a-3, dre-mir-181a-5, dre-mir-181b-3, dre-mir-181d, dre-mir-128-3
Our results show miRNAs have a wide variety of different expression profiles in neural cells, including: expression in neuronal precursors and stem cells (for example, miR-92b); expression associated with transition from proliferation to differentiation (for example, miR-124); constitutive expression in mature neurons (miR-124 again); expression in both proliferative cells and their differentiated progeny (for example, miR-9); regionally restricted expression (for example, miR-222 in telencephalon); and cell-type specific expression (for example, miR-218a in motor neurons). [score:15]
Figure 6 miR-218a is expressed in embryonic cranial and spinal motor-neurons. [score:3]
miR-218a expression in the zebrafish brain. [score:3]
Yellow cells express both miR-218a and GFP in the NVII and NX cranial motor nuclei. [score:3]
miR-218a expression is shown in red in (e) and (f) is a superimposition of the miR-218a staining (red) and anti-GFP immunostaining (green). [score:3]
Click here for file 7 miR-218a expression in the zebrafish brain. [score:3]
For instance, miR-218a is exclusively expressed in cranial motor nuclei (NIII, NV, NVI, NVII, NX) and spinal motor neurons (MN, Figure 6a-f;7, and Table E in7). [score:3]
Similar to miR-34, miR-218a expression expands rostrally in the adult brain. [score:3]
Additional data file 17 is a figure showing miR-218a expression in the zebrafish brain. [score:3]
For instance, miR-218a is predominantly expressed in most motor neurons. [score:3]
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[+] score: 15
miR-155 and miR-218 backbones lead to potent knockdownpME -RNAi651, pME -RNAi661 and pME -RNAi671 constructs with green fluorescent protein (GFP) marker followed by a synthetic pre-miR directed against the 3′-UTR of mCherry were cloned downstream of the ubiquitin promoter in a mini-tol2-R4R2 multisite gateway-compatible destination plasmid (Supplementary Fig. 3). [score:3]
hsa-miR218 -based plasmids: An artificial miRNA -expressing hsa-miR218 cassette was generated in our laboratory. [score:3]
However, the backbone based on dre-miR30 achieved only weak red fluorescence inhibition compared with mmu-miR155 or hsa-miR218 backbones. [score:2]
miR-155 and miR-218 backbones lead to potent knockdown. [score:2]
According to the cell-specific observations above, miR218 and miR155 backbones led to potent global knockdown with ∼74 and 83% reduction in red fluorescence, respectively, while the miR30 backbone reduced fluorescence modestly by ∼33%. [score:2]
Pri-hsa-miR218-2 was amplified and cloned into pME -RNAi651 in two steps to allow the insertion of a 2 × BsmBI repeat at the pre-miR218 position (Fig. 1). [score:1]
The third plasmid, based on an hsa-miR218 sequence, was made in our laboratory. [score:1]
pME -RNAi651 is based on a mmu-miR155 backbone, pME -RNAi661 on a dre-miR30 backbone and pME -RNAi671 on a hsa-miR218 backbone. [score:1]
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4
[+] score: 12
[53] [,] [71] [,] [72] miR-218 knock-down in zebrafish results in a phenotype similar to robo1 overexpression, suggesting functional regulation of Slit–Robo signalling by miR-218. [score:5]
Additionally, cross-talk was found between Robo1, Vegfa, and the Vegfr2 receptor to control heart field migration, indicating a Slit/miR-218/Robo/Vegf feedback regulatory loop regulating heart field migration. [score:3]
[71] miR-218 is able to repress expression of both robo1 and robo2 mRNA. [score:3]
Microrna-218 regulates vascular patterning by modulation of Slit-Robo signaling. [score:1]
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5
[+] score: 5
Since miR-23 (JX994633), miR-218 (JX994383) and miR-338 (JX994406) are present in the elephant shark, these conserved miRNAs are likely to be involved in the regulation of Runx2 expression in elephant shark, possibly during chondrogenic differentiation through mechanisms similar to that in other jawed vertebrates. [score:4]
Of these, binding sites for miR-23, miR-218 and miR-338 were found conserved in the 3′UTR of elephant shark Runx2, while only that for miR-28 is present in zebrafish and fugu Runx2 (Fig. 8B). [score:1]
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[+] score: 4
Several other miRNA clusters including miR-126, miR-218, miR-23/27 clusters are documented in the regulation of angiogenesis [39, 42– 44], whether, all these families of miRNAs function independently or in concert are unclear. [score:2]
An earlier study has demonstrated the role of miR-218 in vascular patterning by modulating Robo-Slit signaling [39]. [score:1]
MicroRNA-218 regulates vascular patterning by modulation of Slit-Robo signaling. [score:1]
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[+] score: 4
In fact, we proved that in mouse cardiac cells and zebrafish embryos, Tbx5 is able to regulate several miRNAs and, in particular, miR-218 and miR-19 (Chiavacci et al., 2012, 2015). [score:2]
A slit/miR-218/robo regulatory loop is required during heart tube formation in zebrafish. [score:2]
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