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9 publications mentioning dre-mir-132-2

Open access articles that are associated with the species Danio rerio and mention the gene name mir-132-2. Click the [+] symbols to view sentences that include the gene name, or the word cloud on the right for a summary.

1
[+] score: 323
Other miRNAs from this paper: dre-mir-132-1
To examine whether miR-132 is important for brain vascular development, we downregulated the expression of miR-132 using two morpholino oligonucleotides (MOs), which targeted mature miR-132 (“ miR-132 MO”, see also ref. [score:9]
To demonstrate the leakage of blood cells in the brain, we knocked down miR-132 expression in double transgenic zebrafish Tg(Flk1:eGFP;Gata1:DsRed) larvae, in which ECs express enhanced green fluorescent protein (eGFP) and blood cells express DsRed. [score:8]
In comparison with control larvae, in which neurons expressed tdT (“ HuC:tdT”), larvae with neurons expressing miR-132-S exhibited severe intracranial hemorrhage (Figure 3B and 3C; P < 0.01) and increased DAPI leakage (Figure 3D and 3E; P < 0.05) and reduced Cdh5 expression (Figure 3F; P < 0.05). [score:7]
In comparison with tdT expression in ECs (“ Flk1:tdT”), miR-132-S expression in ECs resulted in severe intracranial hemorrhage (Figure 3H; P < 0.01) and reduction of Cdh5 expression (Figure 3I; P < 0.01). [score:7]
To study the consequences of downregulating the level of miR-132 in neurons, we transiently expressed miR-132 sponge (miR-132-S) in neurons. [score:6]
To address this point, we specifically downregulated the level of miR-132 in ECs by transiently expressing miR-132-S driven by the promoter of the EC-specific gene Flk1 (“ Flk1:tdT-miR-132-S”). [score:6]
Importantly, the expression of eEF2K in zebrafish larvae was decreased or increased by the overexpression or knockdown of miR-132, respectively (Figure 6D and 6E; P < 0.05). [score:6]
Interestingly, up- and downregulation of the miR-132 level in neurons resulted in a coordinated change of the miR-132 level in ECs, and EC-specific reduction of miR-132 also impaired Cdh5 expression as well as the brain vascular integrity. [score:6]
By overexpressing or downregulating miR-132 in cultured cortical neurons, we found that the miR-132 level in isolated neuronal exosomes positively correlated with that in neurons (Figure 4J and 4K; P < 0.01). [score:6]
Treatment with the nSMase2 inhibitor spiroepoxide (10 μM) or nSMase2 knockdown with MO led to severe intracranial hemorrhage accompanied with decreased expression of miR-132 in ECs of zebrafish larvae (Figure 5B, 5C and Supplementary information, Figure S8D-S8F; P < 0.05). [score:6]
The expression of miR-132 in zebrafish larvae was efficiently downregulated by these MOs (Supplementary information, Figure S1D; P < 0.05). [score:6]
Through secreting exosomes, neurons can translocate miR-132 to ECs to regulate the expression of the vascular junction protein Cdh5 by targeting eef2k (Figure 7). [score:6]
The non-overlapping expression pattern of HuC:tdT and Flk1:eGFP ensured that the coordinated changes in endothelial miR-132 were not due to the non-specific expression of HuC plasmids in ECs (Supplementary information, Figure S7). [score:5]
Taken together, these results indicate that eef2k is a direct target of miR-132 in ECs to regulate the integrity of brain vasculature. [score:5]
As the expression of miR-132 is positively regulated by sensory experience and neural activity 38, 39, 40, it is of interest to examine whether enriched environment or enhanced neural activity can promote the development of brain vascular integrity by increasing miR-132 levels. [score:5]
MiR-132 is necessary for the brain vascular integrity in larval zebrafishMiRNAs are small non-coding RNAs that post-transcriptionally regulate the expression of target mRNAs [21]. [score:5]
MiR-132 targets eef2k in ECs to regulate Cdh5 expression and brain vascular integrity. [score:5]
Conversely, overexpression of miR-132 in neurons, through the transient expression of HuC:tdT-miR-132, increased the miR-132 level in ECs (Figure 3G; P < 0.05). [score:5]
Knockdown or mutation of miR-132 caused severe intracranial hemorrhage and disruption of brain vascular integrity in zebrafish larvae with reduced expression of the adherens junction protein vascular endothelial cadherin (VE-cadherin, also known as Cdh5) and its intracellular partner β-catenin. [score:5]
As the impairment of brain vascular integrity will lead to the ingress of plasma components into the brain and compromise synaptic and neuronal functions 1, 2, the regulation of brain vascular integrity by miR-132 may indirectly contribute to the role of miR-132 in neural development and function. [score:4]
Moreover, knockdown of eef2k alleviated the intracranial hemorrhage (Figure 6G; P < 0.01), DAPI leakage (Figure 6H and Supplementary information, Figure S10C; P < 0.05) and reduction of Cdh5 expression (Figure 6I; P < 0.05) in miR-132 morphants. [score:4]
Furthermore, we identified eukaryotic elongation factor 2 kinase (eef2k) as a direct target of miR-132. [score:4]
This indicates that miR-132 in ECs can regulate expression of Cdh5 and the integrity of the brain vasculature. [score:4]
This defect of brain vascular integrity was a specific consequence of downregulation of miR-132, because co-injection of miR-132 RNA with miR-132 MO alleviated the hemorrhagic phenotype in morphants (Figure 1J; P < 0.001). [score:4]
Here we found that knockdown of miR-132 did not affect the pericyte coverage, suggesting no direct involvement of pericytes in the regulation of brain vascular integrity by miR-132. [score:4]
These results indicate that eef2k is a direct target of miR-132. [score:4]
Moreover, the level of miR-132 in b. End3 cells could be further increased after incubation with the exosomes isolated from neurons overexpressing miR-132 (Figure 4L; P < 0.001). [score:3]
Interestingly, reduction of miR-132 in neurons by transiently expressing HuC:tdT-miR-132-S also decreased the level of miR-132 in ECs (Figure 3G; P < 0.05). [score:3]
The sequence of miR-132 guide RNA (gRNA) (5′-TTGGTAACAGTCTACAGCCA-3′) was designed to target the sequence of mature miR-132 (Supplementary information, Figure S4A). [score:3]
However, previous reports showed that miR-132 was also expressed in pericytes and glial cells 43, 44. [score:3]
The real-time PCR with SYBR Premix Ex Taq II (Takara) was performed on the cDNA to detect the relative miR-132 expression. [score:3]
The knockout efficiency of mature miR-132 transcription was examined by real-time PCR, and hemorrhagic phenotypes were examined in F0 embryos which carried miR-132 mutations. [score:3]
The sponge contained ten repeats of the miR-132 antisense sequence and efficiently inhibited miR-132 function by chelating miR-132 (Supplementary information, Figure S6; P < 0.001) [31]. [score:3]
As miR-132 expression is kept at a high level in the brain [39], it is possible that the mechanism we have identified may also contribute to the maintenance of brain vascular integrity in adult brain. [score:3]
The expression of β-catenin was reduced in miR-132 morphants (P < 0.05), whereas we observed no significant change for α-catenin (Figure 2A and 2B). [score:3]
In hemorrhagic miR-132 morphants, the expression of Cdh5, an important component of adherens junctions [26], but not Claudin-5, Occludin, ZO-1 or N-cadherin was markedly reduced (Figure 2A-2C; P < 0.01). [score:3]
To reduce miR-132 expression, miR-132 sponge (miR-132-S) containing 10 repeated miR-132 antisense sequences was synthesized by GeneArt and cloned into HuC:tdT, Flk1:tdT or Fugw vectors. [score:3]
To manipulate the expression of miR-132 or label exosomes in cultured neurons, dissociated rat cortical neurons were transfected with 2 μg plasmid or 100 nM FAM-tagged miR-132 (Genepharma) with a Rat Neuron Nucleofector Kit (Amaxa, VPG1003) by using an electroporator (Amaxa, Program O-03). [score:3]
The miR-132-S was inserted into the 3′ untranslated region (3′ UTR) of the reporter gene tdTomato (tdT) and driven by the promoter of the neuron-specific gene HuC (“ HuC:tdT-miR-132-S”). [score:3]
To examine the effect of neuronal miR-132 manipulations on the expression of miR-132 and eEF2K in ECs, Tg(Flk1:eGFP) larvae microinjected with HuC:tdT, HuC:tdT-miR-132 or HuC:tdT-miR-132-S were used for both neuron and EC sorting. [score:3]
This increase was not affected by co-treatment with the RNA polymerase II inhibitor DRB (5, 6-dichloro-1-b-D-ribofuranosylbenzimidazole; Figure 4H; P = 0.9), suggesting neuronal exosomes can transfer mature miR-132 to ECs. [score:3]
Combining flow cytometry and real-time PCR analysis, we found that, in zebrafish larvae, expression of miR-132 was much higher in neurons than in ECs (Figure 3A; P < 0.001). [score:3]
More importantly, by combining flow cytometry and, we found that the expression of eEF2K in ECs was significantly increased after sponge -mediated reduction of miR-132 in neurons (Figure 6J; P < 0.05). [score:3]
miR-132 MO: 5′-AGCGACCATGGCTGTAGACTGTTAC-3′ miR-132 loop MO: 5′-GGCTGTAGACTGTTACCAAAAATTC-3′ Cdh5 MO: 5′-TACAAGACCGTCTACCTTTCCAATC-3′ nSMase2 MO: 5′-CCACCTGCACCTGCACAAAACAACA-3′ eef2k MO: 5′-AGCTCCTCTTCAGCCATGATGCCCC-3′ control MO: 5′-CCTCTTACCTCAGTTACAATTTATA-3′ miR-132 RNA: 5′-UAACAGUCUACAGCCAUGGUCG-3′ control RNA: 5′-UUGUACUACACAAAAGUACUG-3′ CRISPR/Cas9 -mediated mutation of miR-132 in zebrafish embryosThe CRISPR (clustered regularly interspaced short palindromic repeats)/Cas9 system was applied to introduce miR-132 gene mutation in zebrafish embryos as previously reported 58, 59, 60. [score:3]
Application of the eEF2K inhibitor NH125 (2.5 μM) significantly alleviated the hemorrhagic defect in miR-132 morphants (Figure 6F; P < 0.001). [score:3]
We then chose to examine the effect of miR-132 knockdown on endothelial transcytosis and pericytes that can also regulate vascular permeability in the brain [4]. [score:3]
Because only about 40% of miR-132 morphants exhibited severe intracranial hemorrhage (Figure 1C), we examined the level of miR-132 in hemorrhagic and non-hemorrhagic miR-132 morphants, and found that the expression of miR-132 was comparable in the two groups (Supplementary information, Figure S3A). [score:3]
Considering that less than 5% neurons in the brain were labeled by HuC promoter -driven transient gene expression, the effects of neuronal manipulations on miR-132 level in ECs are underestimated. [score:3]
Gain- and loss-of-function experiments showed that eef2k in ECs mediated the action of miR-132 on Cdh5 expression and brain vascular integrity. [score:3]
Supplementary information, Figure S9Prediction of the target genes of miR-132 in zebrafish. [score:3]
To compare the expression level of miR-132 in zebrafish ECs and neurons, Tg(Flk1:eGFP) and Tg(HuC:GFP) larvae were used for EC and neuron sorting, respectively. [score:3]
Therefore, application of miR-132-containing exosomes may be a safe and efficient future strategy for alleviating brain vascular dysfunctions associated with neurological and brain vascular diseases. [score:3]
Novel function of miR-132 in regulating brain vascular integrity MiR-132, a neuron-enriched miRNA, plays important roles in the development and activity -dependent plasticity of neural systems in a cell-autonomous manner. [score:3]
We then examined whether miR-132 in ECs can also regulate the brain vascular integrity. [score:2]
MiR-132, a neuron-enriched miRNA, plays important roles in the development and activity -dependent plasticity of neural systems in a cell-autonomous manner. [score:2]
In the present study, we found that, neurons transfer miR-132, an evolutionarily conserved and neuron-enriched miRNA 19, 20, into ECs via secreting exosomes to regulate the brain vascular integrity. [score:2]
Taken together, these in vitro and in vivo findings suggest that neuronal exosomes containing miR-132 can mediate neuronal regulation of brain vascular integrity. [score:2]
To increase the expression of miR-132, zebrafish pri- miR-132 was amplified from the zebrafish genomic DNA by using primers (forward: 5′-CGCCTCGAGCAGTCTACAGTCATGGCTACTGACG-3′ reverse: 5′-GCGTCTAGACCTGTTCACTTGCATGCAAGG-3′) and cloned into HuC:tdT, pCS2: GFP or Fugw vectors. [score:2]
CRISPR/Cas9 -mediated mutation of miR-132 in zebrafish embryos. [score:2]
At a cellular level, miR-132 regulates neurite growth and arborization 20, 36, 37, and synaptic structure and function 19, 38. [score:2]
Neuronal miR-132 regulates brain vascular integrity via affecting vascular miR-132 level. [score:2]
Collectively, these results suggest that miR-132 regulates the brain vascular integrity through affecting adherens junction proteins rather than transcytosis or pericytes. [score:2]
Similar to the effects of miR-132 knockdown, Cdh5 morphants also displayed increased intracranial hemorrhage (see also ref. [score:2]
As ECs are the main constituent of the brain vasculature, we thus proposed that miR-132 in neurons may regulate the brain vascular integrity by affecting miR-132 levels in ECs. [score:2]
As the contents of exosomes are abundant, other factors besides miR-132 in neuronal exosomes may also participate in the neural regulation of brain vascular integrity. [score:2]
MiR-132 is a neuron-enriched miRNA and plays crucial roles in neural development and plasticity 19, 20. [score:2]
miR-132 MO: 5′-AGCGACCATGGCTGTAGACTGTTAC-3′ miR-132 loop MO: 5′-GGCTGTAGACTGTTACCAAAAATTC-3′ Cdh5 MO: 5′-TACAAGACCGTCTACCTTTCCAATC-3′ nSMase2 MO: 5′-CCACCTGCACCTGCACAAAACAACA-3′ eef2k MO: 5′-AGCTCCTCTTCAGCCATGATGCCCC-3′ control MO: 5′-CCTCTTACCTCAGTTACAATTTATA-3′ miR-132 RNA: 5′-UAACAGUCUACAGCCAUGGUCG-3′ control RNA: 5′-UUGUACUACACAAAAGUACUG-3′ The CRISPR (clustered regularly interspaced short palindromic repeats)/Cas9 system was applied to introduce miR-132 gene mutation in zebrafish embryos as previously reported 58, 59, 60. [score:2]
Zebrafish eef2k 3′ UTR (500 bp) containing miR-132 target sequences was amplified from the zebrafish cDNA with primers (forward: 5′-CGCCTCGAGTTTACAGATTGATCAAAATGGTTTA-3′ reverse: 5′-CGCTCTAGACGCGCGGCCGCTCCAGCAAAAGTGATCACACA-3′) and cloned into psiCHECK-2 or psiCHECK-2 :tdTomato vector. [score:2]
Novel function of miR-132 in regulating brain vascular integrity. [score:2]
MiR-132 is evolutionarily conserved among animal species and highly expressed in the brain of zebrafish larvae (Supplementary information, Figure S1A and S1B; see also ref. [score:2]
Thus, it is of interest to examine whether miR-132 in pericytes and glial cells can also regulate brain vascular integrity. [score:2]
Neuronal miR-132 regulates brain vascular integrity via affecting vascular miR-132 levelIn mammals, miR-132 is enriched in neurons 19, 20. [score:2]
This study discovers a previously unidentified function of miR-132 and reveals that neuronal exosomes serve as a novel carrier in mediating the neural regulation of brain vascular integrity. [score:2]
These in vitro findings show that neurons can regulate the level of miR-132 in ECs through exosome -mediated intercellular transfer of miR-132. [score:2]
Moreover, miR-132 mutations induced by co-injecting miR-132 guide RNA (gRNA) and zebrafish codon-optimized Cas9 mRNA also led to a significant increase of intracranial hemorrhage in F0 embryos (Figure 1K and Supplementary information, Figure S4; P < 0.001). [score:2]
Supplementary information, Figure S4Mutation of miR-132 by CRISPR/Cas9. [score:2]
We found that vsg1 mRNA was reduced rather than increased in miR-132 morphants (Figure 2F; P < 0.01), suggesting that at least transcytosis is not enhanced by miR-132 knockdown. [score:2]
In the present study, we found that miR-132 exerts a non-cell-autonomous function in regulating the integrity of the brain vasculature. [score:2]
Together, these results suggest that neuronal miR-132 may regulate brain vascular integrity through coordinately affecting miR-132 level in ECs. [score:2]
The miR-132 gene mutation in F0 embryos was examined by PCR and sequencing analysis with primers (forward: 5′-CGCCTCGAGCAGTCTACAGTCATGGCTACTGACG-3′ reverse: 5′-GCGTCTAGACCTGTTCACTTGCATGCAAGG-3′). [score:1]
To address whether neuronal exosomes containing miR-132 can be internalized into ECs, we first labeled purified exosomes with the green fluorescent lipid dye PKH67 and incubated them with the mouse brain microvascular EC line (b. End3). [score:1]
In comparison with embryos injected with a control MO (“Ctrl MO”), a substantial proportion of miR-132 morphants displayed intracranial hemorrhage (Figure 1A and 1C; Ctrl MO: 3.3% ± 0.7%; miR-132 MO: 38.0% ± 2.8%; miR-132 loop MO: 37.1% ± 7.9%; mean ± SEM, P < 0.001) without any marked embryonic death or defects in gross morphology (Supplementary information, Figure S1E and S1F). [score:1]
600 pg z Cas9 mRNA and 100 pg miR-132 gRNA were co -injected into zebrafish embryos at one-cell stage. [score:1]
Exosomes transfer neuronal miR-132 from neurons to ECsExosomes are newly identified vehicles for intercellular communication [15]. [score:1]
Consistent with the microarray data and the prediction that the zebrafish eef2k 3′UTR contains two miR-132 binding sites (Figure 6A), we found that miR-132 markedly repressed the luciferase activity of the eef2k 3′UTR (, Figure S9B). [score:1]
Supplementary information, Figure S10Role of eef2k in mediating miR-132 effects on brain vascular integrity. [score:1]
In mammals, miR-132 is enriched in neurons 19, 20. [score:1]
Collectively, these results indicate that neuronal exosomes can transfer miR-132 into ECs. [score:1]
The defect in the brain vascular integrity was mimicked by neuron-specific reduction of miR-132. [score:1]
EC-EC contacts in control larvae showed numerous and extensive junctions (Figure 1G and 1H) whereas junctions between brain ECs in hemorrhagic miR-132 morphants was discontinuous, junction density was reduced, and the cleft between ECs was increased (Figure 1G and 1I). [score:1]
Importantly, miR-132 was detected in the isolated neuronal exosome and its level was increased with the increased amount of exosomes (Figure 4D; P < 0.001). [score:1]
Combining experiments on cultured rodent brain cells, we found that neurons secreted miR-132-containing exosomes, which were then internalized into brain ECs, leading to an increased level of miR-132 in ECs, and impairment of exosome secretion in zebrafish larvae caused intracranial hemorrhage. [score:1]
The Taqman real-time PCR was only used to detect the absolute quantity of miR-132 in different amount of neuronal exosomes. [score:1]
We then examined whether eEF2K mediates the effect of miR-132 on the brain vascular integrity. [score:1]
The tdTomato-eef2k 3′UTR mRNA (50 pg) and GFP mRNA (30 pg), together with control RNA (200 pg) or miR-132 RNA (200 pg), were co -injected into zebrafish embryos at the one-cell stage. [score:1]
Two repeated miR-132 antisense sequences were cloned into psiCHECK-2 vector as a miR-132 sensor. [score:1]
Both in vitro and in vivo reporter assays showed that eef2k 3′ UTR was sufficient to confer miR-132 regulation (Figure 6B and Supplementary information, Figure S10A and S10B; P < 0.001), and the second binding site was indispensable (Figure 6A and 6C). [score:1]
Zebrafish whole-mount in situ hybridization was performed as previously described 22, 62 with a digoxigenin-labeled miR-132 Locked Nucleic Acid (LNA) probe (5′-CGACCATGGCTGTAGACTGTTA -3′, Exiqon) and a scramble LNA probe (5′-GTGTAACACGTCTATACGCCCA-3′, Exiqon). [score:1]
Supplementary information, Figure S6Design and efficiency of miR-132 sponge. [score:1]
Supplementary information, Figure S1Conserved miR-132 is necessary for brain vascular integrity. [score:1]
Consistent with a previous finding that miR-132 can facilitate pathological angiogenesis [25], we also found the brain vascular density was decreased in miR-132 morphants (Supplementary information, Figure S2; P < 0.01). [score:1]
Thus, neuronal miR-132 is necessary for the integrity of brain vasculature. [score:1]
In contrast to control embryos, red fluorescent beads were readily observed to leak out from the brain vessels of miR-132 morphants (Supplementary information, Figure S1I and S1J). [score:1]
Exosomes transfer neuronal miR-132 from neurons to ECs. [score:1]
Furthermore, incubation with neuronal exosomes significantly increased the level of miR-132 in b. End3 cells (Figure 4H; P < 0.05). [score:1]
The luminal side of brain vessels in miR-132 morphants was tortuous and rough (Figure 1G). [score:1]
Supplementary information, Figure S3Impairment of brain vascular integrity in nonhemorrhagic miR-132 morphants. [score:1]
Supplementary information, Figure S2 MiR-132 knockdown reduces brain vascular density. [score:1]
It was reported that neurons can transfer functional materials to recipient cells via secreting exosomes 11, 32 leading us to postulate that neuronal exosomes may transfer miR-132 from neurons to ECs. [score:1]
Zebrafish embryos were microinjected at the one-cell stage with 8 ng miR-132 MO, 8 ng miR-132 loop MO, 0.5 ng Cdh5 MO, 0.5 - 1 ng eef2k MO, 4 ng nSMase2 MO, or equivalent control MO. [score:1]
A significant increase of DAPI -positive parenchymal cell nuclei as well as dextran leakage was observed in miR-132 morphants (Figure 1D, 1E and Supplementary information, Figure S1H; P < 0.001). [score:1]
A pair of oligonucleotides containing the miR-132 gRNA sequence were annealed and cloned into the pT7-gRNA plasmid. [score:1]
We noted, however, in those miR-132 morphants that did not exhibit hemorrhage, brain vascular integrity was also disrupted as evidenced by a significant increase of DAPI leakage from the brain vasculature (Supplementary information, Figure S3B and S3C; P < 0.01). [score:1]
Taken together, these results indicate that miR-132 is necessary for the integrity of the brain vasculature. [score:1]
More importantly, 17 out of 18 leakage events observed occurred at functional vessels which already exhibited blood flow (Figure 1F and Supplementary information, Figure S1J; data obtained from 9 miR-132 morphants). [score:1]
Then miR-132 gRNA was synthesized with MAXIscript T7 kit (Ambion, AM1312M) and purified with mirVana miRNA isolation kit (Ambion, AM1560). [score:1]
Page's trend tests were applied for examining whether there is an increasing trend in the level of miR-132 as the amount of exosomes increases in Figure 4D. [score:1]
[23]) or precursor miR-132 loop (“ miR-132 loop MO”, Supplementary information, Figure S1C). [score:1]
To examine the level of endothelial miR-132 after neuronal exosome treatment, b. End3 cells were incubated with the isolated neuronal exosomes at 37 °C for 24 h. The addition of exosomes isolated from 50 ml neuronal conditioned media into 0.5 ml ECs culture medium was counted as concentrating 100 times (100×). [score:1]
In addition, formulated nanoparticle -mediated miR-132 delivery into ECs can improve EC survival in vitro and EC transplantation efficiency in mice [56]. [score:1]
On the other hand, treatment with the eEF2K non-specific activator rapamycin (2 μM) led to intracranial hemorrhage in wildtype larvae (Figure 6F; P < 0.05) and further aggravated the hemorrhagic defect of miR-132 morphants (Figure 6F; P < 0.001). [score:1]
This suggested that the vascular leakage in brains of miR-132 morphants is due to defects in the integrity of brain vasculature. [score:1]
Next, by transfecting neurons with carboxyfluorescein (FAM)-tagged miR-132, we observed fluorescence -positive exogenous miR-132 in neuronal exosome -treated b. End3 cells (Figure 4G). [score:1]
These allowed us to determine that pericyte coverage was not significantly changed in miR-132 morphants (Figure 2G and 2H). [score:1]
In miR-132 rescue experiments, 8 ng miR-132 MO was co -injected with 20 nM miR-132 RNA or control RNA (Genepharma). [score:1]
Whole-mount in situ hybridizationZebrafish whole-mount in situ hybridization was performed as previously described 22, 62 with a digoxigenin-labeled miR-132 Locked Nucleic Acid (LNA) probe (5′-CGACCATGGCTGTAGACTGTTA -3′, Exiqon) and a scramble LNA probe (5′-GTGTAACACGTCTATACGCCCA-3′, Exiqon). [score:1]
At a system level, miR-132 is essential for experience -dependent structural and functional plasticity of the visual cortex 39, 40. [score:1]
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2
[+] score: 13
Other miRNAs from this paper: dre-mir-219-1, dre-mir-219-2, dre-mir-132-1, dre-mir-219-3
We show by qPCR that miR132 and miR219 are rhythmically expressed during zebrafish development (p<0.05; Figure 3A and 3B). [score:4]
tefα knock down does not significantly affect miR132 and miR219 expression levels, consistent with the absence of PARREs in their promoters (data not shown). [score:4]
miR219 and miR132 temporal expression pattern. [score:3]
0012542.g003 Figure 3(A) qPCR analysis showing the temporal oscillation of miR132 and (B) miR219 transcription during the first four days of development in embryos raised under a 12∶12 LD cycle. [score:2]
[1 to 20 of 4 sentences]
3
[+] score: 12
Following LH/hCG stimulation in the ovarian cells miR-132 and miR-212 were found to be highly up regulated and computational analysis has identified nearly 77 putative mRNA as potential targets of miR-212 and miR-132 in granulosa cells [60]. [score:4]
Besides their multiple roles in neuronal development, increasing evidence point towards an important involvement of miR-212 and miR-132 in mediating many other biological processes, including inflammation [52], immune function [53] and other cellular dysfunctions such as cancer. [score:2]
miR-212 and miR-132 are evolutionary conserved tandem miRNAs, well known for their essential role in the development, maturation and function of neurons [42]. [score:2]
Furthermore, recent evidence has demonstrated that miR-212 and miR-132 play an important role as post-transcriptional regulators in granulosa cells [60]. [score:2]
miR-212 and miR-132 are closely related as they have identical seed sequences and the mature miRNA differs only by four nucleotides. [score:1]
miR-212 arises from the miR-212/132 cluster (which comprises miR-212 and miR-132). [score:1]
[1 to 20 of 6 sentences]
4
[+] score: 3
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-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-218a-2, 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
Other miRNAs with expression in the retina include miR-454a (Figure C in5), miR-132 (Figure E in5), miR-125b (Figure F in5) and miR-181a (Figure G in3). [score:3]
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5
[+] score: 2
Other miRNAs from this paper: hsa-let-7a-1, hsa-let-7a-2, hsa-let-7a-3, hsa-let-7b, hsa-let-7e, hsa-mir-20a, hsa-mir-21, hsa-mir-23a, hsa-mir-24-1, hsa-mir-24-2, hsa-mir-26b, hsa-mir-27a, hsa-mir-29a, hsa-mir-31, hsa-mir-29b-1, hsa-mir-29b-2, hsa-mir-103a-2, hsa-mir-103a-1, hsa-mir-199a-1, hsa-mir-148a, hsa-mir-7-1, hsa-mir-7-2, hsa-mir-7-3, hsa-mir-10b, hsa-mir-181a-2, hsa-mir-181b-1, hsa-mir-181c, hsa-mir-199a-2, hsa-mir-199b, hsa-mir-203a, hsa-mir-204, hsa-mir-212, hsa-mir-181a-1, hsa-mir-221, hsa-mir-23b, hsa-mir-27b, hsa-mir-128-1, hsa-mir-132, hsa-mir-133a-1, hsa-mir-133a-2, hsa-mir-143, hsa-mir-200c, hsa-mir-181b-2, hsa-mir-128-2, hsa-mir-200a, hsa-mir-30e, hsa-mir-148b, hsa-mir-338, hsa-mir-133b, dre-mir-7b, dre-mir-7a-1, dre-mir-7a-2, dre-mir-10b-1, dre-mir-181b-1, dre-mir-181b-2, dre-mir-199-1, dre-mir-199-2, dre-mir-199-3, dre-mir-203a, dre-mir-204-1, dre-mir-181a-1, dre-mir-221, dre-mir-222a, 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-7e, dre-mir-7a-3, dre-mir-10b-2, dre-mir-20a, dre-mir-21-1, dre-mir-21-2, dre-mir-23a-1, dre-mir-23a-2, dre-mir-23a-3, dre-mir-23b, dre-mir-24-4, dre-mir-24-2, dre-mir-24-3, dre-mir-24-1, dre-mir-26b, dre-mir-27a, dre-mir-27b, dre-mir-29b-1, dre-mir-29b-2, dre-mir-29a, dre-mir-30e-2, dre-mir-101b, dre-mir-103, dre-mir-128-1, dre-mir-128-2, dre-mir-132-1, dre-mir-133a-2, dre-mir-133a-1, dre-mir-133b, dre-mir-133c, dre-mir-143, dre-mir-148, dre-mir-181c, dre-mir-200a, dre-mir-200c, dre-mir-203b, dre-mir-204-2, dre-mir-338-1, dre-mir-338-2, dre-mir-454b, hsa-mir-181d, dre-mir-212, dre-mir-181a-2, hsa-mir-551a, hsa-mir-551b, dre-mir-31, dre-mir-722, dre-mir-724, dre-mir-725, dre-mir-735, dre-mir-740, hsa-mir-103b-1, hsa-mir-103b-2, dre-mir-2184, hsa-mir-203b, dre-mir-7146, dre-mir-181a-4, dre-mir-181a-3, dre-mir-181a-5, dre-mir-181b-3, dre-mir-181d, dre-mir-204-3, dre-mir-24b, dre-mir-7133, dre-mir-128-3, dre-mir-7132, dre-mir-338-3
26 +2.14 miR-132 +1.83 (1.71e-3) +0.52 miR-2184 -2.63 (2.54e-5) -2.25 -2.50 miR-222a +1.54 (1.13e-2) +3.24 miR-24 -1.36 (1.9e-2) -1.41 -0.73 miR-454b +1.14 (4.93e-2) +0.14 miR-133a -1.72 (2.67e-3) -4.25 -5.07 miR-101b -2.52 (3.44e-5) -3.43 miR-338 -2.23 (1.90e-4) -2.90 -1.57 miR-26b -1.91 (1.84e-3) -3. 67 miR-204 -2.60 (4.76e-5) -0.57 -2.36 miR-203b -1.77 (3.45e3 -0.21 miR-10b -1.36 (2.90e-2) -1.78 miR-725 -1.29 (3.23e-2) -1.62 Zebrafish + Axolotl Zebrafish SymbolZebrafish log [2] Fold-change (p-value)Axolotl log [2] Fold-change SymbolZebrafish log [2] Fold-change (p-value) miR-27a +1.57 (7.96e-3) +2.15 miR-27b +1.38 (2.44e-2) miR-29b -2.05 (1.28e-2) -0.97 miR-143 +1.31 (2.89e-2) miR-30e +1.18 (4.80e-2) miR-200c -1.85 (1.72e-3) miR-200a -1.74 (3.66e-3) miR-23a -1.35 (2.05e-2) 10. [score:1]
26 +2.14 miR-132 +1.83 (1.71e-3) +0.52 miR-2184 -2.63 (2.54e-5) -2.25 -2.50 miR-222a +1.54 (1.13e-2) +3.24 miR-24 -1.36 (1.9e-2) -1.41 -0.73 miR-454b +1.14 (4.93e-2) +0.14 miR-133a -1.72 (2.67e-3) -4.25 -5.07 miR-101b -2.52 (3.44e-5) -3.43 miR-338 -2.23 (1.90e-4) -2.90 -1.57 miR-26b -1.91 (1.84e-3) -3. 67 miR-204 -2.60 (4.76e-5) -0.57 -2.36 miR-203b -1.77 (3.45e3 -0.21 miR-10b -1.36 (2.90e-2) -1.78 miR-725 -1.29 (3.23e-2) -1.62 Zebrafish + Axolotl Zebrafish SymbolZebrafish log [2] Fold-change (p-value)Axolotl log [2] Fold-change SymbolZebrafish log [2] Fold-change (p-value) miR-27a +1.57 (7.96e-3) +2.15 miR-27b +1.38 (2.44e-2) miR-29b -2.05 (1.28e-2) -0.97 miR-143 +1.31 (2.89e-2) miR-30e +1.18 (4.80e-2) miR-200c -1.85 (1.72e-3) miR-200a -1.74 (3.66e-3) miR-23a -1.35 (2.05e-2) 10. [score:1]
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6
[+] score: 1
Other miRNAs from this paper: hsa-mir-132, dre-mir-132-1
Furthermore, this pathway appears to be important for dendritic arborization where activity -dependent NMDAR activation of the γ isoform of CaMKI results in MEK/Erk -mediated CREB regulated transcription of Wnt-2 and microRNA132 [108]. [score:1]
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7
[+] score: 1
Other miRNAs from this paper: hsa-mir-210, hsa-mir-132, dre-mir-210, dre-mir-132-1
We also find sites close to mir210 and mir-132/212 which may be involved in the hypoxic response. [score:1]
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8
[+] score: 1
The induction of members of the miR-21, miR-29, and miR-146 families was in line with earlier microarray studies, which reported these along with some other miRNAs, like miR-9, miR-132, miR-147, and miR-155 as infection-inducible [13, 26, 43, 44]. [score:1]
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9
[+] score: 1
Likewise, miR-1, miR-124, miR-125b, miR-132, bantam, miR-34 and the miR-310 cluster have all been implicated in the modulation of synaptic homeostasis [70]– [76]. [score:1]
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