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6 publications mentioning dre-mir-141

Open access articles that are associated with the species Danio rerio and mention the gene name mir-141. Click the [+] symbols to view sentences that include the gene name, or the word cloud on the right for a summary.

[+] score: 114
Other miRNAs from this paper: dre-mir-429a, dre-mir-200a, dre-mir-200b, dre-mir-200c, dre-mir-429b
In contrast, embryos injected with miR-141/429a inhibitors showed only 5.3% increase in body length, because the expression change of GH/IGF axis genes was more remarkable in embryos treated with miR-141/429a mimics than with their inhibitors (Fig. 5E). [score:7]
As the results, ectopic expression of miR-141 resulted in a reduction expression of GH and GHRb to 12.8% and 17.6% at 24 hpf, 11.2% and 66.4% at 48 hpf (Fig. 2C), while miR-429a reduced the expression of GH, GHRa, GHRb and IGF2a to 62.3%, 37.1%, 59%, 72% at 24 hpf and 20%, 14%, 6.5%, 52.5% at 48 hpf (Fig. 2D) compared to the control microRNA mimic. [score:6]
The indicated concentration of control mimic and inhibitor were used as control for the miR-141/429a mimics and inhibitors, and they have no obvious toxic effect on the embryo development. [score:6]
Comparing with the control -mimic injected embryos (Fig. 4C-a), ectopic expression of miR-141/429a resulted in significantly higher level of apoptotic cells in brain and tails (Fig. 4C-b) that could be rescued by the miR-141/429a inhibitors (Fig. 4C-c). [score:5]
The cell apoptosis led by overexpression of miR-141/429a could be efficiently rescued by miR-141/429a inhibitors (Fig. 4C-d–f). [score:5]
Moreover, miR-141/429a inhibitors could rescue the defect of somatic growth resulted by miR-141/429a overexpression, whereas partially rescue the phenotype of pericardial edema (Fig. 3A). [score:5]
Co-injection of either 10 μM miR-141/429a with 40 μM inhibitor or 20 μM miR-141/429a with 80 μM inhibitor produced a statistically significant recovery in length to 3507 ± 103 μm or 3480 ± 73 μm. [score:5]
The expression levels of miR-141 and -429a were efficiently reduced to 51.59% and 23.98% by inhibitors (Fig. 5D). [score:5]
Ectopic expression of miR-141/429a mimics lead to pericardial edema in zebrafish embryos, which could be partially rescued by miR-141/429a inhibitors (Fig. 3A). [score:5]
Apart from inhibiting body growth in embryo, overexpression of miR-141/429a resulted in cell cycle arrest and cell apoptosis (Fig. 4). [score:5]
Finally, an average length of 3529 ± 76 μm (80 μM control inhibitor injection) were elevated to 3717 ± 64 μm by injection of 80 μM miR-141/429a inhibitors, for a 5.3% increase in body length. [score:5]
Accordingly, we detected that expression of miR-141 and miR-429a were increased by injection of p53 mRNA into zebrafish embryos compared to the control groups (Fig. 6C), whereas the GH mRNA was reduced by ectopic expression of p53 (Fig. 6D). [score:4]
The results in our study suggest that over -expression of miR-141/429a may affect embryo heart development. [score:4]
However, injection of miR-141/429a inhibitors did not cause any observable developmental defects in zebrafish embryos, that was the same phenotype as injection of morpholinos of miR-200 family members 35 36. [score:4]
miR-141/429a repressed the luciferase activity of GH 3′ UTR-pmirGLO, whereas mutation of either predicted miR-200a/141 or miR-200b/200c/429a/429b binding site attenuated this repression, and mutation in both binding sites abrogated this repression (Fig. 5A). [score:3]
To check the expression of miR-200 family members during normal embryonic development, we synthesized cDNA with a mixture of stem-loop RT primers of miR-141/200a, miR-429a/429b and miR-200b/200c, respectively. [score:3]
For the following experiments, miR-141 and miR-429a mimics or inhibitors were 1:1 mixed to give working solutions. [score:3]
Among all three binding sites of miR-200s in GHRb gene, mutation of either binding site 1 or 3 attenuated the repression of luciferase activity by miR-141/429a, and mutation in both binding sites 1 and 3 abrogated this repression (Fig. 5B). [score:3]
In comparison to the control, overexpression of miR-141/429a increased percentage of cells in G1 (approximately 10.67%) and reduced percentages of cells in S (approximately 5.26%) and G2/M (about 5.42%) (Fig. 4A,B). [score:3]
To examine the ability of miR-200s inhibitors to repress miR-200s levels in vivo, we injected zebrafish embryos with anti-miR-141, anti-miR-429a or a scrambled control. [score:3]
Moreover, the inductions of both miR-141 and miR-429a by GH injection were abrogated in p53 mutant embryos, suggesting that p53 is necessary for the increased miR-200s expression by GH activation in zebrafish embryos. [score:3]
Taken together, our observations suggest that miR-141/429a inhibits cell proliferation and induces cell apoptosis. [score:3]
Moreover, the miR-141/429a inhibitors could efficiently rescue the defects of cell cycle arrest. [score:3]
Ectopic expression of miR-141/429a led to pericardial edema in the embryos. [score:3]
Dose -dependent suppression of somatic growth was clearly observed in miR-141/429a injected embryo at 72 hpf (Fig. 3B). [score:3]
At 72 hpf, over -expression of miR-141/429a dramatically reduced body length when compared to control mimic -injected embryos that have similar body length to the uninjected embryos. [score:2]
Further, whole-mount in situ hybridization at 48 hpf demonstrated a dramatic reduction of GH mRNA in pituitary following miR-141/429a injection (Fig. 2E,F). [score:1]
By analysis, we observed a reduction of GH protein in the zebrafish embryos subjected to miR-141/429a injection (Fig. 2G). [score:1]
In mammals, miR-141 and miR-200c co-existed in one gene cluster without miR-429, whereas miR-429b, another duplicated copy of miR-429 appears in zebrafish and co-existed with miR-141/200c in chromosome 6 (Fig. 1A). [score:1]
Moreover, IGF1, a major downstream mediator of the growth hormone pathway, was also significantly reduced by both miR-141 and miR-429a (Fig. 2C,D). [score:1]
Notably, both miR-141 and miR-429a were increased after GH injection (Fig. 6E). [score:1]
Injection of synthetic miR-141 and -429a mimic significantly increased the level of miR-141 and -429a transcript present (Fig. 2B). [score:1]
Moreover, the mRNA levels of GH, GHRa, GHRb, IGF2a and IGF1 were significantly elevated when miR-141/429a was repressed (Fig. 5E). [score:1]
An average body length of 3543 ± 94 μm (10 μM control miRNA mimic injection) and 3524 ± 94 μm (20 μM control miRNA mimic injection) were reduced to 3131 ± 140 μm (11.7% decrease in body length) and 2938 ± 136 μm (16.7% decrease in body length) by injection of 10 μM and 20 μM miR-141/429a, respectively (Fig. 3B). [score:1]
[1 to 20 of 34 sentences]
[+] score: 26
Other miRNAs from this paper: mmu-let-7g, mmu-let-7i, mmu-mir-124-3, mmu-mir-140, mmu-mir-141, mmu-mir-152, mmu-mir-182, mmu-mir-183, mmu-mir-191, mmu-mir-199a-1, mmu-mir-200b, mmu-mir-205, mmu-let-7d, mmu-mir-200a, mmu-let-7a-1, mmu-let-7a-2, mmu-let-7b, mmu-let-7c-1, mmu-let-7c-2, mmu-let-7e, mmu-let-7f-1, mmu-let-7f-2, mmu-mir-96, mmu-mir-200c, mmu-mir-214, mmu-mir-199a-2, mmu-mir-199b, mmu-mir-124-1, mmu-mir-124-2, mmu-mir-7a-1, mmu-mir-7a-2, mmu-mir-7b, dre-mir-7b, dre-mir-7a-1, dre-mir-7a-2, dre-mir-182, dre-mir-183, dre-mir-199-1, dre-mir-199-2, dre-mir-199-3, dre-mir-205, dre-mir-214, dre-mir-430a-1, dre-mir-430b-1, dre-mir-430c-1, mmu-mir-429, mmu-mir-449a, dre-mir-429a, 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-96, 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-140, dre-mir-152, dre-mir-200a, dre-mir-200b, dre-mir-200c, 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, mmu-mir-449c, mmu-mir-449b, dre-mir-429b, mmu-let-7j, mmu-let-7k, mmu-mir-124b
Embryos injected with either miR-141/miR-200a or miR-200b/miR-429 pairs of antisense morpholinos showed lack of expression of the corresponding miR-200 members with a given 5′ seed but did not display any change in OMP expression relative to wild-type controls (data not shown). [score:5]
Finally, 8 of 24 miRNA probes, including miR-200a and miR-200b, as well as miR-96, miR-141, miR-182, miR-183, miR-191, and miR-429, revealed robust expression in the MOE and VNO neuroepithelium, with weaker expression in the adjacent respiratory epithelium (Figure 2A, right column, and Table S3). [score:5]
In addition, in situ hybridization analyses (Figure 7C) show that a mixture of all three morpholinos (Triple MO mix: miR-141 MO, miR-200b MO, and miR-429 MO) was sufficient to simultaneously inhibit the expression of all five mature zebrafish miR-200 family members to threshold levels of detection. [score:5]
As predicted from sequence analyses and thermal stability calculations, miR-141 MO specifically inhibited miR-200a and miR-141, miR-200b MO specifically inhibited miR-200b and miR-200c, and miR-429 MO specifically inhibited miR-429 (Figure S4B). [score:5]
However, miR-141 and -200a express different 5′ seed heptamers from miR- 200b, -200c, and -429 and are thus likely to form two functional subgroups within the miR-200 family (Figure 2C; Doench and Sharp, 2004; Lewis et al., 2005). [score:3]
One of these families, miR-200 family comprising miR-200a, miR-200b, miR-200c, miR-429, and miR-141, also highly detected by microarray, was among the most frequently cloned species in all olfactory tissues examined (Table S2). [score:1]
In mouse, the miR-200 family is composed of five family members (miR-141, -200a, -200b, -200c, -429) clustered into two loci of chromosomes 4 and 6 (Figure 2C). [score:1]
In order to test the specificity of each morpholino (MO) sequence, we systematically injected one-cell zebrafish embryos with either miR-141 MO, miR-200b MO, or miR-429 MO and performed in situ hybridization against all five miRNAs of the miR-200 family. [score:1]
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[+] score: 26
Other miRNAs from this paper: hsa-let-7a-1, hsa-let-7a-2, hsa-let-7a-3, hsa-let-7b, hsa-let-7c, hsa-let-7d, hsa-let-7e, hsa-let-7f-1, hsa-let-7f-2, hsa-mir-96, mmu-let-7g, mmu-let-7i, mmu-mir-124-3, mmu-mir-9-2, mmu-mir-141, mmu-mir-152, mmu-mir-182, mmu-mir-183, mmu-mir-199a-1, hsa-mir-199a-1, mmu-mir-200b, mmu-mir-205, hsa-mir-7-1, hsa-mir-7-2, hsa-mir-7-3, hsa-mir-182, hsa-mir-183, hsa-mir-199a-2, hsa-mir-199b, hsa-mir-205, hsa-mir-214, hsa-mir-200b, mmu-let-7d, mmu-mir-130b, hsa-let-7g, hsa-let-7i, hsa-mir-124-1, hsa-mir-124-2, hsa-mir-124-3, hsa-mir-141, hsa-mir-152, hsa-mir-9-1, hsa-mir-9-2, hsa-mir-9-3, mmu-mir-200a, mmu-let-7a-1, mmu-let-7a-2, mmu-let-7b, mmu-let-7c-1, mmu-let-7c-2, mmu-let-7e, mmu-let-7f-1, mmu-let-7f-2, mmu-mir-96, hsa-mir-200c, mmu-mir-200c, mmu-mir-214, mmu-mir-199a-2, mmu-mir-199b, mmu-mir-124-1, mmu-mir-124-2, mmu-mir-9-1, mmu-mir-9-3, mmu-mir-7a-1, mmu-mir-7a-2, mmu-mir-7b, hsa-mir-200a, hsa-mir-130b, hsa-mir-376a-1, mmu-mir-376a, dre-mir-7b, dre-mir-7a-1, dre-mir-7a-2, dre-mir-182, dre-mir-183, dre-mir-199-1, dre-mir-199-2, dre-mir-199-3, dre-mir-205, dre-mir-214, hsa-mir-429, mmu-mir-429, hsa-mir-450a-1, mmu-mir-450a-1, dre-mir-429a, 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-96, 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-130b, dre-mir-152, dre-mir-200a, dre-mir-200b, dre-mir-200c, hsa-mir-450a-2, dre-let-7j, hsa-mir-376a-2, mmu-mir-450a-2, dre-mir-429b, mmu-let-7j, mmu-let-7k, mmu-mir-9b-2, mmu-mir-124b, mmu-mir-9b-1, mmu-mir-9b-3
We found eight miRs differentially expressed, six down-regulated (miR-9, miR-141, miR-200a, miR-200b, miR-429 and miR-376a) and two up-regulated (miR-450a-5p and miR130b*) in the Dlx5 [−/−] OE (Fig.  1a). [score:9]
We observed a reduction of miR-9, miR-141 and miR-429 signal in the Dlx5 [−/−] OE, compared to the WT (Fig.  1c), while hybridization with two positive controls, Sp8 (expressed in the OE) and Sox5 (expressed in chondrogenic condensations), yielded an equivalent positive signal in both genotypes, indicating adequate RNA preservation. [score:4]
For miR-141/ 200a, the enriched categories included regulation of cell differentiation, neurogenesis, development and regulation of transcription (Suppl. [score:4]
miR-200a, miR-200b, miR-141 and miR-429 share the same seed sequence and likely target the same mRNAs; for this reason they are grouped in a single miR class (named miR-200-class). [score:3]
As a further confirmation, we carried out in situ hybridization on sections of WT and Dlx5 [−/−] embryonic OE, at the age E12.5, to detect miR-9, miR-141 and miR-429, using specific mouse DIG -labelled probes. [score:1]
The miR-200a, - 200b and - 429 loci are closely located on chromosome 4, while miR-141 and -200c are closely located on chromosome 6. miR-376a is clustered with 16 other miRs on chromosome 12. [score:1]
Since miR-200a, miR-200b, miR-141 and miR-429 share very similar seed sequences (Suppl. [score:1]
No Dlx5 binding site was predicted within a 50 kb range from the miR-9.1, miR-141, miR-200c and miR-376a loci. [score:1]
Hybridization was carried out with DIG -labelled riboprobes that specifically detect the mature form of mouse miR-9 and miR-141 (Exiqon) in according with manufactory instruction. [score:1]
We carried out the same prediction and categorization analyses for the miR of the -200 class; in this case the two subfamilies (miR-141/ 200a and miR-200b/ c/ 429/ 548a) were examined separately, and indeed yielded lists which were similar but not identical. [score:1]
[1 to 20 of 10 sentences]
[+] score: 23
B, shown is a time series qRT-PCR data of miR-141 and miR-200b expression in zeb1b -overexpressing embryos (left side; injected with 100 pg zeb1b mRNA and 30 pg gfp mRNA) or zeb1a/b double morphants (right side; injected with 4 ng zeb1a/b TBMO) relative to control embryos (left side; injected with 130 pg gfp mRNA; right side; injected with 4 ng SCMO). [score:5]
Expression of miR-141 and -200b was significantly decreased in zeb1b -overexpressing embryos compared with control siblings during gastrulation and early segmentation. [score:4]
We measured the expression of miR-141 and miR-200b, located in the two different miR-200 family clusters, in zeb1b -overexpressing embryos and zeb1a/b morphants by qRT-PCR. [score:3]
To investigate their functional relevance, we generated miR-200 morphants by injection of a triple anti-miR-200 MO mix (miR-141 MO, miR-200b MO, and miR-429 MO) that was shown to efficiently knockdown all five members of the miR-200 family (23) and controlled our knockdown experiment for the absence of expression of these by whole-mount ISH of 2-day-old embryos (data not shown). [score:3]
miR-141 and miR-200b expression in control embryos was set to 1 (n = 4 per condition; values represent the mean ± S. E. ). [score:3]
To verify the efficacy of anti-miR-200 family MOs, one-cell stage embryos were injected with an anti-miR-200 MO mix (miR-141, -200b, -429) or SCMO, fixed at 48 h post fertilization (hpf), and assayed for miR-141, 200a/b/c, and -429 expression by whole-mount ISH. [score:2]
miR-200c and miR-141 map closely on chromosome 6, and the stem-loop sequences are separated by a 118-base pair spacer sequence. [score:1]
MOs against the miR-200 family are as published (23): anti-miR-141 (5′-GCA TCG TTA CCA GAC AGT GTT A-3′), anti-miR-200b (5′-GTC ATC ATT ACC AGG CAG TAT TA-3′), and anti-miR-429 (5′-ACGGCATTACCAGACAGTATTA-3′). [score:1]
Finally, we show that Zeb1b represses transcription of miR-141 and -200b, two members of the miR-200 family. [score:1]
[1 to 20 of 9 sentences]
[+] score: 8
The family of microRNAs 200 (miR-200a, miR-200b, miR-200c, miR-141 and miR-429) and the miR-205A regulate the expression of the transcriptional repressors of E-cadherin ZEB-1 and ZEB-2 and, consequently, the levels of E-cadherin in breast cancer cells and tissues. [score:4]
Regulation of miR-200c, miR-141 and miR-205 by ERβ1. [score:2]
The figure shows the regulation of miR-200c, miR-141 and miR-205 by ERβ1. [score:2]
[1 to 20 of 3 sentences]
[+] score: 5
Notably, cardiac-specific miR-1, miR-133, miR-208 and miR-499 were all suppressed by two or more orders of magnitude [34], [35], as were the stemness and cell cycle repressors miR-141 and miR-137 [36]; in contrast, the proliferative miRNAs, miR-222 [37], increased dramatically in MDCs, and miR-221 was undetectable in myocytes but highly expressed in MDCs (Figure 5D). [score:5]
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