sort by

14 publications mentioning rno-mir-433

Open access articles that are associated with the species Rattus norvegicus and mention the gene name mir-433. Click the [+] symbols to view sentences that include the gene name, or the word cloud on the right for a summary.

1
[+] score: 182
Thus, the expression of human miR-127 was ∼20 times higher than human miR-433, the expression of rat miR-127 was ∼47 times higher than rat miR-433, and the expression of dog miR-127 was ∼40 times higher than dog miR-433. [score:7]
Similarly, the rat miR-433 and miR-127 was ∼210 fold and ∼10000 fold ovexpressed (Figure 6f) and the dog miR-433 and miR-127 was ∼4 fold and ∼160 fold ovexpressed (Figure 6g), respectively. [score:5]
0007829.g005 Figure 5(a) The miR-433/127 loci expression plasmid of human, rat, or dog was expressed in mouse Hepa-1 cells (different species), and the binding of ERRγ to the endogenous promoter of miR-433 and of miR-127 of each species was detected using specific ERRγ antibodies. [score:5]
We next determined expression levels of the mature miR-433 and miR-127 in Hepa-1 cells after recombinant vector over -expression. [score:5]
Artificial Expression of miR-433 and miR-127 In Vitro in CellsOur previous studies showed that the mouse miR-433 and miR-127 genes overlapped and the expression of mouse miR-433 and miR-127 was controlled by independent promoters [3], [4]. [score:5]
The miR-433/127 loci cloned from human, rat, or dog was overexpressed in mouse Hepa-1 cells by transfection of an expression plasmid containing the loci of each species (Figure S2, see below description), respectively. [score:5]
Potential PCR amplification from genomic DNA contamination was eliminated by treating the total RNA with DNase I. As shown in Figures 6a–c, primary transcripts of the human (a), rat (b), or dog (c) miR-433 and miR-127 were easily detected in cells that over-expressed the recombinant expression vector, respectively. [score:5]
The recombinant human, rat, or dog miR-433/127 loci expression vector (designated pMIR-REPORT-NoMp-human, rat or dog) was then transfected into Hepa-1 cells and the expression of miR-433 and miR-127 primary transcripts was examined using semi-quantitative RT-PCR. [score:5]
For instance, if mutations occurred in the region between pre-miR-433 and pre-miR-127, it would be likely to affect both the processing of mature miR-433 and the regulation of miR-127 expression. [score:5]
0007829.g006 Figure 6(Panels a–c) Semi-quantitative RT-PCR analysis of pri-miR-433 and pri-miR-127 expression transcribed from the human (a), rat (b), and dog (c) miR-433/127 loci expression plasmid. [score:5]
Our studies provide evidence for a conserved gene structure and ERR/SHP dependent regulation of miR-433 and miR-127 gene expression in mammals. [score:4]
Based on this information, we made a direct comparison between the expression level of miR-433 and miR-127. [score:4]
Based on the identification of the same binding motifs, we predicted that a common regulatory mechanism of miR-433 and miR-127 expression may exist among different mammalian species. [score:4]
Compared with non-vector transfected cells, the human miR-433 was ∼100 fold over-expressed whereas the human miR-127 was ∼2000 fold over-expressed (Figure 6e). [score:4]
These results suggest that the expression of miR-433/127 is not only under transcriptional control as elucidated in our previous [3], [4] and the present study, but also subjects to epigenetic regulation. [score:4]
We recently have shown that gene expression of miR-433 and miR-127 in mice was regulated via a nuclear receptor ERRγ/SHP dependent mechanism [4]. [score:4]
Figure S2 Procedures for cloning the miR-433/127 loci expression vector of human, rat, or dog. [score:3]
In order to avoid the effect of endogenous miR-127 and miR-433 primary transcripts in Hela cells, we overexpressed the pMIR-Report human433/127 loci, pMIR-Report rat433/127 loci, and pMIR-Report dog433/127 loci in Hepa1 cells. [score:3]
This would allow us to determine if the transcriptional expression of miR-433 or miR-127 could be driven by its own promoter from the endogenous miR-433/127 loci. [score:3]
Our previous studies showed that the mouse miR-433 and miR-127 genes overlapped and the expression of mouse miR-433 and miR-127 was controlled by independent promoters [3], [4]. [score:3]
On the other hand, we observed a common transcriptional mechanism governing the expression of miR-433 and miR-127 in mammals, which involved ERR family members and orphan receptor SHP. [score:3]
Due to high expression of primary transcript of miR-433 and mIR-127, different PCR cycles were used (see Figure 6). [score:3]
In addition, the expression level of pri-miR-433 was markedly lower than that of pri-miR-127 (Figure 6d) in all three species, suggesting pri-miR-433 and pri-miR-127 were transcribed differentially from an independent transcription unit. [score:3]
Transcriptional expression of miR-433 and miR-127 from the miR-433/127 loci in human, rat, and dog. [score:3]
Artificial Expression of miR-433 and miR-127 In Vitro in Cells. [score:3]
As expected, ERRγ dose -dependently activated promoters of miR-433 and miR-127 of human (Figure 4a), rat (Figure 4b), and dog (Figure 4c), which was repressed by co -expression of SHP. [score:3]
These differential expression results provided further evidence that miR-433 and miR-127 produced from the miR-433-127 loci were transcribed from two separate promoters in human, rat, and dog. [score:3]
However, the question remains to be determined whether molecular details of miR-433 and miR-127 regulation by ERR/SHP are restricted to mouse or whether they apply to other species. [score:2]
In conclusion, our studies for the first time provide evidence for a conserved structure and transcriptional regulation of the clustered miR-433 and miR-127 genes in mammals, including humans. [score:2]
Common Regulation of miR-433 and miR-127 Promoter Activity among Mammalian Species. [score:2]
Primers used to determine the expression of primary transcripts of miR-433 and of miR-127 are located surrounding the precursors of miR-433 and of miR-127. [score:2]
We elucidated a common regulatory mechanism governing miR-433 and miR-127 promoter activities, which was dependent on nuclear receptor estrogen related receptor gamma (ERRγ, NR3B3) and small heterodimer partner (SHP, NR0B2) [4]. [score:2]
Our published results showed that miR-433 and miR-127 genes are overlapped in a 5′–3′ unidirectional way in mouse [3] and these two non-coding genes have an antisense transcript, RTL1 [19]. [score:2]
The expression level of primary transcript of miR-433 and miR-127 was determined by semi-quantitative PCR using primers listed in Supplementary Material Table S3. [score:2]
The conservation of the transcriptional regulation of miR-433 and miR-127 further supports the notion that the miR-433/127 loci in mammals might be evolved from an ancient common origin. [score:2]
Table S1 Primers used to generate miR-433/127 loci expression vector. [score:2]
We recently have reported that the full length primary transcripts of mouse miR-433 and miR-127 overlapped in a 5′–3′ unidirectional way [3]. [score:2]
In this study, we used pMIR-Report-human 433/127, pMIR-Report-rat433/127, pMIR-Report-dog433/127 plasmids as the standard template to determine the PCR efficiency, then compared the expression level of miR-433 and miR-127 primary transcripts. [score:2]
Our results presented in this study provide evidence that the miR-433 and miR-127 overlapping genes have a higher rate of conservation in mammalian species. [score:1]
ERRγ was co-immunoprecipitated on the ERRE containing the endogenous promoter regions of miR-433 and miR-127 in the liver of human and rat, and dog spleen, respectively (Figure 5b). [score:1]
Although the miR-433/127 loci were located on different chromosomes (Chr) in those species (human, Chr 14; Chimpanzee, Chr14; Horse, Chr 24; Dog, Chr 8; Monkey, Chr 7; Rat, Chr 6; Cow, Chr 21; mouse, Chr 12), multiple sequence alignment (MSA) of the precursors, pre-miR-433 and pre-miR-127, showed that the sequence similarity of pre-miR-433 hairpins was ∼95% (Figure 1a) and of pre-miR-127 was 100% (Figure 1b) among those species. [score:1]
BLASTN search of genome sequences of different species was completed online and a 5 kb genomic sequence surrounding the miR-433 and miR-127 precursors in each species was extracted manually. [score:1]
Finally, the long DNA fragments containing human, rat or dog miR-433 and miR-127 loci were inserted into Asc I and Pac I sites of pMIR-REPORT-NoMp. [score:1]
Comparison of Gene Structure of miR-433/127 Loci from Different Mammalian Species. [score:1]
Why is the miR-433 and miR-127 overlapping gene structure in mammalian species so conserved? [score:1]
Using mouse miR-433 and miR-127 precursor hairpin structure sequences as a query, we searched the genome databases of seven other species, including human, chimpanzee, horse, dog, monkey, rat, and cow. [score:1]
Representative common TF binding motifs (1°∼4°) are shown, and their positions appear to be conserved in the promoter region of miR-433 and of miR-127 among different species. [score:1]
MatInspector of Genomatix Software Suite was used to predict the transcription factor binding sites in the promoter regions of miR-433 and miR-127 in different species, which was completely using Default parameters (http://www. [score:1]
The conservation of pre-miR-433 and pre-miR-127 hairpin sequences as well as the distance between them among different mammalian species raised the possibility that miR-433 and miR-127 might be evolved from the same DNA origin during evolution. [score:1]
The promoter of pri-miR-433 and of pri-miR-127 from each species was cloned into a pGL3-basic vector, respectively. [score:1]
Conserved response elements in the promoters of miR-433 and miR-127 of eight mammalian species. [score:1]
Unique potential binding motifs were also identified in the promoter region of miR-433 and of miR-127 in each species. [score:1]
Multiple sequence alignment (MSA) of miR-433 and miR-127 precursor hairpin sequences in eight mammalian species. [score:1]
zFive µg of recombinant plasmid of miR-433/127 loci of human, rat and dog was transfected into Hepa-1 cells, respectively. [score:1]
Predicted ERRE sites on the miR-433 and miR-127 gene promoters. [score:1]
Based on their overlapping gene structure and transcriptional initiation and termination sites, we subsequently cloned promoters of miR-433 and miR-127. [score:1]
The precursor sequences of miR-433 and miR-127 were downloaded from the Sanger Institute (http://microrna. [score:1]
MSA of miR-433 and miR-127 gene promoters in eight mammalian species. [score:1]
Transient transfection assays to determine ERRγ and SHP regulation of miR-433 and miR-127 promoter (pro. ) [score:1]
0007829.g002 Figure 2 (a) MSA of sequences 2 kb before pre-miR-433. [score:1]
The sequence similarity in either the miR-433 promoter region (Figure 2a) or the genomic region between pre-miR-433 and pre-miR-127 (Figure 2b) was low among the eight species. [score:1]
To further confirm this result, the direct association of ERRγ with miR-433 and miR-127 promoters of each species in vivo was assessed using ChIP assays. [score:1]
Semi-Quantitative RT-PCR for miR-433 and miR-127 Primary Transcripts. [score:1]
This resulted in the cloning of the gene cluster encoding mouse miR-433 and miR-127, which provided the first report for an overlapping code usage of the paired miR-433/127 gene [3]. [score:1]
Promoter analysis of miR-433 and miR-127 luciferase reporters of human, rat and dog. [score:1]
0007829.g001 Figure 1(a) Pre-miR-433 alignment in eight different species. [score:1]
In the present study, we analyzed genes encoding miR-433 and miR-127 and determined the promoter transactivation of miR-433 and miR-127 from other mammalian species, including humans. [score:1]
The promoters of pri-miR-433 and pri-miR-127 were cloned into a pGL3-basic vector, respectively. [score:1]
We used MatInspector of Genomatix Software Suite to identify transcription factor binding motifs and position preference in the upstream promoter regions of miR-433 and of miR-127 in eight mammalian species. [score:1]
The mature sequences of miR-433 and miR-127 were identical among the eight species. [score:1]
The promoters of miR-433 and miR-127 from human, rat and dog were cloned into a pGL3 basic vector, respectively. [score:1]
Figure S1 Transient transfection assays to determine ERRα and ERRβ regulation of miR-433 and miR-127 promoter (pro. ) [score:1]
To determine if miR-433 and miR-127 in human, rat, and dog can be independently and differentially transcribed using each miRNA's own promoter, we cloned a large (∼4.5 kb) human, rat, or dog genomic DNA fragment containing miR-433 and miR-127 and their promoter regions into pMIR-REPORT vector (Figure S2). [score:1]
Based on the above gene structure analysis and sequence prediction referenced from our published mouse data [3], [4], we hypothesized that the genomic location of promoters of miR-433 and miR-127 was similar in other mammalian species as in mouse. [score:1]
ChIP analysis of ERRγ Co-immunoprecipitation (Co-IP) on the miR-433 and miR-127 promoter region containing putative ERRE in human, rat, and dog. [score:1]
Conserved Transcription Factor Binding Motifs in the Upstream Region of miR-433 and of miR-127 among Mammalian Species. [score:1]
The 4.5 kb genomic sequences centered miR-433 and miR-127 were extracted. [score:1]
We found that miR-433 and miR-127 had almost identical PCR amplification efficiency (Supplementary Material Table S4). [score:1]
The distance between miR-433 and miR-127 showed a striking similarity: 986 bp in human, chimpanzee, horse, dog, and monkey, 989 bp in rat, 988 bp in cow, and 1007 bp in mouse. [score:1]
0007829.g004 Figure 4Transient transfection assays to determine ERRγ and SHP regulation of miR-433 and miR-127 promoter (pro. ) [score:1]
As shown in Figure 5, ERRγ was found to Co-IP on both the miR-433 and miR-127 promoters of human, rat, or dog. [score:1]
Five µg of pMIR-REPORT-NoMp vector containing miR-433/127 loci of human, rat or dog, respectively, was transfected into Hepa-1 cell on 60 mm culture plate. [score:1]
Although the miR-433/127 gene loci was located on different chromosomes in different species, the distance between miR-433 and miR-127 is very similar, which is ∼1 kb. [score:1]
We cloned the promoters of miR-433 and miR-127 into pGL3 luciferase reporters using genomic DNAs isolated from liver specimens of human, rat and dog. [score:1]
ERRa, but not ERRβ, showed strong activation of miR-433 and miR-127 promoters of human, rat, and dog (Figure S1). [score:1]
The response elements of the miR-433 and miR-127 genes from eight different species are illustrated. [score:1]
0007829.g003 Figure 3 The response elements of the miR-433 and miR-127 genes from eight different species are illustrated. [score:1]
It has been reported that the miR-433/127 locus is located in the imprinted region Dlk1/Gtl2 and transcribed in an antisense orientation to a retrotransposon-like gene Rtl1 [21]– [24]. [score:1]
Despite lower sequence similarity, analysis of miR-433 and miR-127 promoters of those species predicted common nuclear receptor binding sites, including ERRE (Figure 3 and Table 1). [score:1]
[1 to 20 of 89 sentences]
2
[+] score: 132
These results demonstrated that both miR-21-3p and miR-433 can regulate FSHb expression by directly binding to the FSHb 3′UTR and inhibiting the FSHb expression levels through the degradation of mRNA and inhibition of translation. [score:13]
To determine the transfection efficiency achieved with a 100 nM concentration of the negative controls, mimics, inhibitor negative controls and inhibitors of miR-21-3p and miR-433, we measured the expression levels of the two miRNAs, and the results showed that transfection of the miR-21-3p mimic significantly increased the expression level of miR-21-3p, whereas transfection of the miR-21-3p inhibitor significantly decreased the expression level of miR-21-3p (Figure 4E). [score:11]
To examine whether the silencing of FSHb is mediated by the specific, direct interaction of miR-21-3p and miR-433 with the FSHb target site, we predicted the respective target positions of the two miRNAs in the FSHb 3′UTR using the TargetScan program (Figures 3A and 3B), and we then mutated the complementary sites of the two miRNA seed regions to generate pmiR-FSHb-3′UTR-MUT and pmiR-FSHb-3′UTR-MUT1 (Supplementary File 3). [score:8]
Validation of the interaction between the miRNAs and FSHb in vitroTo examine whether the silencing of FSHb is mediated by the specific, direct interaction of miR-21-3p and miR-433 with the FSHb target site, we predicted the respective target positions of the two miRNAs in the FSHb 3′UTR using the TargetScan program (Figures 3A and 3B), and we then mutated the complementary sites of the two miRNA seed regions to generate pmiR-FSHb-3′UTR-MUT and pmiR-FSHb-3′UTR-MUT1 (Supplementary File 3). [score:8]
Furthermore, miR-433 inhibits retinoblastoma by suppressing the expression levels of notch homolog 1 (Notch1) and paired box protein Pax-6 (PAX6) [48]. [score:7]
In another study, Xiao-chun Wang et al. observed that miR-433 acts as a tumor suppressor and inhibits oral squamous cell carcinoma (OSCC) cell growth, invasion and migration by targeting histone deacetylase 6 (HDAC6) [47]. [score:7]
Taken together, our results show that both miR-21-3p and miR-433 down-regulate FSHb expression and cause FSH secretion decreased. [score:6]
We then randomly selected two miRNAs from the set of 13 down-regulated miRNAs (miR-21-3p and miR-433) for subsequent analysis, and the results suggested that miR-21-3p and miR-433 down-regulated FSHb in the sexual maturity stage compared with the non-sexual maturity stage (Figures 2C and 2D). [score:6]
Figure 5 (A-B) Rat anterior pituitary cells were transfected with mimic negative controls (NC), mimics, inhibitor negative controls (I-NC) and inhibitors of miR-21-3p and miR-433. [score:5]
Rat anterior pituitary cells were transfected with the mimic negative controls (NC), mimics, inhibitor negative controls (I-NC) and inhibitors of miR-21-3p and miR-433. [score:5]
We then used a screening system based on the luciferase reporter plasmid carrying the full-length 3′UTR of the FSHb mRNA and found that 18 miRNAs, specifically miR-433-3p, miR-323-3p, miR-328a-3p, miR-3573-3p, miR-204-5p, miR-206-5p, miR-31a-5p, miR-7a-5p, miR-880-3p, miR-186-5p, miR-503-5p, miR-383-5p, miR-324-5p, miR-505-5p, miR-27b-3p, miR-221-5p, miR-320-3p and miR-21-3p, could suppress the expression of the reporter by more than 30% (Figure 1). [score:5]
We observed a similar pattern for miR-433: the expression level was significantly increased in the mimic group and significantly decreased in the inhibitor group (Figure 4F). [score:5]
However, our results show that miR-433 can regulate the FSHb expression levels, which provides data on the regulation of hormone secretion in the pituitary by miRNAs. [score:5]
Moreover, a 0.74-fold decrease (P<0.05) in the FSHb expression level was observed after transfection with the miR-433 mimic, and a 1.37-fold increase (P<0.05) was detected after transfection with the miR-433 inhibitor (Figure 5B). [score:5]
Therefore, the results suggested that miR-21-3p and miR-433 can regulate the expression of FSHb. [score:4]
miR-21-3p- and miR-433 -mediated regulation of the FSHb expression levels in and FSH secretion by rat primary pituitary cells. [score:4]
To verify that both miR-21-3p and miR-433 target the FSHb gene and to gain further insights into their regulation of reproduction, we measured the expression levels of FSHb in rat primary anterior pituitary cells by quantitative RT-PCR and the secretion of FSH by these cells through ELISA. [score:4]
35 rno-miR-383-5p 820-826 7mer-1A −0.11 rno-miR-409a-5p 639-645 7mer-1A −0.19 rno-miR-433-3p 1044-1050 7mer-m8 −0.14 rno-miR-449c-3p 674-680 7mer-m8 −0.13 rno-miR-503-5p 763-769 7mer-1A −0.22 rno-miR-505-5p 111-117 7mer-1A −0.14 rno-miR-7a-5p 572-578 7mer-1A −0.01 rno-miR-880-3p 586-592 7mer-1A −0.11 rno-miR-9a-3p 272-278 7mer-1A −0.1 Figure 1Effects of the predicted 45 miRNAs on the reporter gene expression of the pmiR-FSHb-3′UTR-WT vector. [score:3]
35 rno-miR-383-5p 820-826 7mer-1A −0.11 rno-miR-409a-5p 639-645 7mer-1A −0.19 rno-miR-433-3p 1044-1050 7mer-m8 −0.14 rno-miR-449c-3p 674-680 7mer-m8 −0.13 rno-miR-503-5p 763-769 7mer-1A −0.22 rno-miR-505-5p 111-117 7mer-1A −0.14 rno-miR-7a-5p 572-578 7mer-1A −0.01 rno-miR-880-3p 586-592 7mer-1A −0.11 rno-miR-9a-3p 272-278 7mer-1A −0.1 Figure 1Effects of the predicted 45 miRNAs on the reporter gene expression of the pmiR-FSHb-3′UTR-WT vector. [score:3]
We introduced site-specific mutations into the pmiR-FSHb-3′UTR-WT plasmid to interrupt the binding sites of miR-21-3p and miR-433, producing the pmiR-FSHb-3′UTR-MUT and pmiR-FSHb-3′UTR-MUT1 plasmids (Supplementary File 3). [score:2]
In addition, miR-433 and miR-21-3p exert the same regulatory effects on FSH secretion. [score:2]
Recent reports have shown that miR-433 exerts functions in human tumorigenesis and development [42]. [score:2]
Similar to miR-21, the role of miR-433 in pituitary hormone secretion remains largely unknown due to a lack of relevant studies. [score:1]
miR-433 is located on chromosome 14q32 and exhibits functions in many types of mammalian cells [41]. [score:1]
After a 24-h transfection period, the rat primary pituitary cells in the blank group (A), the negative control group (B), the miR-21-3p mimic group (C), and the miR-433 mimic group (D) are shown. [score:1]
Figure 4After a 24-h transfection period, the rat primary pituitary cells in the blank group (A), the negative control group (B), the miR-21-3p mimic group (C), and the miR-433 mimic group (D) are shown. [score:1]
Similarly, co-transfection of miR-433 and pmiR-FSHb-3′UTR-WT into 293T cells yielded a more than a 30% decrease in luciferase activity, whereas cotransfection of miR-433 and pmiR-FSHb-3′UTR-MUT1 yielded no changes in luciferase activity (Figure 3D). [score:1]
Effect of miR-21-3p and miR-433 transfection on rat primary pituitary cells. [score:1]
Effect of transfecting rat primary pituitary cells with miR-21-3p and miR-433. [score:1]
For the analysis of miR-21-3p and miR-433, 293T cells were cotransfected with the mimics, negative controls, pmiR-FSHb-3′UTR-WT, pmiR-FSHb-3′UTR-MUT, pmiR-FSHb-3′UTR-MUT1 and pmiR-RB-REPORT [TM]. [score:1]
Some researchers have found an association between miR-433 and human glioma, gastric carcinoma, myeloproliferative neoplasms and ovarian, liver and other cancers [42– 46]. [score:1]
miR-21-3p and miR-433 were selected for the subsequent experiment. [score:1]
Regarding hormone secretion, in 2012, Riester et al. reported that ACTH stimulation could modulate the adrenal response by influencing miR-433 to act as an endogenous modulator of the glucocorticoid receptor (Nr3c1) [49]. [score:1]
To detect the growth of cultured primary pituitary cells after transfection with miR-21-3p and miR-433, we observed the growth of the pituitary cells and noted that they appeared to be in good condition (Figures 4A-4D). [score:1]
[1 to 20 of 34 sentences]
3
[+] score: 99
To further validate the regulation of miR-433-3p on DKK1 expression level, protein immunoblotting assay showed that increased miR-433-3p inhibited over 90% DKK1 protein expression (Fig 2C, p<0.0001 compared to control group). [score:6]
2. miRNA-433-3p targeted DKK1 protein expression. [score:5]
Furthermore, we validated that miR-433-3p directly regulated DKK1 expression through epigenetic modulation mechanism. [score:5]
Protein immunoblotting assay showed miR-433-3p inhibited DKK1 expression up to 90% of total protein (C). [score:4]
However, we don't have direct evidences to show miR-433-3p was secreted by osteoblasts and targeted osteoclasts to reduce DKK-1 sercretion via exosomes. [score:4]
Data showed mutant miR-433-3p lost the regulation ability on DKK1 expression. [score:4]
In agreement with Jess Morhayim, Sylvia Weilner and Cheng' studies[15, 27, 28], we showed miR-433-3p and miR-106b were up-regulated in OVX rat mo del. [score:4]
The authors further emphasized the vital role of miR-433-3p in DKK1/WNT/β-catenin pathway through decreasing DKK1 expression and inducing osteoblasts differentiation. [score:3]
Schematic figure showed miR-433-3p targeting DKK1 mRNA 3'UTR, mapping from site 554 to 560 (A). [score:3]
As no study reported DKK1 regulated by miR-433-3p, we further confirmed such regulation by mutant miR-433-3p method. [score:3]
Importantly, miR-433-3p was increased in serum and was contained in osteoblast secreted exosomes which targeted umbilical cord blood cells[15]. [score:3]
When human hFOB1.19 cells were infected with recombinant lentivirus which stably expressed miR-433-3p, results showed increased mRNA level of osteogenic markers RUNX2 and osteocalcin. [score:3]
Rat bone marrow derived osteoblasts were infected with miR-433-3p stable expression lentivirus. [score:3]
We have shown the direct regulation of miR-433-3p on DKK1, but the effect of miR-433-3p on osteoblasts was still not clear. [score:3]
Lentivirus mediated miR-433-3p stable expression increased ALP activity of immortalized human hFOB1.19 and rat ROS 17/2.8 cells (A, p<0.01, triple experiments). [score:3]
0179860.g002 Fig 2 Schematic figure showed miR-433-3p targeting DKK1 mRNA 3'UTR, mapping from site 554 to 560 (A). [score:3]
Validation of miR-433-3p targeting DKK1 mRNA 3’UTR. [score:3]
showed that lentivirus mediated miR-433-3p stable expression increased ALP activity both in human and rat derived immortalized cells compared to controls (Fig 3A, mean ± SE of triple experiments, p<0.01). [score:2]
sham rat) Peers' studies hsa-miR-34a-3p 2.63 upUp, Jess Morhayim[15] hsa-miR-433-3p 1.24 up This study hsa-miR-106b 2.24 up This study hsa-miR-23a 0.48 downDown, Sylvia Weilner[27] hsa-miR-328-3p 0.38 down Down, Sylvia Weilner hsa-miR-29b-3p 2.1 up Up, Jess Morhayim hsa-miR-146a-5p 2.68 up Up, Jess Morhayim hsa-miR-148a-3p 1.85 upUp, Cheng[28] We noted that DKK1 played important role in the development of osteoporosis. [score:2]
Data showed that miR-433-3p potentially regulated DKK1 mRNA. [score:2]
showed that lentivirus mediated miR-433-3p stable expression also increased osteoblasts ALP activity compared to blank lentivirus (Fig 3B, mean ± SE, p<0.01). [score:2]
In order to elucidate if primary osteoblasts harbor high level of miR-433-3p, we quantified the miR-433-3p in cells using real-time PCR. [score:1]
We further analyzed the miR-433-3p level in bone tissue of rat femur bone using ALP staining method and in situ hybridization method. [score:1]
Alizarin red staining figures indicated that miR-433-3p promoted Ca [2+] deposited within osteoblasts (Fig 3C, under microscopy counting for ten views, mean ± SE, p<0.01). [score:1]
We further showed the association of serum DKK1 and circulating miR-433-3p (r = 0.7520, p = 0.046). [score:1]
miR-433-3p oligonucleotide was stained by rhodamine B, which would emit red color through excitation. [score:1]
Effects of miR-433-3p on osteoblasts differentiation and maturation. [score:1]
Locked nucleic acid -based miR-433-3p probe was labeled with DIG at the 3' end (Focofish, Guangzhou). [score:1]
Cells were infected with lentivirus in which miR-433-3p sequence was constructed (plenty 7.3/V5-DEST). [score:1]
In agreement with the above findings, we showed that osteoblasts harbored high level of miR-433-3p (Fig 3) which might secret to circulating or tissue space. [score:1]
Furthermore, the correlation of serum DKK1 with circulating miR-433-3p level was analyzed by SPSS software. [score:1]
Alizarin red staining results indicated that miR-433-3p promoted Ca [2+] deposited within osteoblasts (D, p<0.01). [score:1]
Correlation of serum DKK1 with circulating miR-433-3p. [score:1]
In the design of this study, we hypothesized that high level of miR-433-3p in osteoblasts might be associated with the negative feedback of high DKK1 level in serum. [score:1]
Correlation of serum DKK1 with circulating miR-433-3p (B, linear regression, r = 0.7520, p = 0.046). [score:1]
Increased ALP activity was not detected in miR-433 sponge vector group. [score:1]
We also used miRNA sponge technology to silence miR-433-3p level, and found that miRNA sponge decrease ALP activity in the present of miR-433-3p in hFOB1.19 and ROS 17/2.8 cells. [score:1]
3. Administration of miRNA-433-3p promoted osteoblasts differentiation in vitro. [score:1]
Sections were incubated with miR-433-3p probe in a moist chamber at 50°C overnight. [score:1]
Importantly, this study linked the association of high level of DKK1 and miR-433-3p in OVX rat. [score:1]
miR-433-3p also increased primary bone marrow induced ostetoblasts ALP activity, but not in miR-433-3p plus sponge vector group (B, **, p<0.01). [score:1]
Infection of lentivirus miR-433-3p to human hFOB1.19 cells showed increased mRNA level of osteogenic markers RUNX2 and osteocalcin (C, **, p<0.01). [score:1]
When the miR-433-3p binding site in 3’UTR was mutant, such reduction was prohibited (Fig 2B, column 4). [score:1]
We found miR-433-3p and miR-106b were not reported previously in OVX rat circulating serum. [score:1]
DIG-labeled antisense of miR-433-3p probe was detected by anti-DIG secondary antibody, thus red color was observed under microscopy with 510–530 nm excitation (C, Rhodamine labeled, p<0.05). [score:1]
from in situ hybridization data showed that high level of miR-433-3p was found in femur bone osteoblasts (Fig 4C, p<0.05, ten countings of microscopy views). [score:1]
miRNA-433-3p quantification and staining in bone tissue. [score:1]
4. Osteoblasts harbored high level of miRNA-433-3p. [score:1]
Alizarin red staining results indicated that miR-433-3p promoted Ca2+ deposited within osteoblasts. [score:1]
Blank or constructed vectors were co -transfected with miR-433-3p oligonucleotide into cells using Fugene HD lipid (Roche, # 04709705001). [score:1]
[1 to 20 of 50 sentences]
4
[+] score: 19
Other miRNAs from this paper: hsa-mir-17, hsa-mir-18a, hsa-mir-19a, hsa-mir-19b-1, hsa-mir-19b-2, hsa-mir-20a, hsa-mir-21, hsa-mir-23a, hsa-mir-24-1, hsa-mir-24-2, hsa-mir-27a, hsa-mir-30a, hsa-mir-32, hsa-mir-92a-1, hsa-mir-92a-2, hsa-mir-93, hsa-mir-107, hsa-mir-129-1, hsa-mir-30c-2, hsa-mir-139, hsa-mir-181c, hsa-mir-204, hsa-mir-212, hsa-mir-181a-1, hsa-mir-222, hsa-mir-15b, hsa-mir-23b, hsa-mir-132, hsa-mir-138-2, hsa-mir-140, hsa-mir-142, hsa-mir-129-2, hsa-mir-138-1, hsa-mir-146a, hsa-mir-154, hsa-mir-186, rno-mir-324, rno-mir-140, rno-mir-129-2, rno-mir-20a, rno-mir-7a-1, rno-mir-101b, hsa-mir-29c, hsa-mir-296, hsa-mir-30e, hsa-mir-374a, hsa-mir-380, hsa-mir-381, hsa-mir-324, rno-mir-9a-1, rno-mir-9a-3, rno-mir-9a-2, rno-mir-15b, rno-mir-17-1, rno-mir-18a, rno-mir-19b-1, rno-mir-19b-2, rno-mir-19a, rno-mir-21, rno-mir-23a, rno-mir-23b, rno-mir-24-1, rno-mir-24-2, rno-mir-27a, rno-mir-29c-1, rno-mir-30e, rno-mir-30a, rno-mir-30c-2, rno-mir-32, rno-mir-92a-1, rno-mir-92a-2, rno-mir-93, rno-mir-107, rno-mir-129-1, rno-mir-132, rno-mir-138-2, rno-mir-138-1, rno-mir-139, rno-mir-142, rno-mir-146a, rno-mir-154, rno-mir-181c, rno-mir-186, rno-mir-204, rno-mir-212, rno-mir-181a-1, rno-mir-222, rno-mir-296, rno-mir-300, hsa-mir-20b, hsa-mir-431, rno-mir-431, hsa-mir-433, hsa-mir-410, hsa-mir-494, hsa-mir-181d, hsa-mir-500a, hsa-mir-505, rno-mir-494, rno-mir-381, rno-mir-409a, rno-mir-374, rno-mir-20b, hsa-mir-551b, hsa-mir-598, hsa-mir-652, hsa-mir-655, rno-mir-505, hsa-mir-300, hsa-mir-874, hsa-mir-374b, rno-mir-466b-1, rno-mir-466b-2, rno-mir-466c, rno-mir-874, rno-mir-17-2, rno-mir-181d, rno-mir-380, rno-mir-410, rno-mir-500, rno-mir-598-1, rno-mir-674, rno-mir-652, rno-mir-551b, hsa-mir-3065, rno-mir-344b-2, rno-mir-3564, rno-mir-3065, rno-mir-1188, rno-mir-3584-1, rno-mir-344b-1, hsa-mir-500b, hsa-mir-374c, rno-mir-29c-2, rno-mir-3584-2, rno-mir-598-2, rno-mir-344b-3, rno-mir-466b-3, rno-mir-466b-4
Finally, other subsets of miRNAs were either up-regulated (miR-23a-3p, miR132-3p, miR-146a-5p, miR-154-3p, miR-181d-5p, miR-212-3p, miR-212-5p, miR-344b-5p, miR-380-3p, miR-410-3p, miR-433-3p and miR-3584; Fig. 2, Supplementary Fig. S4), or down-regulated (miR-29c-5p, miR-30a-5p, miR-30c-2-3p, miR-30e-3p, miR-138-5p, miR-140-3p, miR-551b-3p and miR-652-3p; Fig. 2, Supplementary Fig. S5) during all phases of the disease. [score:9]
Moreover, we and Gorter et al. 24 observed the up-regulation of miR-212-5p, whereas we and Bot et al. 23 observed the up-regulation of miR-433-3p. [score:7]
Even if displaying the same patterns observed with the microarray, the expression levels of mir-181c-5p, miR-433-3p, miR-505-3p and miR-551b-3p were not significantly different from controls (Fig. 4). [score:3]
[1 to 20 of 3 sentences]
5
[+] score: 17
0018613.g004 Figure 4Three general trends of miRNA expression trajectories were observed for Wistar islets at 2.8G vs 16.7G: i) increased expression as exhibited by rno-miR-132, rno-miR-212 and rno-miR-409-3p, ii) decreased expression as in the case of rno-miR-124, rno-miR-142-3p, rno-miR-375, rno-miR-335, rno-miR-130a and rno-miR-708 and, iii) no change as seen in rno-miR-376a, rno-miR-142-5p and rno-miR-433. [score:7]
Three general trends of miRNA expression trajectories were observed for Wistar islets at 2.8G vs 16.7G: i) increased expression as exhibited by rno-miR-132, rno-miR-212 and rno-miR-409-3p, ii) decreased expression as in the case of rno-miR-124, rno-miR-142-3p, rno-miR-375, rno-miR-335, rno-miR-130a and rno-miR-708 and, iii) no change as seen in rno-miR-376a, rno-miR-142-5p and rno-miR-433. [score:7]
In general, aside from more significant changes in expression levels of miRNAs at 24 h incubation compared to 1 h incubation, three trends in terms of expression changes are also observed in the Wistar islet upon stimulation at 16.7G as compared to 2.8G: i) increasing miRNA levels, as displayed by rno-miR-132, rno-miR-212 and rno-miR-409-3p, ii) decreasing miRNA levels as exhibited by rno-miR-124, rno-miR-142-3p, rno-miR-375, rno-miR-335, rno-miR-130a and rno-miR-708, and iii) no significant change as displayed by rno-miR-376a, rno-miR-142-5p and rno-miR-433. [score:3]
[1 to 20 of 3 sentences]
6
[+] score: 16
However, no association between the SNP in FGF20, microRNA-433, or α- synuclein expression and Parkinson's disease have been reported (Wider et al., 2009; de Mena et al., 2010). [score:5]
Variation in the miRNA-433 binding site of FGF20 confers risk for Parkinson disease by overexpression of alpha-synuclein. [score:5]
The risk allele disrupts a binding site for microRNA-433, increasing FGF20 mRNA translation. [score:3]
FGF20 rs12720208 SNP and microRNA-433 variation: no association with Parkinson's disease in Spanish patients. [score:3]
[1 to 20 of 4 sentences]
7
[+] score: 10
However, circulating levels of miR-296 and miR-433 were found to be downregulated in hypertension and congenital heart disease, respectively [56, 57]. [score:6]
Few of the highly upregulated microRNAs were: miR-79, miR-183, miR-206, miR-207, miR-296-3p, miR-298, miR-380-5p, miR-433, miR-449b, miR-705, miR-761 (S1 Table). [score:4]
[1 to 20 of 2 sentences]
8
[+] score: 7
On the 14th day after injury, 25 miRNAs, including miR-31a-3p, miR-17-5p, miR-146b-5p, miR-154-3p, and miR-363-3p, were upregulated (Figure  2C), and 18 miRNAs were downregulated, including miR-433-3p and miR-496-3p (Figure  2D). [score:7]
[1 to 20 of 1 sentences]
9
[+] score: 6
Variation in the miR-433 binding site of FGF20 confers risk for Parkinson diseases by up-regulation of α-Synucein [16]. [score:6]
[1 to 20 of 1 sentences]
10
[+] score: 4
MicroRNA-433 inhibits the proliferation and migration of HUVECs and neurons by targeting hypoxia-inducible factor 1 alpha. [score:4]
[1 to 20 of 1 sentences]
11
[+] score: 3
MicroRNA-433 dampens glucocorticoid receptor signaling, impacting circadian rhythm and osteoblastic gene expression. [score:2]
GC function was related to miR-338 (Zhang et al., 2016) and miR-433 (Smith et al., 2016) in osteoclast formation. [score:1]
[1 to 20 of 2 sentences]
12
[+] score: 3
Other miRNAs from this paper: mmu-mir-30a, mmu-mir-101a, mmu-mir-125a, mmu-mir-125b-2, mmu-mir-132, mmu-mir-134, mmu-mir-135a-1, mmu-mir-138-2, mmu-mir-142a, mmu-mir-150, mmu-mir-154, mmu-mir-182, mmu-mir-183, mmu-mir-24-1, mmu-mir-194-1, mmu-mir-200b, mmu-mir-122, mmu-mir-296, mmu-mir-21a, mmu-mir-27a, mmu-mir-92a-2, mmu-mir-96, rno-mir-322-1, mmu-mir-322, rno-mir-330, mmu-mir-330, rno-mir-339, mmu-mir-339, rno-mir-342, mmu-mir-342, rno-mir-135b, mmu-mir-135b, mmu-mir-19a, mmu-mir-100, mmu-mir-139, mmu-mir-212, mmu-mir-181a-1, mmu-mir-214, mmu-mir-224, mmu-mir-135a-2, mmu-mir-92a-1, mmu-mir-138-1, mmu-mir-181b-1, mmu-mir-125b-1, mmu-mir-194-2, mmu-mir-377, mmu-mir-383, mmu-mir-181b-2, rno-mir-19a, rno-mir-21, rno-mir-24-1, rno-mir-27a, rno-mir-30a, rno-mir-92a-1, rno-mir-92a-2, rno-mir-96, rno-mir-100, rno-mir-101a, rno-mir-122, rno-mir-125a, rno-mir-125b-1, rno-mir-125b-2, rno-mir-132, rno-mir-134, rno-mir-135a, rno-mir-138-2, rno-mir-138-1, rno-mir-139, rno-mir-142, rno-mir-150, rno-mir-154, rno-mir-181b-1, rno-mir-181b-2, rno-mir-183, rno-mir-194-1, rno-mir-194-2, rno-mir-200b, rno-mir-212, rno-mir-181a-1, rno-mir-214, rno-mir-296, mmu-mir-376b, mmu-mir-370, mmu-mir-433, mmu-mir-466a, rno-mir-383, rno-mir-224, mmu-mir-483, rno-mir-483, rno-mir-370, rno-mir-377, mmu-mir-542, rno-mir-542-1, mmu-mir-494, mmu-mir-20b, mmu-mir-503, rno-mir-494, rno-mir-376b, rno-mir-20b, rno-mir-503-1, mmu-mir-1224, mmu-mir-551b, mmu-mir-672, mmu-mir-455, mmu-mir-490, mmu-mir-466b-1, mmu-mir-466b-2, mmu-mir-466b-3, mmu-mir-466c-1, mmu-mir-466e, mmu-mir-466f-1, mmu-mir-466f-2, mmu-mir-466f-3, mmu-mir-466g, mmu-mir-466h, mmu-mir-504, mmu-mir-466d, mmu-mir-872, mmu-mir-877, rno-mir-466b-1, rno-mir-466b-2, rno-mir-466c, rno-mir-872, rno-mir-877, rno-mir-182, rno-mir-455, rno-mir-672, mmu-mir-466l, mmu-mir-466i, mmu-mir-466f-4, mmu-mir-466k, mmu-mir-466j, rno-mir-551b, rno-mir-490, rno-mir-1224, rno-mir-504, mmu-mir-466m, mmu-mir-466o, mmu-mir-466c-2, mmu-mir-466b-4, mmu-mir-466b-5, mmu-mir-466b-6, mmu-mir-466b-7, mmu-mir-466p, mmu-mir-466n, mmu-mir-466b-8, rno-mir-466d, mmu-mir-466q, mmu-mir-21b, mmu-mir-21c, mmu-mir-142b, mmu-mir-466c-3, rno-mir-322-2, rno-mir-503-2, rno-mir-466b-3, rno-mir-466b-4, rno-mir-542-2, rno-mir-542-3
Those miRNAs differentially expressed on the microarrays with greatest fold changes, miRNA-101a, miRNA-142-3p, miRNA-433 and miRNA-96, were further analyzed. [score:3]
[1 to 20 of 1 sentences]
13
[+] score: 2
Furthermore, we previously found that miR-21-3p and miR-433 both decrease FSH secretion by regulating FSHb [16]. [score:2]
[1 to 20 of 1 sentences]
14
[+] score: 1
Other miRNAs from this paper: mmu-mir-1a-1, mmu-mir-127, mmu-mir-134, mmu-mir-136, mmu-mir-154, mmu-mir-181a-2, mmu-mir-143, mmu-mir-196a-1, mmu-mir-196a-2, mmu-mir-21a, rno-mir-329, mmu-mir-329, mmu-mir-1a-2, mmu-mir-181a-1, mmu-mir-181b-1, mmu-mir-181c, mmu-mir-375, mmu-mir-379, mmu-mir-181b-2, rno-mir-21, rno-mir-127, rno-mir-134, rno-mir-136, rno-mir-143, rno-mir-154, rno-mir-181c, rno-mir-181a-2, rno-mir-181b-1, rno-mir-181b-2, rno-mir-196a, rno-mir-181a-1, mmu-mir-196b, rno-mir-196b-1, mmu-mir-412, mmu-mir-370, oar-mir-431, oar-mir-127, oar-mir-432, oar-mir-136, mmu-mir-431, mmu-mir-433, rno-mir-431, ssc-mir-181b-2, ssc-mir-181c, ssc-mir-136, ssc-mir-196a-2, ssc-mir-21, rno-mir-370, rno-mir-412, rno-mir-1, mmu-mir-485, mmu-mir-541, rno-mir-541, rno-mir-493, rno-mir-379, rno-mir-485, mmu-mir-668, bta-mir-21, bta-mir-181a-2, bta-mir-127, bta-mir-181b-2, bta-mir-181c, mmu-mir-181d, mmu-mir-493, rno-mir-181d, rno-mir-196c, rno-mir-375, mmu-mir-1b, bta-mir-1-2, bta-mir-1-1, bta-mir-134, bta-mir-136, bta-mir-143, bta-mir-154a, bta-mir-181d, bta-mir-196a-2, bta-mir-196a-1, bta-mir-196b, bta-mir-329a, bta-mir-329b, bta-mir-370, bta-mir-375, bta-mir-379, bta-mir-412, bta-mir-431, bta-mir-432, bta-mir-433, bta-mir-485, bta-mir-493, bta-mir-541, bta-mir-181a-1, bta-mir-181b-1, ssc-mir-1, ssc-mir-181a-1, mmu-mir-432, rno-mir-668, ssc-mir-143, ssc-mir-181a-2, ssc-mir-181b-1, ssc-mir-181d, ssc-mir-196b-1, ssc-mir-127, ssc-mir-432, oar-mir-21, oar-mir-181a-1, oar-mir-493, oar-mir-433, oar-mir-370, oar-mir-379, oar-mir-329b, oar-mir-329a, oar-mir-134, oar-mir-668, oar-mir-485, oar-mir-154a, oar-mir-154b, oar-mir-541, oar-mir-412, mmu-mir-21b, mmu-mir-21c, ssc-mir-196a-1, ssc-mir-196b-2, ssc-mir-370, ssc-mir-493, bta-mir-154c, bta-mir-154b, oar-mir-143, oar-mir-181a-2, chi-mir-1, chi-mir-127, chi-mir-134, chi-mir-136, chi-mir-143, chi-mir-154a, chi-mir-154b, chi-mir-181b, chi-mir-181c, chi-mir-181d, chi-mir-196a, chi-mir-196b, chi-mir-21, chi-mir-329a, chi-mir-329b, chi-mir-379, chi-mir-412, chi-mir-432, chi-mir-433, chi-mir-485, chi-mir-493, rno-mir-196b-2, bta-mir-668, ssc-mir-375
Other families that had a high abundance of reads were miR-134, miR-136, miR-154, miR-370, miR-412, miR-431, miR-432, miR-433, miR-485, miR-493, miR-541; a total of 11 miRNA families. [score:1]
[1 to 20 of 1 sentences]