sort by

27 publications mentioning dre-mir-133a-1

Open access articles that are associated with the species Danio rerio and mention the gene name mir-133a-1. Click the [+] symbols to view sentences that include the gene name, or the word cloud on the right for a summary.

1
[+] score: 95
In our findings, the downregulation of miRs-133a and b started at 24 h and peaked at 2–3 days post the surgery, whereas miR-1 peaked already at 24 h. Thus, we suggest that the early expression of is necessary to contrast the caspase protein translation in all injured hearts (due to miR-133 downregulation). [score:11]
The miR-133 expression is regulated by extracellular signal-regulated kinase 1/2 activation and is inversely correlated with vascular growth [23], since it is strongly related to FGF-receptor expression [24]. [score:7]
a Expression of miR-1; b expression of miR-133a; c expression of miR-133b. [score:7]
miR-133a instead acts directly on blocking the expression of the receptor of FGF and on the expression of the PP2AC that promotes the activity of ERK. [score:6]
At 7 days after amputation (dpa), the level of miR-133 expression in the ventricle of the heart was lower than control individuals and suggested that miR-133 is an endogenous inhibitor of EC proliferation [25]. [score:5]
Most of these genes were demonstrated to be, directly or indirectly, a target of miR-1 and miR-133a and miR-133b (ref. [score:5]
Liu N MicroRNA-133a regulates cardiomyocyte proliferation and suppresses smooth muscle gene expression in the heartGenes Dev. [score:5]
Particularly, miR-1, miR-133a and miR-133b have been detected in 1 dpa in different data sets of down-regulated transcripts. [score:4]
miR-133a has significantly downregulated at 24 hpa in both portions (EPCs, 0.329 ± 0.056; RC, 0.388 ± 0.152; P < 0,001) vs control (EPCs, 1 ± 0.377; RC 0.880 ± 0.219). [score:4]
Moreover, miR-133a is probably a key miR that can activate the epicardium because it showed a more significant downregulation already at 1 dpa. [score:4]
However, in the reference panorama, information is still lacking about the timing of the downregulation of the miRs, about the possible involvement of miRs-1 and of the isoforms miR-133a and -133b in the heart differentiation and regeneration. [score:4]
In zebrafish, transgenic-inducing elevation of miR-133 levels after injury provoked an inhibition of myocardial regeneration, while the knockout of miR-133 showed increased CM proliferation [30]. [score:4]
Xu C The muscle-specific microRNAs miR-1 and miR-133 produce opposing effects on apoptosis by targeting HSP60, and caspase-9 in cardiomyocytesJ. [score:3]
In zebrafish, miR-133 antagonism that occurred during FGF-receptor inhibition has accelerated the regeneration of appendage or heart damage through increased proliferation within the regeneration blastema [25]. [score:3]
Regarding miR-133a (Fig.   1b), the qPCR data show that at 24 hpa there is a decrease (but not statistically significant, 0.707 ± 0.065), while the values of expression on days 2, 3 and 7 are similar to those of the miR-1 (0.519 ± 0.079, 0.255 ± 0.016, 0.560 ± 0.145, respectively) (Fig.   2). [score:3]
For example, among the target genes of miR-133, the genes for fibroblast growth factor receptor 1 (FGFR1) and protein phosphatase-2A-catalytic subunit (PP2AC, including Ppp2ca and Ppp2cb) seem to be promising to understand the possible induction. [score:3]
Tbx18, a target of miR-133a, is specific for epicardium and it would be a key transcription factor to induce the mesenchymal transient cells to differentiate into the precursors of CM 24, 29. [score:3]
Hearts were harvested from 24 h to 30 dpa, and analysed for miRs (miR-1 and miR-133a/miR-133b) by qPCR to know how their expression levels vary at different stages of regeneration. [score:3]
miR-1 is the most conserved miRNA during evolution [16], whereas a gene duplication probably has formed the miR-133 gene, which in fact is positioned in the same genetic locus of the miR-1 [31] and, in mammals, it regulates transcription of myoD [19]. [score:2]
Feng Y A feedback circuit between miR-133 and the ERK1/2 pathway involving an exquisite mechanism for regulating myoblast proliferation and differentiationCell Death Dis. [score:2]
Previous studies indicated that during myogenesis, the signalling pathway of MyoD are regulated by both miR-133a and miR-133b [24]. [score:2]
Fig. 7 A proposed schematic mo del of miR-1 and miR-133 actions in blocking the FGF -dependent transduction pathway in the cells involved in cardiac regeneration: CMs, fibroblast, EPCs and endocardial cells. [score:1]
Particularly, miR-133 has two isoforms, miR-133a and miR-133b, and their activity seems to be similar at the moment [23]. [score:1]
There are two members in the miR-133 family: miR-133a and miR-133b. [score:1]
miR-1/miR-133 are mainly implicated in post lesion in mammals as well as in zebrafish 14, 17, 22, 23. [score:1]
Recently, an involvement of miRs has been shown by the array analysis at 7 days post operation dpa [25], and in particular of miR-133 [31]. [score:1]
[1 to 20 of 26 sentences]
2
[+] score: 53
Liu N. Bezprozvannaya S. Williams A. H. Qi X. Richardson J. A. Bassel-Duby R. Olson E. N. microRNA-133a regulates cardiomyocyte proliferation and suppresses smooth muscle gene expression in the heart Genes Dev. [score:6]
By targeting the same transcription factors that regulate miR-1/miR133 expression and control cardiac progenitor cell proliferation and differentiation, miR-1 and miR-133 fine-tune multiple nodes of the genetic networks that control cardiac muscle differentiation. [score:6]
miR-1 and miR-133 are for the most part co-expressed and contribute to the establishment of a muscle specific gene expression program while having somewhat antagonistic roles in the control of proliferation and differentiation [94]. [score:5]
An older study using knock-outs for miR-133a-1 and miR-133-a2 with removal of the selection markers also supports the redundancy of these genes during heart development, as only the double knock-out mice displayed detectable cardiac phenotypes [115]. [score:4]
Interestingly, both miR-1 and miR-133 have been shown to be negative regulators of the same cardiogenic transcription factors that, in addition to promoting their expression, activate protein-coding genes involved in muscle function (e. g., sarcomere genes) [34, 92, 94, 95]. [score:4]
These include marked changes in the cardiac contractibility apparatus, with a switch from fetal specific to adult isoforms of several sarcomeric proteins, and the silencing of smooth muscle proteins expressed early during cardiomyocyte differentiation, which appears to be regulated by both miR-1 and miR-133. [score:4]
As discussed above, miR-1 was later found to be encoded in two bicistronic clusters together with miR-133a, which displays the same overall expression pattern and is also a key regulator of muscle and cardiac cell differentiation. [score:4]
In the embryonic heart, expression of the miR-1/miR-133 locus is transcriptionally regulated by the myogenic transcription factors SFR, MYOCD and MEF2. [score:4]
Thus, the available data support the view that miR-1 and miR-133 play a critical synergistic role in the suppression the cardiac fetal gene program and enforcement of adult skeletal muscle properties, driving cardiac maturation. [score:3]
Figure 5 Transcriptional regulatory networks controlled by miR-1 and miR-133 during cardiac muscle differentiation. [score:2]
In mammals, the duplicated miR-1/miR-133 locus is transcribed into a bicistronic transcript that is regulated by multiple independent upstream intronic enhancers. [score:2]
For the miR-133 d KO animals, albeit a modest reduction in viability is observed during embryonic development, along with a high number of VSD related deaths soon after birth (day P0/P1), about half of the mice hearts developed with a relatively normal morphology [115]. [score:2]
miR-1 is encoded by two genes, miR-1-1 and 1-2, which are clustered with miR-133a-2 and miR-133a-1, respectively. [score:1]
The first report of an equivalent reprogramming event used an ‘educated guess’ approach to test the individual and combined effects of six miRs with reported cardiac functions (miR-1; miR-126-3p; miR-133a; miR-138, miR-206; miR-208a) to induce fibroblast trans-differentiation [90]. [score:1]
Interestingly, the lack of miR-1/miR133 seems to affect multiple cellular pathways required for this transition. [score:1]
Indeed, while miR-1 is acknowledged to trigger differentiation of both mouse and human embryonic stem (ES) cells into the cardiomyocytes, miR-133 was found to act in partial opposition to miR-1, by promoting muscle progenitor expansion and preventing terminal differentiation [82]. [score:1]
This is in sharp contrast with the previously described defect of miR-133a d KO mice, which becomes apparent only at later stages [115]. [score:1]
Interestingly, miR-133 is also conserved in Drosophila, but it is not clustered with the single dm-miR-1 gene. [score:1]
Chen J. F. Man del E. M. Thomson J. M. Wu Q. Callis T. E. Hammond S. M. Conlon F. L. Wang D. Z. The role of microRNA-1 and microRNA-133 in skeletal muscle proliferation and differentiation Nat. [score:1]
[1 to 20 of 19 sentences]
3
[+] score: 48
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-132-2, dre-mir-133a-2, 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
Three of the 107 genes are previously identified targets of the downregulated miRNAs, including mmp14, a known target of miR-133 [64], mmp9 (targeted by miR-204 and miR-338) and timp2 (targeted by miR-24 and miR-204). [score:12]
Conversely, miR-204 was downregulated in zebrafish and bichir, miR-133a was downregulated in bichir, and miR-2184, miR-338 and miR-24 were downregulated in axolotl. [score:10]
S24 Table Zebrafish Ensembl gene identifiers for 107 genes upregulated in three mo dels with predicted miRNA binding sites for miR-2184, miR-204, miR-338, miR-133a and miR-24 and members of the network of commonly up- and downregulated genes with functional interactions to 11 blastema -associated genes. [score:7]
We performed similar analyses to capture potential target genes for the 5 commonly downregulated miRNAs (miR-2184, miR-204, miR-338, miR-133a and miR-24). [score:6]
S23 Table Zebrafish Ensembl gene identifiers for 205 genes upregulated in three mo dels with predicted miRNA binding sites for miR-2184, miR-204, miR-338, miR-133a and miR-24 in all three mo dels. [score:4]
Within this subset of differentially regulated zebrafish miRNAs, we identified 10 miRNAs: miR-21, miR-181c, miR-181b, miR-31, miR-7b, miR-2184, miR-24, miR-133a, miR-338 and miR-204, that showed conserved expression changes with both bichir and axolotl regenerating samples (Table 1). [score:4]
Recently, zebrafish appendage regeneration studies have revealed two differentially regulated miRNAs, miR-133 [27] and miR-203 [28], as essential regulators of caudal fin regeneration. [score: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]
[1 to 20 of 9 sentences]
4
[+] score: 35
Other miRNAs from this paper: hsa-mir-23a, hsa-mir-29a, hsa-mir-29b-1, hsa-mir-29b-2, hsa-mir-107, hsa-mir-205, hsa-mir-214, hsa-mir-221, hsa-mir-1-2, hsa-mir-122, hsa-mir-133a-1, hsa-mir-133a-2, hsa-mir-184, hsa-mir-193a, hsa-mir-1-1, hsa-mir-29c, hsa-mir-133b, dre-mir-205, dre-mir-214, dre-mir-221, dre-mir-430a-1, dre-mir-430b-1, dre-mir-430c-1, dre-mir-1-2, dre-mir-1-1, dre-mir-23a-1, dre-mir-23a-2, dre-mir-23a-3, dre-mir-29b-1, dre-mir-29b-2, dre-mir-29a, dre-mir-107a, dre-mir-122, dre-mir-133a-2, dre-mir-133b, dre-mir-133c, dre-mir-184-1, dre-mir-193a-1, dre-mir-193a-2, dre-mir-202, 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, hsa-mir-202, hsa-mir-499a, dre-mir-184-2, dre-mir-499, dre-mir-724, dre-mir-725, dre-mir-107b, dre-mir-2189, hsa-mir-499b, dre-mir-29b3
This network visualization shows that (1) all modules contain at least 2 genes that are predicted targets of a deregulated miRNA identified in this study, except the module “Apoptosis and NAFLD”; (2) dre-miR-2189, the only DE miRNA that was downregulated, targets many genes in modules that are predominantly upregulated such as Cell cycle (4 target mRNAs), Apoptosis and Autophagy (19 targets), Epigenetics and Apoptosis/Autophagy (2 targets) and Receptors (4 targets); (3) certain miRNAs have only 1 target gene in the selected modules, including dre-miR-184 (“Oxidative phosphorylation”), dre-miR-430a and dre-miR-430b (“Apoptosis and Autophagy”); (4) while other miRNAs have common target genes in the same modules, i. e., dre-miR-725/dre-miR-724/dre-miR-193a, dre-miR-202, dre-miR-205 and dre-miR-133a that have several common target genes in modules “Oxidative phosphorylation and NAFLD”, “Apoptosis/Autophagy”, “NAFLD” and “Cell cycle”. [score:26]
Renaud L. Harris L. G. Mani S. K. Kasiganesan H. Chou J. C. Baicu C. F. Van Laer A. Akerman A. W. Stroud R. E. Jones J. A. HDACs regulate miR-133a expression in pressure overload -induced cardiac fibrosisCirc. [score:4]
Dre-miR-430a and dre-miR-133a have more targets in common than with any other miR-430 family members. [score:3]
Chen J. -F. Man del E. M. Thomson J. M. Wu Q. Callis T. E. Hammond S. M. Conlon F. L. Wang D. -Z. The role of microRNA-1 and microRNA-133 in skeletal muscle proliferation and differentiationNat. [score:1]
For the species Danio rerio, miRNAs are labeled “dre-miRNAs”, i. e., dre-miR-133a. [score:1]
[1 to 20 of 5 sentences]
5
[+] score: 28
Down-regulation of miR-133a contributes to up-regulation of Rhoa in bronchial smooth muscle cells. [score:7]
In order to address this possibility, we used several MAPK inhibitors, such as JNK inhibitor II, SB203580 for p38 and PD98059 and U0126 for ERK1/2, to identify the signals involved in morphine -induced miR-133a regulation. [score:6]
miR-145, miR-133a and: tumor-suppressive target FSCN1 in esophageal squamous cell carcinoma. [score:5]
Expression of miR-1, miR-133a, and miR-206 increases during development of human skeletal muscle. [score:4]
The muscle-specific microRNAs miR-1 and miR-133 produce opposing effects on apoptosis by targeting HSP60, HSP70, and caspase-9 in cardiomyocytes. [score:3]
Caveolin-1 mediates tumor cell migration and invasion and its regulation by miR-133a in head and neck squamous cell carcinoma. [score:2]
Three different miR-133 sequences are known: miR-133a-1,-2, and. [score:1]
[1 to 20 of 7 sentences]
6
[+] score: 24
Other miRNAs from this paper: dre-mir-196a-1, dre-mir-199-1, dre-mir-199-2, dre-mir-199-3, dre-mir-203a, dre-mir-210, dre-mir-214, 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-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-1-2, dre-mir-1-1, 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-21-1, dre-mir-21-2, dre-mir-25, dre-mir-30e-2, dre-mir-101a, dre-mir-103, dre-mir-107a, dre-mir-122, 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-126a, dre-mir-129-2, dre-mir-129-1, dre-mir-130b, dre-mir-130c-1, dre-mir-130c-2, dre-mir-133a-2, dre-mir-133b, dre-mir-133c, dre-mir-135c-1, dre-mir-135c-2, dre-mir-140, dre-mir-142a, dre-mir-142b, dre-mir-150, dre-mir-152, dre-mir-462, dre-mir-196a-2, dre-mir-196b, dre-mir-202, dre-mir-203b, dre-mir-219-3, dre-mir-365-1, dre-mir-365-2, dre-mir-365-3, dre-mir-455-1, 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-135b, dre-mir-135a, dre-mir-499, dre-mir-738, dre-mir-429b, dre-mir-1788, dre-mir-196c, dre-mir-107b, dre-mir-455-2, dre-mir-222b, dre-mir-126b, dre-mir-196d, dre-mir-129-3, dre-mir-129-4
Indeed, deletion of miR-1 altered regulation of cardiogenesis, electrical conduction and cell cycle of cardiomyocites, and miR-133 plus miR-1 regulate cardiac hypertrophy, as their over expression inhibits it. [score:7]
Dre-miR-133 expression was higher in muscle and dre-miR-430 showed higher expression in developmental samples. [score:6]
Dre-miR-1 and dre-miR-133a were expressed in muscle and heart, where they play an important regulatory role in other organisms [60, 61]. [score:4]
The expression of miR-133a was confirmed by qRT-PCR and its relative concentration was higher in muscle than in other tissues (Figure 5). [score:3]
The heart showed accumulation of dre-miR-101a, dre-miR-130b, dre-miR-130c, dre-miR-221 and dre-miR-499, while dre-miR-1 and dre-miR-133a expression was detected in both muscle and heart. [score:3]
Dre-miR-499 was heart specific, dre-miR-1 and dre-miR-133a were detected in both muscle and heart and dre-miR-103 and dre-miR-122 were gut/liver specific. [score:1]
[1 to 20 of 6 sentences]
7
[+] score: 22
This causes increased expression of miR-133 target genes such as cx43 (Yin et al., 2012; Banerji et al., 2016). [score:5]
Although rescue using Tg(hsp70:miR-133sp [pd48]) supports our mo del that cx43 is functionally activated downstream of Esco2 and Smc3, because miR-133 has multiple targets (Yin et al., 2008), we cannot rule out the possibility that a different target gene is responsible for the rescue. [score:5]
In this line, heat shock induces expression of the miR-133 target sequence fused to EGFP and therefore sequesters the miR-133. [score:5]
Knocking down miR-133 (which targets cx43 for degradation) via the ‘sponge’ transgene (three miR-133 binding sites) results in the increase of cx43 levels (Yin et al., 2012). [score:4]
Regulation of zebrafish heart regeneration by miR-133. [score:2]
Fgf -dependent depletion of microRNA-133 promotes appendage regeneration in zebrafish. [score:1]
[1 to 20 of 6 sentences]
8
[+] score: 18
Specifically, miRNA-seq analysis identified 5 up-regulated cardiac specific miRNAs (miR-29a, miR-29b, miR-133, miR-193 and miR-223) previously identified for being regulators of cardiac development and homeostasis (Fig.   2). [score:6]
Targetscan software [50] predicted about 51 common targets for miR-29a, miR-29b, miR-133, miR-193 and miR-223 (Fig.   2C, middle panel). [score:5]
Table  2, miR-29a, miR-29b, miR-133, miR-193 and miR-223 were selected among the 10 most up-regulated miRNAs associated to the aging heart 43, 47– 49. [score:4]
Venn diagrams depicting the distribution of miR-133, miR-193, miR-29a/b, miR-223 predicted targets (middle panel). [score:3]
[1 to 20 of 4 sentences]
9
[+] score: 17
The role of as a suppressor of cardiomyocyte proliferation is supported by both double -knockout (miR-133a-1/miR-133a-2) mouse studies showing that is essential for regulating cardiomyocyte proliferation and normal heart development [17], and zebrafish studies, where was significantly reduced in regenerative/proliferative cardiac tissue [7]. [score:6]
A comparison of in regenerated versus un-injured zebrafish myocardium identified miR-133 as being specifically down-regulated during the period of cardiomyocyte proliferation and regeneration [7]. [score:4]
There are three genomic loci producing miR-133 with only-1 and-2 being expressed in the heart [15]. [score:3]
miR-133 is one of the most abundant cardiac miRNA [16] and is essential for normal cardiogenesis in mice, through regulation of serum response factor (SRF) [GenBank: NM_020493] dependent transcription [17]. [score:2]
miR-133a. [score:1]
Microarray miR-133 miR-590 miR-199a Cardiomyocyte Proliferation From late gestation, the majority of human cardiomyocytes cease proliferating due to either an absence of karyokinesis and/or cytokinesis [1– 3]. [score:1]
[1 to 20 of 6 sentences]
10
[+] score: 12
For example, the main function of miR-1, miR-133 and miR-206 is inhibition of their target genes in order to promote differentiation of muscle cells [7]– [9]. [score:5]
The expressions of miR-1, miR-133, miR-206 and miR-208 in muscle cells are mainly controlled by MRFs, serum response factor (SRF) and MEF2 [12]– [15]. [score:3]
The target genes for zebrafish miR-1 and miR-133 are involved in actin -binding, as well as actin-related and vesicular transport [11]. [score:3]
Absence of miR-1 and miR-133 by co-injection of mopholinos (MOs) into embryos disturbs the organization of actin in muscle fibers. [score:1]
[1 to 20 of 4 sentences]
11
[+] score: 10
3.4In addition to myofilament proteins, the expression of four microRNAs (miRNA, miR) involved in cardiac development and function was analysed (Fig. 2B): miR-133a and b, miR-1 and miR-499. [score:4]
In addition to myofilament proteins, the expression of four microRNAs (miRNA, miR) involved in cardiac development and function was analysed (Fig. 2B): miR-133a and b, miR-1 and miR-499. [score:4]
MiR-133a and b (a regulator of myocyte enhancer protein 2) and miR-1 (important in myoblast to myotube differentiation) significantly increased over time in developing mouse hearts yet were present at very low levels in the adult zebrafish heart. [score:2]
[1 to 20 of 3 sentences]
12
[+] score: 9
Expression of miR-1, miR-133a, miR-133b and miR-206 increases during development of human skeletal muscle. [score:4]
Regulation of zebrafish heart regeneration by miR-133. [score:2]
A feedback circuit between miR-133 and the ERK1/2 pathway involving an exquisite mechanism for regulating myoblast proliferation and differentiation. [score:2]
Fgf -dependent depletion of microRNA-133 promotes appendage regeneration in zebrafish. [score:1]
[1 to 20 of 4 sentences]
13
[+] score: 8
miR-133 acts in a negative feedback loop with serum response factor (SRF) to promote myoblast differentiation in vitro, and suppresses BMP2 -induced osteogenesis by targeting Runx2 [77], [78]. [score:5]
Of the 22 non-coding transcripts, we identified 2 differentially expressed genes in the proximal tail categorized within the miRNA precursor families miR-133 and miR-324. [score:3]
[1 to 20 of 2 sentences]
14
[+] score: 8
Connective tissue growth factor (CTGF) is a target of miR-133, and it is down-regulated by miR-133 (Duisters et al., 2009). [score:6]
miR-133 and miR-30 regulate connective tissue growth factor: implications for a role of microRNAs in myocardial matrix remo deling. [score:2]
[1 to 20 of 2 sentences]
15
[+] score: 6
miR-133 also underwent changes in the CNS that were important enough to produce changes in the expression of its target gene: the transcription factor Pitx3. [score:5]
Accordingly, the major changes observed in our qPCR experiments (Fig. 4A) occurred at the periphery (Fig. 4M), although miR-133 also displayed changes in the CNS to a lesser extent (Fig. 4G). [score:1]
[1 to 20 of 2 sentences]
16
[+] score: 6
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-15a, hsa-mir-17, hsa-mir-18a, hsa-mir-19a, hsa-mir-19b-1, hsa-mir-20a, hsa-mir-24-1, hsa-mir-24-2, hsa-mir-27a, hsa-mir-92a-1, hsa-mir-92a-2, mmu-let-7g, mmu-let-7i, mmu-mir-1a-1, mmu-mir-15b, mmu-mir-23b, mmu-mir-27b, mmu-mir-130a, mmu-mir-133a-1, mmu-mir-140, mmu-mir-24-1, hsa-mir-196a-1, mmu-mir-199a-1, hsa-mir-199a-1, mmu-mir-200b, mmu-mir-206, hsa-mir-30c-2, hsa-mir-196a-2, hsa-mir-199a-2, hsa-mir-199b, hsa-mir-200b, mmu-mir-301a, mmu-let-7d, hsa-let-7g, hsa-let-7i, hsa-mir-1-2, hsa-mir-15b, hsa-mir-23b, hsa-mir-27b, hsa-mir-130a, hsa-mir-133a-1, hsa-mir-133a-2, hsa-mir-140, hsa-mir-206, mmu-mir-30c-1, mmu-mir-30c-2, mmu-mir-196a-1, mmu-mir-196a-2, 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-15a, mmu-mir-18a, mmu-mir-20a, mmu-mir-24-2, mmu-mir-27a, mmu-mir-92a-2, hsa-mir-200c, hsa-mir-1-1, mmu-mir-1a-2, mmu-mir-17, mmu-mir-19a, mmu-mir-200c, mmu-mir-199a-2, mmu-mir-199b, mmu-mir-19b-1, mmu-mir-92a-1, hsa-mir-30c-1, hsa-mir-200a, hsa-mir-301a, mmu-mir-133a-2, mmu-mir-133b, hsa-mir-133b, hsa-mir-196b, mmu-mir-196b, dre-mir-196a-1, dre-mir-199-1, dre-mir-199-2, dre-mir-199-3, hsa-mir-18b, 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-1-2, dre-mir-1-1, dre-mir-15a-1, dre-mir-15a-2, dre-mir-15b, dre-mir-17a-1, dre-mir-17a-2, dre-mir-18a, dre-mir-18b, dre-mir-18c, dre-mir-19a, dre-mir-20a, dre-mir-23b, dre-mir-24-4, dre-mir-24-2, dre-mir-24-3, dre-mir-24-1, dre-mir-27a, dre-mir-27b, dre-mir-27c, dre-mir-27d, dre-mir-27e, dre-mir-30c, dre-mir-92a-1, dre-mir-92a-2, dre-mir-92b, dre-mir-130a, dre-mir-133a-2, dre-mir-133b, dre-mir-133c, dre-mir-140, dre-mir-196a-2, dre-mir-196b, dre-mir-200a, dre-mir-200b, dre-mir-200c, dre-mir-206-1, dre-mir-206-2, dre-mir-301a, dre-let-7j, hsa-mir-92b, mmu-mir-666, mmu-mir-18b, mmu-mir-92b, mmu-mir-1b, dre-mir-196c, dre-mir-196d, mmu-mir-3074-1, mmu-mir-3074-2, hsa-mir-3074, mmu-mir-133c, mmu-let-7j, mmu-let-7k, dre-mir-24b
Other groups have performed miRNA expression profiling of the developing mouse orofacial region using microarrays (Mukhopadhyay et al., 2010) and have found similar differential expression across time for miRNAs that included Mir133a and Mir133b. [score:5]
The role of microRNA-1 and microRNA-133 in skeletal muscle proliferation and differentiation. [score:1]
[1 to 20 of 2 sentences]
17
[+] 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]
[1 to 20 of 1 sentences]
18
[+] score: 4
Other miRNAs from this paper: dre-mir-1-2, dre-mir-1-1, dre-mir-133a-2, dre-mir-133b
For the first time the research of Ceci et al., has demonstrated the early activation of the heart of zebrafish from 24 h (hrs) post injury due to downregulations of miR1, miR133a, and miR133b. [score:4]
[1 to 20 of 1 sentences]
19
[+] score: 3
However, the expression levels of miR-124-3p, miR-124-5p, miR-124-6-5p, miR-133a-3p, miR-133b-3p, miR-135b-3p, miR-135b-5p, miR-137-3p and some other miRNAs were rather low (Excel S1). [score:3]
[1 to 20 of 1 sentences]
20
[+] score: 3
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-16-1, hsa-mir-17, hsa-mir-21, hsa-mir-22, hsa-mir-28, hsa-mir-29b-1, hsa-mir-16-2, mmu-let-7g, mmu-let-7i, mmu-mir-1a-1, mmu-mir-29b-1, mmu-mir-124-3, mmu-mir-9-2, mmu-mir-133a-1, mmu-mir-145a, mmu-mir-150, mmu-mir-10b, mmu-mir-195a, mmu-mir-199a-1, hsa-mir-199a-1, mmu-mir-200b, mmu-mir-206, mmu-mir-143, hsa-mir-10a, hsa-mir-10b, hsa-mir-199a-2, hsa-mir-217, hsa-mir-218-1, hsa-mir-223, hsa-mir-200b, mmu-let-7d, hsa-let-7g, hsa-let-7i, hsa-mir-1-2, hsa-mir-124-1, hsa-mir-124-2, hsa-mir-124-3, hsa-mir-133a-1, hsa-mir-133a-2, hsa-mir-143, hsa-mir-145, hsa-mir-9-1, hsa-mir-9-2, hsa-mir-9-3, hsa-mir-150, hsa-mir-195, hsa-mir-206, 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-16-1, mmu-mir-16-2, mmu-mir-21a, mmu-mir-22, mmu-mir-29c, rno-let-7d, rno-mir-329, mmu-mir-329, rno-mir-331, mmu-mir-331, rno-mir-148b, mmu-mir-148b, rno-mir-135b, mmu-mir-135b, hsa-mir-200c, hsa-mir-1-1, mmu-mir-1a-2, mmu-mir-10a, mmu-mir-17, mmu-mir-28a, mmu-mir-200c, mmu-mir-218-1, mmu-mir-223, mmu-mir-199a-2, mmu-mir-124-1, mmu-mir-124-2, mmu-mir-9-1, mmu-mir-9-3, mmu-mir-7b, mmu-mir-217, hsa-mir-29c, hsa-mir-200a, hsa-mir-365a, mmu-mir-365-1, hsa-mir-365b, hsa-mir-135b, hsa-mir-148b, hsa-mir-331, mmu-mir-133a-2, mmu-mir-133b, hsa-mir-133b, rno-let-7a-1, rno-let-7a-2, rno-let-7b, rno-let-7c-1, rno-let-7c-2, rno-let-7e, rno-let-7f-1, rno-let-7f-2, rno-let-7i, rno-mir-7b, rno-mir-9a-1, rno-mir-9a-3, rno-mir-9a-2, rno-mir-10a, rno-mir-10b, rno-mir-16, rno-mir-17-1, rno-mir-21, rno-mir-22, rno-mir-28, rno-mir-29b-1, rno-mir-29c-1, rno-mir-124-3, rno-mir-124-1, rno-mir-124-2, rno-mir-133a, rno-mir-143, rno-mir-145, rno-mir-150, rno-mir-195, rno-mir-199a, rno-mir-200c, rno-mir-200a, rno-mir-200b, rno-mir-206, rno-mir-217, rno-mir-223, dre-mir-7b, dre-mir-10a, dre-mir-10b-1, dre-mir-217, dre-mir-223, hsa-mir-429, mmu-mir-429, rno-mir-429, mmu-mir-365-2, rno-mir-365, dre-mir-429a, hsa-mir-329-1, hsa-mir-329-2, hsa-mir-451a, mmu-mir-451a, rno-mir-451, dre-mir-451, 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-1-2, dre-mir-1-1, 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-10b-2, dre-mir-16a, dre-mir-16b, dre-mir-16c, dre-mir-17a-1, dre-mir-17a-2, dre-mir-21-1, dre-mir-21-2, dre-mir-22a, dre-mir-22b, dre-mir-29b-1, 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-133a-2, dre-mir-133b, dre-mir-133c, dre-mir-143, dre-mir-145, dre-mir-150, dre-mir-200a, dre-mir-200b, dre-mir-200c, dre-mir-206-1, dre-mir-206-2, dre-mir-365-1, dre-mir-365-2, dre-mir-365-3, dre-let-7j, dre-mir-135b, rno-mir-1, rno-mir-133b, rno-mir-17-2, mmu-mir-1b, dre-mir-429b, rno-mir-9b-3, rno-mir-9b-1, rno-mir-9b-2, rno-mir-133c, mmu-mir-28c, mmu-mir-28b, hsa-mir-451b, mmu-mir-195b, mmu-mir-133c, mmu-mir-145b, mmu-mir-21b, mmu-let-7j, mmu-mir-21c, mmu-mir-451b, mmu-let-7k, rno-let-7g, rno-mir-29c-2, mmu-mir-9b-2, mmu-mir-124b, mmu-mir-9b-1, mmu-mir-9b-3
For example, miR-1 and miR-133 are specifically expressed in muscles. [score:3]
[1 to 20 of 1 sentences]
21
[+] score: 2
Regulation of zebrafish heart regeneration by miR-133. [score:2]
[1 to 20 of 1 sentences]
22
[+] score: 2
Other miRNAs from this paper: hsa-mir-133a-1, hsa-mir-133a-2, dre-mir-133a-2
DCM caused by deregulation of miRNAs such as miRNA-133a has been recently described in animal mo dels (Chen et al, 2008; Meder et al, 2008; van Rooij et al, 2007). [score:2]
[1 to 20 of 1 sentences]
23
[+] score: 2
Additional data indicate that FGF and BMP signaling pathway interactions are regulated by negative feedback loops involving microRNAs, particularly miR-130 and miR-133 [48, 49]. [score:2]
[1 to 20 of 1 sentences]
24
[+] score: 1
Other miRNAs from this paper: dre-mir-133a-2, dre-mir-133b, dre-mir-133c
Fgfr1 control of growth rate is exerted by miR-133 mediation (Yin and Poss, 2008). [score:1]
[1 to 20 of 1 sentences]
25
[+] score: 1
For instance miR-1 and miR-133, whose origin remounts to a common ancestor of Protostomia and Deuterostomia [25], were amongst the most conserved miRNAs (Table  2). [score:1]
[1 to 20 of 1 sentences]
26
[+] score: 1
Similarly reports suggest that linc-MD1 could interact with miR-133 and miR-135 and promote muscle differentiation [38]. [score:1]
[1 to 20 of 1 sentences]
27
[+] score: 1
Yin VP Fgf -dependent depletion of microRNA-133 promotes appendage regeneration in zebrafishGenes Dev. [score:1]
[1 to 20 of 1 sentences]