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8 publications mentioning dre-mir-29b3

Open access articles that are associated with the species Danio rerio and mention the gene name mir-29b3. Click the [+] symbols to view sentences that include the gene name, or the word cloud on the right for a summary.

1
[+] score: 171
Specifically, in the heart, miR-29 family up-regulation is associated with cardiac development and growth regulation [59] whereas its down-regulation is involved in cardiac tissue remo deling after myocardial infarction [43]. [score:9]
Age -dependent miR-29 family up-regulation correlates with regulation of collagen and methylation levels in Nothobranchius furzeri heartMiR-29 family, one of the most upregulated miRNAs, was further evaluated for its well-known role during aging and cardiovascular diseases. [score:8]
Red dots show miR-29-sponge up-regulated genes, blue dots show Wild Type up-regulated genes. [score:7]
The increased expression levels of col1a1, col1a2 and col15a1, all known direct targets of miR-29, further confirmed an accumulation of collagen deposition in the miR-29-sponge heart (Fig.   6 panel C). [score:6]
In HCF derived from old donors, all miR-29 family members were upregulated (Figure  S1 panel A), with a parallel decrease of col3a1 expression (Figure  S1 panel B) and global 5mC level (Figure  S1 panel C). [score:6]
Consistently, the DNMT inhibitor RG108 exerted the same effect of miR-29a or miR-29b mimics (Fig.   9 panel C), further suggesting a potential role for miR-29 family in preventing hypoxia -dependent hypermethylation via down-regulation of DNMTs 66, 67. [score:6]
Interestingly, the analysis of miRNA expression performed in different Nfu organs, including brain, liver, heart and skin, revealed miR-29 family together with miR-27d as one of the only two consistently up-regulated miRNAs during aging in all the four tissues (Figure  S5) [34]. [score:6]
Age -dependent miR-29 family up-regulation correlates with regulation of collagen and methylation levels in Nothobranchius furzeri heart. [score:5]
Noteworthy, the ROS scavenger N-acetyl cysteine (NAC) counteracted the effect of H [2]O [2] on expression of miR-29 expression (Figure  S2 panel A and Fig.   4 panel A) suggesting a link between miR-29 and oxidative stress. [score:5]
To functionally analyze the role of miR-29 in the heart we generated a transgenic zebrafish mo del where miR-29 biological activity was antagonized by the stable expression of a competitive inhibitor (a 3′-UTR containing seven repeats of the miR-29 binding site: miR-29-sponge) under the control of the actin beta-2 promoter (actb2:eGFP-sponge-29) of Danio renio 35, 62. [score:5]
Full-length blot is presented in Supplementary Figure 6. (B) qRT-PCR mRNA analysis of hypoxia associated genes: erythropoietin alpha (epoa); hexokinase2 (hk2); heme oxygenase1a (hmox1a); lactate dehydrogenase A (ldha); cyclin -dependent kinase inhibitor 1B (p27) in Wild Type (black circles; n = 4) and miR-29-sponge (gray squares; n = 4) Zebrafish hearts expressed as fold-change versus Wild Type samples. [score:5]
miR-29 family knock-down changes global methylation level and collagen expression in Zebrafish. [score:4]
Of note, the knock-down of miR-29 family in zebrafish transgenic animal embryo by expression of a specific sponge (miR-29-sponge) [35] compromised cardiac function and morphology, enhancing both fibrosis and global DNA methylation. [score:4]
Genes regulated by miR-29 depletion ( ± 0.5 log2 fold change, basemean > 5, fdr < 0.05) derived from mRNASeq of zebrafish samples were imported into the Ingenuity Pathways Analysis Software (Qiagen - Version 39480507) to reveal top disease affected categories by genetic networks. [score:4]
Biological function gene ontology of up-regulated genes in miR-29-sponge Zebrafish hearts (red bars). [score:4]
Given the up-regulation of miR-29 during aging in multiple organs, this protective action could represent a general phenomenon. [score:4]
List of genes is provided also in supplemental table  5. (B) Volcano plot of differentially regulated genes expressed in the heart of Wild Type and miR-29-sponge Zebrafish. [score:4]
Figure 3Age -dependent miR-29 family up-regulation affects collagen and methylation levels in N. furzeri heart. [score:4]
Despite age -dependent upregulation, antagonism of miR-29 exacerbates brain aging indicating that miR-29 has a protective role in neurons [35]. [score:4]
Intriguingly, after treatment with H [2]O [2], the transcripts coding for miR-29 target genes, including col1a1, col11 and dnmt1, dnmt3a and dnmt3b, were down regulated while NAC partially restored their normal mRNA levels (Fig.   4 panels B and C). [score:4]
Moreover, gene ontology analysis of biological functions obtained by Gene set enrichment analysis (GSEA) pointed out an up-regulation of cellular response to stress and methylation (Fig.   7 panel D; red bar graph) as well as a down-modulation of response to oxidative stress and cardiac morphology and functions (Fig.   7 panel D; blue bar graph), which fully correlate with our experimental evidences on miR-29 sponge fish in comparison to Wild Type. [score:4]
Myocardial infarction, in fact, induces a down-regulation of miR-29 which event, in turn, is partially responsible for fibrosis [43]. [score:4]
MiR-29 family, one of the most upregulated miRNAs, was further evaluated for its well-known role during aging and cardiovascular diseases. [score:4]
Interestingly, these miRNAs control the expression of collagen genes and are themselves controlled by TGF-β [44] suggesting for a direct link between miR-29 family and the progress of inflammatory responses. [score:4]
Figure 9Hypoxia affects miR-29 family and its related targets. [score:3]
Similarly, expression of miR-29 counteracts age -dependent oxidative damage in the brain [35]. [score:3]
Figure 4Oxidative stress affects miR-29 family and its targets. [score:3]
Of note, exogenous expression of miR-29a/b mimics rescued the hypoxic and fibrotic phenotype (Fig.   9 panel B) suggesting a possible protective role of miR-29 family to counteract hypoxia-related collagen deposition and consequently fibrosis. [score:3]
Oxidative stress induces expression of microRNA-29 family. [score:3]
Upon miR-29 knockdown, no significant changes were detected in terms of survival during the first year of age (data not shown). [score:2]
Ingenuity pathway analysis on genes regulated by miR-29 depletion ( ± 0.5 log2 fold change, basemean > 5, fdr < 0.05) revealed a predicted activation of the hypertrophic response in miR-29 sponge fish, perfectly fitting with the observed cardiac phenotype (Fig.   7 panel C). [score:2]
Interestingly, 350 transcripts were found up regulated in the miR-29-sponge compare to Wild type hearts (suppl. [score:2]
Taken altogether, these data suggested that miR-29 family is regulated by ROS. [score:2]
In the cardiovascular system, miR-29 family has multiple roles: i) is known to be involved in atrial fibrillation [69]; ii) may act as a negative regulator of fibrosis counteracting miR-21 function 43, 70, 71; iii) controls cardiomyocytes apoptosis and aortic aneurism formation 30, 72. [score:2]
In addition, miR-29 has been described to be up regulated during cardiac aging in mouse [30]. [score:2]
In the present study, by using human cardiac fibroblasts, we demonstrated for the first time that miR-29 family is regulated by oxidative stress level. [score:2]
To further explore the effect of miR-29 family depletion on the cardiac molecular phenotype, RNA sequencing (RNA-seq) was performed on the whole heart of wt and miR-29-sponge fish. [score:1]
Calibration bar = 1 mm (B) Representative echocardiography of Wild Type (left panels) and miR-29-sponge (right panels) Zebrafish hearts showing end-diastolic area (EDA; first and third panel) and end-systolic area (ESA; second and fourth panel) Calibration bar = 1 mm. [score:1]
Hence, we propose here that the physiological accumulation of oxidative stress during aging may control miR-29 family establishing a protective mechanism to limit cardiac fibrosis. [score:1]
Figure 8Hypoxic markers accumulate in miR-29-sponge Zebrafish hearts. [score:1]
This evidence prompted us to investigate miR-29 family expression in cardiac fibroblasts maintained in the presence of 1% O [2], the standard in vitro hypoxic condition. [score:1]
Specifically, miR-29 sponge fish showed a FAC of 16%, whereas control animals had values of about 30% (Fig.   5 panel D). [score:1]
For long RNA sequencing, RNA was isolated from 3 zebrafish hearts for each condition (wt and miR-29-sponge) using the miRNeasy micro Kit (Qiagen) combined with on-column DNase digestion (DNase-Free DNase Set, Qiagen) to avoid contamination by genomic DNA. [score:1]
In order to assess cardiac function in Wild type and miR-29-sponge zebrafish, animals were anesthetized with low-dose tricaine solution (0.04 mg/mL) and placed in a Petri dish filled with a custom-made sponge, with the ventral side upward. [score:1]
To investigate the effect of hypoxia on miR-29 family and its targets, HCFs were exposed to 1% O [2] concentration for 48 hours. [score:1]
In this perspective, miR-29 family members are of particular interest for cardiac pathophysiology. [score:1]
miR-29 family resulted sensitive to 200 µM H [2]O [2] already after 24 h of treatment (Figure  S2 panel A and Fig.   4 panel A). [score:1]
Morphologically, we found a significant cardiac spherization in fish injected with miR-29-sponges detectable by 2D-echo analysis (Fig.   5 panel B) and visible hypertrophy that were confirmed by histological examinations (Fig.   5 panel E). [score:1]
Indeed, our results suggest that the miR-29 family strongly affects gene transcription possibly via age-associate DNA methylation changes in Nfu. [score:1]
Because of its biological relevance in cardiac pathophysiology, we focused our attention on miR-29 family. [score:1]
Moreover, miR-29 family play a role during DNA methylation / demethylation control [57] and cellular reprogramming [58]. [score:1]
The sensitivity of miR-29a and miR-29b to O [2] reduction was confirmed also by pri-miR-29 analysis. [score:1]
Hematoxylin/eosine-stained sections were prepared to visualize ventricle of wt and miR-29-sponge zebrafish. [score:1]
To investigate the potential relationship between the accumulation of ROS in the heart (see Fig.   1 panels D and E) and the increase in miR-29 family member expression (Fig.   3 panel A), differentiated H9C2 rat cardiomyoblasts and human cardiac fibroblasts (HCF) were exposed to H [2]O [2] [46]. [score:1]
Hypoxia induces hypermethylation and fibrosis by miR-29 family down-modulation. [score:1]
Figure 7Identification of miR-29 associated cardiac transcriptome. [score:1]
In these experiments, we detected a transient down-modulation of miR-29a and miR-29b leading to collagen deposition and fibrosis, a molecular scenario similar to that observed in the heart of the miR-29-sponge transgenic fish. [score:1]
Calibration bar = 25 µm (B) Collagen deposition quantification in sections derived from Wild Type (black circles; n = 8) and miR-29-sponge (gray squares; n = 8) Zebrafish hearts. [score:1]
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[+] score: 18
Other miRNAs from this paper: dre-mir-10a, dre-mir-10b-1, dre-mir-183, dre-mir-430a-1, dre-mir-430b-1, dre-mir-430c-1, dre-let-7a-1, dre-let-7a-2, dre-let-7a-3, dre-let-7a-4, dre-let-7a-5, dre-let-7a-6, dre-mir-1-2, 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-10c, dre-mir-10d, dre-mir-15a-1, dre-mir-15a-2, dre-mir-17a-1, dre-mir-17a-2, dre-mir-20a, dre-mir-29b-1, dre-mir-29b-2, dre-mir-29a, dre-mir-92a-1, dre-mir-92a-2, dre-mir-92b, dre-mir-101a, dre-mir-101b, 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-145, 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-mir-499, ola-mir-430a-1, ola-mir-430c-1, ola-mir-430b-1, ola-mir-430c-2, ola-mir-430c-3, ola-mir-430d-1, ola-mir-430a-2, ola-mir-430c-4, ola-mir-430d-2, ola-mir-430a-3, ola-mir-430a-4, ola-mir-430c-5, ola-mir-430d-3, ola-mir-430b-2, ola-mir-430c-6, ola-mir-430c-7, ola-mir-20a-1, ola-mir-92a-2, ola-mir-9a-2, ola-mir-101a, ola-mir-9b-1, ola-mir-499, ola-let-7a-1, ola-mir-9a-3, ola-mir-183-1, ola-let-7a-2, ola-mir-29b-1, ola-mir-29a, ola-mir-124-1, ola-mir-124-2, ola-mir-9a-4, ola-mir-101b, ola-let-7a-4, ola-mir-10d, ola-mir-9a-1, ola-mir-92b, ola-mir-9b-2, ola-mir-1-2, ola-mir-124-3, ola-mir-15a, ola-mir-10b, ola-mir-92a-1, ola-mir-20a-2, ola-mir-17, ola-mir-29b-2, ola-mir-29c, ola-mir-183-2, ola-let-7a-3, ola-mir-9a-5, ola-mir-145
Mir-29 family members are up-regulated during aging in a variety of different tissues including muscle, skin, brain and aorta [2, 18, 46, 54, 56, 66] and appear to be key regulators of age -dependent gene expression [6, 51]. [score:6]
We found e. g., miR-10, miR-29 and miR-92 showing potential to be significantly involved in the down-regulation of genes in the aging brain of N. furzeri, like cell cycle regulators (ccne2 [22], nek6 [38], cdk13 [42]) or cancer related genes (mycn [8, 12], vav2 [13, 28]), both processes involved in aging. [score:5]
In O. latipes and T. rubripes, both miR-29 clusters are still present, whereas D. rerio seems to has lost one copy of the miR-29a gene. [score:1]
Whereas for D. rerio the mir-29a-2 gene seems to be lost, we assume that for G. aculeatus the whole second mir-29 cluster (dashed circles) is only missing, because of the low quality genome sequencing and assembly. [score:1]
Another example for an evolutionary conserved miRNA cluster is the miR-29 cluster depicted in Fig. 6d. [score:1]
As from RFAM (version 12.1) and miRBase (release 21), miR-29 genes are mainly identified in vertebrates as well as one Hemichordata and one Arthropoda, so we can only speculate that the original cluster duplication event arose in the early metazoa lineage. [score:1]
d After the ancestral duplication event, the mir-29 cluster is distinguished in the mir-29a/b-1 (filled red and blue dots) and the mir-29a/b-2 cluster (red and blue circles). [score:1]
For G. aculeatus, we were only able to identify one miR-29 cluster. [score:1]
Assuming a complete genome assembly, different scenarios could explain this finding: (1) both original miR-29 clusters were individually duplicated once more, and the fourth miR-29a gene was later lost, (2) one of the two clusters was duplicated as a whole, whereas in the other only miR-29b was copied or (3) both original clusters were duplicated during the same event, and again one of the miR-29a genes was later lost. [score:1]
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3
[+] score: 13
In particular, miR-29, which is down-regulated in response to cardiac injury, has been shown to inhibit the expression of fibrotic genes [148], while miR-21, which is upregulated in response to cardiac stress, has been proposed to promote it [149, 150], although a miR-21 KO mouse mo del raises questions on the essential nature of this response [151]. [score:11]
Van Rooij E. Sutherland L. B. Thatcher J. E. DiMaio J. M. Naseem R. H. Marshall W. S. Hill J. A. Olson E. N. Dysregulation of microRNAs after myocardial infarction reveals a role of miR-29 in cardiac fibrosis Proc. [score:2]
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[+] score: 10
Furthermore, miR-29 was found to suppress immune responses to Listeria monocytogenes and Mycobacterium tuberculosis by targeting IFN-γ [17]. [score:5]
By microarray analysis of miRNA expression in zebrafish we found that miRNAs of the miR-21, miR-29, and miR-146 families were commonly induced by infection of embryos with S. typhimurium and by infection of adult fish with M. marinum. [score:3]
The miR-146 family members were commonly induced during infections of embryos and adult fish, along with miRNAs of the miR-21 and miR-29 families, which also have been implicated in immunity and infection. [score:1]
The induction of members of the miR-21, miR-29, and miR-146 families was in line with earlier microarray studies, which reported these along with some other miRNAs, like miR-9, miR-132, miR-147, and miR-155 as infection-inducible [13, 26, 43, 44]. [score:1]
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[+] score: 5
Other miRNAs from this paper: dre-mir-29b-1, dre-mir-29b-2, dre-mir-29a
Polycomb Group member YY1 was found to be upregulated in RMS cell lines and primary tumors, thus leading to recruitment of EZH2 and HDAC1 to miR-29, silencing this microRNA, and thereby preventing muscle differentiation and facilitating tumor development [12]. [score:5]
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6
[+] score: 4
In zebrafish, miR-29b is part of the miR-29 family that comprises three intergenic members that map to chromosome 4 (miR-29a and miR-29b-2 located within 10Kb of each other; miR-29b-2 referred to as miR-29b herein), and chromosome 6 (miR-29b-1; [34]). [score:1]
Levels of miR-29 and miR-223 were normalized to U6 snRNA and relative fold change between control and crush tissue was determined using 2 [-ΔΔCt] method. [score:1]
HEK293 cells were transfected with either a wild type (WT) or mutated construct (MT), along with a miRNA mimic (miR-29/miR-223) or negative control (miR-NC). [score:1]
The role of miRNAs, including the miR-29 family, in modifying ECM-cell signaling has recently been highlighted [53]. [score:1]
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7
[+] score: 2
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-133a-1, 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
Fabbri M. Garzon R. Cimmino A. Liu Z. Zanesi N. Callegari E. Liu S. Alder H. Costinean S. Fernandez-Cymering C. MicroRNA-29 family reverts aberrant methylation in lung cancer by targeting DNA methyltransferases 3a and 3bEur. [score:2]
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8
[+] score: 1
In another example shown by Wang et al. miR-29 is repressed by NF-kappaB acting through YY1 and the PcG-proteins [40]. [score:1]
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