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34 publications mentioning mmu-mir-328

Open access articles that are associated with the species Mus musculus and mention the gene name mir-328. Click the [+] symbols to view sentences that include the gene name, or the word cloud on the right for a summary.

1
[+] score: 273
However, pre-treatment of macrophages with a p38 inhibitor, doramapimod, or a JNK inhibitor, SP600125, prior to NTHi infection, completely blocked the down-regulation of miR-328 expression (Fig 2H). [score:10]
Among these differentially expressed miRNA we selected miR-328, specifically the 3p strand, as a candidate miRNA for further study as its baseline expression was among the highest observed and most significantly down-regulated following infection. [score:8]
We next determined whether miR-328 was involved in dexamethasone -mediated suppression of immunity and bacterial clearance, and if inhibition of this miRNA could enhance bacterial clearance in these immune suppressed mice. [score:7]
Notably from profiling data, miR-328, a highly conserved miRNA, was significantly down-regulated by infection and its basal level are amongst the highest of all down-regulated miRNA, suggesting a key role in the host response to NTHi infection. [score:7]
Similarly, infection of primary lung macrophages by NTHi also downregulated miR-328 expression in vitro. [score:6]
Here we found that p38 and JNK MAPK is activated by NTHi infection, and inhibition of these MAPK signalling prior to bacterial infection prevents the down-regulation of miR-328 levels. [score:6]
This study is the first to identify a role for miR-328 in regulating bacterial infection in the lung and provides proof-of-principle data that targeting specific host miRNAs could lead to future therapeutics to combat multi-drug resistant bacteria and infection in chronic lung diseases and immune-compromised patients. [score:6]
Although the specific targets of miR-328 remain to be elucidated it is likely that this miRNA targets transcripts involved in regulating phagocytosis and controlling the microbicidal activity of the macrophages and neutrophils. [score:6]
Inhibiting miR-328 enhances bacterial clearance in dexamethasone -mediated immune suppressed mice. [score:5]
Inhibition of miR-328 increased expression of bacterial binding molecules CD14, CD36, and CD11b. [score:5]
Inhibition of miR-328 overcomes corticosteroid -induced immune suppression to clear bacteria. [score:5]
This suggests that NTHi suppresses miR-328 expression via activation of the p38 and JNK MAPK pathway. [score:5]
These data indicate that the inhibition of miR-328 was as effective at clearing bacteria in both immune competent and immune suppressed environments. [score:5]
MiR-328 expression is regulated by p38 and JNK MAPK and inhibition increases bacterial clearance in vitro. [score:5]
Administration of ant-328 inhibited expression of miR-328 (Fig 2A). [score:5]
Notably, inhibition of miR-328 in the lung was effective in amplifying the clearance of infection even in mo dels of corticosteroid -induced immunosuppression and cigarette smoke -induced emphysema. [score:5]
Inhibition of miR-328 with ant-328 substantially increased bacterial clearance suggesting that targeting this miRNA could be potentially used as a new approach to anti-microbial therapy. [score:5]
Inhibition of miR-328 function in human macrophages and neutrophils using ant-328 also resulted in increased bacterial phagocytosis, indicating that our studies are potentially translatable into anti-microbial innate host defence pathways in human cells. [score:5]
Thus, it is possible that miR-328 expression could be regulated by other pathways in a more complex in vivo environment. [score:4]
miR-328 regulates bacterial killing pathways and its expression is controlled by p38 and JNK signalling. [score:4]
Inhibition of miR-328 with ant-328 suggests that this microRNA regulates phagocytosis and killing of bacteria by macrophages and neutrophils in vitro. [score:4]
Here we demonstrate a new role in regulating innate immune cell function, wherein suppression of miR-328 improves bacterial clearance in the lungs. [score:4]
Here we demonstrate that down-regulation of miR-328-3p (termed miR-328 hereafter) is a key element of the innate host defence response to NTHi infection, which facilitates bacterial clearance. [score:4]
Adoptive transfer of miR-328 -depleted macrophages or neutrophils increased bacterial clearance in the lung, further supporting our in vitro observations and directly demonstrating that inhibition of miR-328 in these cells amplifies their ability to clear respiratory infections. [score:4]
did not alter miR-328 expression, suggesting that this miRNA was not directly involved in mediating the effects of corticosteroids (Fig 4A). [score:4]
To investigate the signalling pathways involved in the regulation of miR-328 expression, we used specific inhibitors to block the activation of p38, JNK, and ERK MAPK following NTHi infection. [score:4]
In cancer, miR-328 expression is regulated through the ERK1/2 pathway [38]. [score:4]
Macrophages were purified from lungs of naïve mice and pre -treated with a miRNA inhibitor (antagomir (ant)) with perfect complementarity to miR-328 (ant-328). [score:3]
miR-328 is involved in cancer [36– 38], autoimmunity [39], and neuronal disease [40]. [score:3]
Inhibiting miR-328 increases bacterial uptake in human monocyte-derived macrophages and neutrophils. [score:3]
Ant-328 treatment inhibited miR-328 in both dexamethasone and vehicle -treated mice infected with NTHi to similar levels (Fig 4D). [score:3]
Treatment of macrophages with the mimetic to miR-328 had no effect on bacterial clearance likely because the basal expression level of miR-328 in lung macrophages is already high and so any additive effect becomes masked (S6A and S6B Fig). [score:3]
It will be important, however, to study the chronic impact of altering miR-328 function in murine mo dels, and subsequently in human disease. [score:3]
Using a cigarette smoked -induced mo del of experimental COPD [46], we demonstrated that inhibiting miR-328 brought about a 3-fold increase in bacterial clearance. [score:3]
Although speculative, targeting miR-328 may be more broadly applicable and lead to improvement of innate immune cell function in these immune -deficient patients. [score:3]
We next assessed whether inhibition of miR-328 improved NTHi clearance in vivo, which would indicate whether the use of ant-328 would be a potential therapeutic option for respiratory bacterial infection. [score:3]
Inhibition of miR-328 promotes bacterial clearance in a mo del of cigarette smoke -induced emphysema. [score:3]
Inhibiting miR-328 enhances bacterial clearance in cigarette smoke-exposed mice. [score:3]
Inhibiting miR-328 improves NTHi clearance in the lungs in vivo. [score:3]
Exposure of macrophages to NTHi or vehicle (DMSO) plus NTHi led to a significant 2-fold reduction in miR-328 expression (Fig 2H). [score:3]
MiR-328 is down-regulated after NTHi infection. [score:3]
Moreover, pharmacological inhibition of miR-328 profoundly enhances the clearance of the infection by increasing bacterial uptake by phagocytes, the production of reactive oxygen species (ROS), and microbicidal activity. [score:3]
1004549.g003 Fig 3Inhibiting miR-328 improves NTHi clearance in the lungs in vivo. [score:3]
Inhibition of miR-328 function in macrophages (Fig 2D and 2E) and neutrophils (S3D Fig) substantially enhanced phagocytosis of heat-killed NTHi (significantly increased levels of intracellular CFSE). [score:3]
Interestingly, inhibition of microRNA-328 in mouse and human macrophages increases microbicidal activity by amplifying phagocytosis and production of reactive oxygen species. [score:3]
Likewise, the inhibition of miR-328 in neutrophils produced similar results (S3 E Fig). [score:3]
S3 FigInhibition of miR-328 increases phagocytosis and bacterial clearance by neutrophils in vitro. [score:3]
Inhibition of miR-328 in the lungs promotes bacterial clearance. [score:3]
Inhibition of miR-328 increases phagocytosis and bacterial clearance by neutrophils in vitro. [score:3]
Importantly, dexamethasone administration did not alter miR-328 expression levels despite the increased bacterial load in the lungs. [score:3]
Effect of miR-328 inhibition on ROS generation. [score:3]
We validated the miRNA array data for miR-328 using TaqMan PCR and observed a ~2-fold reduction in expression 24 h after infection (Fig 1E). [score:3]
Although inhibition with an antagomir dramatically promoted NTHi clearance, application of a mimetic (increasing miR-328 levels) failed to delay clearance of NTHi. [score:3]
Inhibition of miR-328 function by ant-328 was confirmed during infection (Fig 3F). [score:3]
Similar to the results observed with murine cells, inhibition of miR-328 significantly increased bacterial uptake by human macrophages (Fig 6A) and neutrophils (Fig 6B) in vitro. [score:3]
Inhibition of miR-328 function also resulted in a decrease in pulmonary compliance (Fig 5D) and an increase in pulmonary elastance (Fig 5E). [score:3]
To determine whether the effects of miR-328 inhibition were due to altered phagocytosis of bacteria, or increased permissibility of phagocytes to active infection, we conducted a phagocytosis assay. [score:2]
MiR-328 regulates bacterial clearance by macrophages and neutrophils in vivo To specifically assess the role of miR-328 in macrophage- and neutrophil -mediated bacterial clearance in vivo we conducted adoptive transfer experiments. [score:2]
Collectively, this data suggests that miR-328 regulates bacterial phagocytosis in neutrophils and macrophages at least partly through the control of cell surface bacterial binding proteins. [score:2]
This indicates that miR-328 regulates phagocytosis and killing of bacteria. [score:2]
Inhibition of miR-328 in dexamethasone pre -treated mice reversed the increased bacteria load compared to controls (Fig 4E). [score:2]
MiR-328 expression following NTHi infection in vivo. [score:2]
Inhibition of miR-328 in neutrophils (S3A Fig) resulted in a 3-fold decrease in bacterial load in the culture supernatant as early as 1 h p. i. and a dramatic increase in bacterial uptake compared to Scr control treatment (S3B–S3C Fig, respectively). [score:2]
MiR-328 was inhibited in (A) macrophages or (C) neutrophils for 12 h ex vivo. [score:2]
miR-328 regulates macrophage and neutrophil bacterial phagocytosis. [score:2]
This suggests that NTHi down regulates miR-328 at least in part through p38 and JNK signalling pathways. [score:2]
Collectively, these data suggest that NTHi activates the p38 and JNK signalling pathways, which regulates the cellular levels of miR-328. [score:2]
Here we show that increased production of ROS in ant-328 treated phagocytes, indicating that this bacterial killing mechanism is also regulated by miR-328. [score:2]
Exposure of the lung to ant-328 resulted in significant reduction in the levels of miR-328 (Fig 5A). [score:1]
We speculate that this is because the levels of endogenous miR-328 are very high, hence masking the effect of mimetic treatment. [score:1]
Thus, we next investigated if inhibition of miR-328 improved bacterial clearance in our mo del of cigarette smoke -induced emphysema. [score:1]
To specifically assess the role of miR-328 in macrophage- and neutrophil -mediated bacterial clearance in vivo we conducted adoptive transfer experiments. [score:1]
Interestingly, miR-328 was decreased within 3 h in infected airways and remain decreased over a 48 h period (S2A Fig). [score:1]
MiR-328 expression levels in (A) airways and (B) lung macrophages measured using Taqman qPCR normalised to sno-202 and expressed as fold change compared to control. [score:1]
S6 Fig Primary lung macrophages were isolated from the lungs of naïve mice and pre -treated with miR-328 mimic for 24 h before infection with NTHi at MOI 100. miR-Scr was used as a control. [score:1]
Similarly, levels of miR-328 are diminished and remain lower in macrophages isolated from the NTHi infected lung over a similar time period (S2B Fig). [score:1]
Thus, miR-328 plays a very specific role in the microbicidal activity of these innate immune cells. [score:1]
Effect of miR-328 on lung inflammation in non-infected mice. [score:1]
MiR-328 regulates bacterial clearance by macrophages and neutrophils in vivo. [score:1]
Exposure of macrophages to NTHi and Scr resulted in a decrease in the levels of miR-328 by ~25% as assessed by TaqMan qPCR (Fig 2A) (this level was similar to NTHi exposure alone). [score:1]
Thus, we determined whether miR-328 plays a role in activating these killing pathways in macrophages and neutrophils. [score:1]
High levels of miR-328 are linked to macrophage homeostasis and thus it is only when levels are dramatically decreased by antagomir treatment that the cell becomes activated to clear bacteria. [score:1]
MiR-328 regulates phagocytosis by human macrophages and neutrophils. [score:1]
Effect of miR-328 mimic on bacterial clearance. [score:1]
The complementary antagomir strand of the miR-328-3p sequence obtained from miRbase was synthesised from Sigma-Aldrich with the following chemical modifications 5’mA. [score:1]
Thus miR-328 plays a critical role in the microbial host defence mechanism of innate immune cells by augmenting phagocytosis, the production of ROS and microbicidal activity. [score:1]
To examine the function of miR-328 in microbial host defence responses in the lung, we isolated the two major innate immune cells that respond to infection and were elevated in the lungs; macrophages and neutrophils. [score:1]
This blocked miR-328 function before the cells were infected with NTHi in vitro. [score:1]
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2
[+] score: 92
Furthermore, the identification of specific miRNAs (miR-140 and miR-328) that regulate lung development, that show increased expression in lung epithelium as development progresses through saccular and alveolar stages, and that functionally suppress the Fgf9 3’ UTR, link Dicer1 activity to Fgf9 mRNA regulation. [score:9]
Collectively, expression patterns and in vitro suppression of the Fgf9 3’ UTR identified miR-140 and miR-328 as candidate miRNAs that could function in vivo to suppress Fgf9 as lung development progresses from pseudoglandular to canalicular stages. [score:8]
Analysis of expression of these miRs at different stages of lung development showed that miR-140-5p and miR-328-3p were expressed at relatively low levels during the pseudoglandular stage of lung development and at relatively higher levels during the saccular stage, while miR-182-5p showed the opposite profile (Fig 3B– 3D). [score:7]
Importantly, several of these miRNAs (miR-24, miR-140, miR-182, miR-183, miR-328) are expressed in fetal or neonatal lung and their relative expression levels are modulated during lung development [26, 27] or in lung cancer [28– 30]. [score:6]
Our demonstration that miR-140 and miR-328 mimics can directly suppress the Fgf9 3’ UTR, shows the therapeutic potential of supplying critical microRNAs directly to lung epithelium during the period of childhood susceptibility to PPB. [score:5]
Insufficient miR-328 in glioblastomas could lead to increased FGF9 expression and thus provide a mechanism to promote disease progression. [score:5]
MiR-140 and miR-328 regulate in vitro lung development and Fgf9 expression. [score:5]
1005242.g004 Fig 4MiR-140 and miR-328 regulate in vitro lung development and Fgf9 expression. [score:5]
To establish whether miR-140 and miR-328 functionally regulate lung development, lung explant cultures were treated with seed -targeting 8-mer LNA oligonucleotides or single mismatch control LNA oligonucleotides (tiny LNAs) [31]. [score:5]
In malignant gliomas (World Health Organization grade IV astrocytic glioblastomas), miR-328 expression is decreased and is associated with worse prognosis [50]. [score:3]
Target sequences and probe design for analysis of miR-140 and miR-328 activity. [score:3]
Increasing evidence suggests that miR-328 also functions as a tumor suppressor in several types of cancers, including malignant glioma, breast, and colorectal carcinomas [49– 52]. [score:3]
miR-328 was also prominently expressed in E18.5 lung epithelium (S5 Fig). [score:3]
Additionally, miR-328 showed reduced expression when comparing levels in grades II and III astrocytoma to those in secondary grade IV glioblastomas [49]. [score:3]
We also show that the Fgf9 3’ UTR is responsive to conserved miRNA-140, miRNA-328, and miR-182, and that miRNA-140 (and miR-328) is an important regulator of lung development. [score:3]
MicroRNA-328 negatively regulates the expression of breast cancer resistance protein (BCRP/ABCG2) in human cancer cells. [score:3]
At a concentration of 10 nM, tiny LNAs effectively blocked miR-140 or miR-328 ability to suppress Fgf9 3’ UTR activity in vitro (Fig 4A and 4B). [score:3]
Expression of miR-328 in E18.5 lung epithelium. [score:3]
Of these, miR-140, miR-183, and miR-328 suppressed luciferase activity, while miR24 and miR-182 increased luciferase activity (Fig 3F, mouse, and S4A Fig and S4B Fig, human). [score:3]
Mature microRNA mimics for miR-24, miR-140, miR-182, miR-183, and miR-328 were then screened for their ability to regulate luciferase activity of the human or mouse FGF9 3’ UTR. [score:2]
The human and mouse FGF9 3’ UTR are highly conserved and are similarly regulated by miR-140, miR-182, miR-183, miR-328. [score:2]
To demonstrate efficacy of tiny LNAs, HEK293 cells, transfected with pFgf9 UTR and miR-140 or miR-328 mimics, were co -transfected with tiny LNA antagomers. [score:1]
S5 FigHistological sections from an E18.5 wild type mouse lung hybridized with a scrambled LNA in situ probe (left) or with an hsa-miR-328 LNA in situ probe (right). [score:1]
Repression of the Fgf9 3’ UTR by 10 nM miR-140 (A) or 10 nM miR-328 (B) transfected into HEK293 cells with a luciferase reporter construct containing a wild type mouse Fgf9 3’ UTR was blocked by adding 10 nM of the corresponding tiny LNAs to the culture medium. [score:1]
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3
[+] score: 79
Putative targets of nine differentially expressed miRNAs that were validated by RT-qPCR (upregulated: mmu-miR-151-3p, mmu-miR-155-5p, mmu-miR-181a-5p, and mmu-miR-328-3p; and downregulated: mmu-miR-21a-5p, mmu-miR-98-5p, mmu-miR-145a-5p, mmu-miR-146b-5p, and mmu-miR-374b-5p) were obtained from the miRWalk database. [score:11]
MyD88 Plays an Important Role in Regulating the Expression of miRNAs During B. abortus InfectionSince innate immunity is the first line of host immune defense against bacterial pathogens and our group has previously demonstrated the important role of MyD88 adaptor molecule during B. abortus infection (25), we evaluated the influence of MyD88 during differential expression of miRNAs upregulated (mmu-miR-181a-5p and mmu-miR-328-3p) or downregulated (mmu-miR-21a-5p, mmu-miR-98-5p, and mmu-miR-146b-5p) by infection. [score:10]
According to the expression levels and fold-change comparing Brucella-infected versus NI libraries, we selected four miRNAs that were upregulated (mmu-miR-151-3p, mmu-miR-155-5p, mmu-miR-181a-5p, and mmu-miR-328-3p) and five miRNAs that were downregulated (mmu-miR-21a-5p, mmu-miR-98-5p, mmu-miR-145a-5p, mmu-miR-146b-5p, and mmu-miR-374b-5p) for validation and further analysis. [score:9]
Differential expression of validated upregulated miRNAs (A) mmu-miR-181a-5p and (B) mmu-miR-328-3p or validated downregulated miRNAs (C) mmu-miR-21a-5p, (D) mmu-miR-98-5p, and (E) mmu-miR-146b-5p were assessed by real-time PCR and normalized to SNORD61 in bone marrow-derived macrophages from C57BL/6 and MyD88 KO mice. [score:9]
We observed a dependence of MyD88 in upregulation of mmu-miR-181a-5p (Figure 5A), while it was not observed differences of upregulation of mmu-miR-328-3p in the absence of MyD88 (Figure 5B). [score:7]
Since innate immunity is the first line of host immune defense against bacterial pathogens and our group has previously demonstrated the important role of MyD88 adaptor molecule during B. abortus infection (25), we evaluated the influence of MyD88 during differential expression of miRNAs upregulated (mmu-miR-181a-5p and mmu-miR-328-3p) or downregulated (mmu-miR-21a-5p, mmu-miR-98-5p, and mmu-miR-146b-5p) by infection. [score:7]
We observed a dependence of MyD88 in upregulation of mmu-miR-181a-5p, while it was not observed differences of upregulation of mmu-miR-328-3p in the absence of MyD88. [score:7]
Validated upregulated miRNAs (F) mmu-miR-181a-5p and (G) mmu-miR-328-3p or validated downregulated miRNAs (H) mmu-miR-21a-5p, (I) mmu-miR-98-5p, and (J) mmu-miR-146b-5p were also assessed by real-time PCR in spleens from C57BL/6 and MyD88 KO mice. [score:7]
For further validation, we chose four upregulated (mmu-miR-151-3p, mmu-miR-155-5p, mmu-miR-181a-5p, and mmu-miR-328-3p) and five downregulated (mmu-miR-21a-5p, mmu-miR-98-5p, mmu-miR-145a-5p, mmu-miR-146b-5p, and mmu-miR-374b-5p) miRNAs (Table S6 in) in infected samples by real-time PCR in macrophages. [score:7]
Four miRNAs were validated by real-time PCR as upregulated: (A) mmu-miR-151-3p, (B) mmu-miR-155-5p, (C) mmu-miR-181a-5p, and (D) mmu-miR-328-3p. [score:4]
C57BL/6 mice were infected intraperitoneally at 1, 3, or 6 days post-infection, and the relative expression of miRNAs: (A) mmu-miR-151-3p, (B) mmu-miR-155-5p, (C) mmu-miR-181a-5p, (D) mmu-miR-328-3p, (E) mmu-miR-21a-5p, (F) mmu-miR-98-5p, (G) mmu-miR-145a-3p, (H) mmu-miR-146b-5p, and (I) mmu-miR-374b-5p were evaluated in mouse spleens. [score:1]
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[+] score: 21
The expressions of miR-711, miR-714, miR-744, miR-2137, miR-5130, miR-1892, miR-328, miR-346, miR-5099, and miR-705 were significantly upregulated in I/R injured heart grafts, while miR-490, miR-491, miR-210, miR-362, miR-24, miR-423, miR-128, miR-328, miR -181, and miR-532 were downregulated. [score:9]
As compared with cells under normxia, miR-711, miR-714, miR-328, miR-346, miR-210, miR-744, miR-5130, miR-181a and miR-2137 were significantly over-expressed in hypoxia/reperfusion treated cardiomyocytes, while the expression of miR-491, miR-211, miR-532, miR-185, miR-425, miR-128, miR-24 was down-regulated (Figure 4B). [score:7]
As expected, miR-2137, miR-210, miR-5130, and miR-328 were highly expressed in cardiomyocytes, while miR-490, miR-491, and miR-211 were expressed at a low level. [score:5]
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5
[+] score: 19
Other miRNAs from this paper: mmu-mir-298, hsa-mir-328, hsa-mir-298
In vivo, we observed decreased expression levels of miR-298 and miR-328 in the hippocampus of aging APPSwe/PS1 mice [8], which supports further the possibility that the loss of miRNA regulation of BACE1 mRNA translation may lead to higher BACE1 protein expression, an enhanced Aß formation and the development of AD. [score:9]
Reported to regulate BACE1 mRNA translation in the context of AD [8], miR-328 has been shown to have a second function, acting as an RNA decoy by binding to heterogeneous nuclear ribonucleoprotein E2 and lifting its translational repression of an mRNA involved in myeloid cell differentiation [11, 12]. [score:6]
In a recent study from our laboratory, we reported similar observations in an animal mo del of AD (APPSwe/PS1 mice) and demonstrated a role for two miRNAs, i. e. miR-298 and miR-328, in the regulation of BACE1 expression, using mainly transiently transfected murine neuronal N2a cells in culture [8]. [score:4]
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6
[+] score: 19
Other miRNAs from this paper: hsa-let-7f-1, hsa-let-7f-2, hsa-mir-24-1, hsa-mir-24-2, hsa-mir-25, hsa-mir-32, mmu-mir-1a-1, mmu-mir-133a-1, mmu-mir-134, mmu-mir-135a-1, mmu-mir-144, mmu-mir-181a-2, mmu-mir-24-1, mmu-mir-200b, mmu-mir-206, hsa-mir-208a, mmu-mir-122, hsa-mir-181a-2, hsa-mir-181b-1, hsa-mir-181c, hsa-mir-181a-1, hsa-mir-214, hsa-mir-200b, mmu-mir-299a, mmu-mir-302a, hsa-mir-1-2, hsa-mir-122, hsa-mir-133a-1, hsa-mir-133a-2, hsa-mir-135a-1, hsa-mir-135a-2, hsa-mir-144, hsa-mir-134, hsa-mir-206, mmu-mir-200a, mmu-mir-208a, mmu-let-7f-1, mmu-let-7f-2, mmu-mir-24-2, hsa-mir-200c, hsa-mir-1-1, mmu-mir-1a-2, hsa-mir-181b-2, mmu-mir-25, mmu-mir-32, mmu-mir-200c, mmu-mir-181a-1, mmu-mir-214, mmu-mir-135a-2, mmu-mir-181b-1, mmu-mir-181c, hsa-mir-200a, hsa-mir-302a, hsa-mir-299, hsa-mir-361, mmu-mir-361, hsa-mir-302b, hsa-mir-302c, hsa-mir-302d, hsa-mir-367, hsa-mir-377, mmu-mir-377, hsa-mir-328, mmu-mir-133a-2, mmu-mir-133b, hsa-mir-133b, mmu-mir-181b-2, hsa-mir-20b, hsa-mir-429, mmu-mir-429, hsa-mir-483, hsa-mir-486-1, hsa-mir-181d, mmu-mir-483, mmu-mir-486a, mmu-mir-367, mmu-mir-20b, hsa-mir-568, hsa-mir-656, mmu-mir-302b, mmu-mir-302c, mmu-mir-302d, mmu-mir-744, mmu-mir-181d, mmu-mir-568, hsa-mir-892a, hsa-mir-892b, mmu-mir-208b, hsa-mir-744, hsa-mir-208b, mmu-mir-1b, hsa-mir-302e, hsa-mir-302f, hsa-mir-1307, eca-mir-208a, eca-mir-208b, eca-mir-200a, eca-mir-200b, eca-mir-302a, eca-mir-302b, eca-mir-302c, eca-mir-302d, eca-mir-367, eca-mir-429, eca-mir-328, eca-mir-214, eca-mir-200c, eca-mir-24-1, eca-mir-1-1, eca-mir-122, eca-mir-133a, eca-mir-144, eca-mir-25, eca-mir-135a, eca-mir-568, eca-mir-133b, eca-mir-206-2, eca-mir-1-2, eca-let-7f, eca-mir-24-2, eca-mir-134, eca-mir-299, eca-mir-377, eca-mir-656, eca-mir-181a, eca-mir-181b, eca-mir-32, eca-mir-486, eca-mir-181a-2, eca-mir-20b, eca-mir-361, mmu-mir-486b, mmu-mir-299b, hsa-mir-892c, hsa-mir-486-2, eca-mir-9021, eca-mir-1307, eca-mir-744, eca-mir-483, eca-mir-1379, eca-mir-7177b, eca-mir-8908j
The downregulated eca-miR-328 had 204 potential target genes reported by TargetScan and these genes significantly enriched five KEGG pathways, from which the most significant was the regulation of actin cytoskeleton (KEGG: 04810, Hyp* = 0.01) with seven genes: fibroblast growth factor 1 (FGF1) and 11 (FGF11), p21 protein (Cdc42/Rac)-activated kinase 6 (PAK6), integrin alpha 5 (fibronectin receptor, alpha polypeptide) (ITGA5), v-rck sarcoma virus CT10 oncogene homolog (avian) (CRK), WAS protein family member 2 (WASF2), and FYVE, RhoGEF and PH domain containing 1 (FGD1). [score:9]
The most significant up- (eca-miR-122) and down-regulated (eca-miR-328) miRNAs in ponies related to Warmblood are shown on Fig.   7a-b. Fig. 7Significantly differentially expressed miRNA in the serum of ponies. [score:6]
A total of 50 miRNAs in serum proved to be potential biomarkers to differentiate specific breed types, of which miR-122, miR-200, miR-483 were over-expressed and miR-328 was under-expressed in ponies compared to Warmbloods. [score:4]
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7
[+] score: 11
Other miRNAs from this paper: hsa-mir-328, hsa-mir-3161
There is growing evidence that microRNAs (miRNAs) can target the expression of both oncogenes and tumour suppressor genes and recently miRNA-328 has been reported to decrease Ptprj expression in epithelial cells [46]. [score:9]
In addition to our observation of multiple lncRNAs originating from the Ptprj locus, the potential for RNA regulation of Ptprj was also recently highlighted by a report showing that PTPRJ is negatively regulated by the short RNA microRNA328 [46]. [score:2]
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8
[+] score: 10
We identified the up-regulation of miR-328, which also potentially targets MeCP2, perhaps implicating the disruption of neurodevelopmental regulatory circuits is a feature of prion disease. [score:10]
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9
[+] score: 10
Expression values were calculated by normalizing to miR-328-3p levels in each sample, and the expression levels were determined using the delta- delta Ct method. [score:3]
The Ct values of miR-328-3p in untreated SKG mice and that in ß-glucan -injected SKG mice were quantified. [score:1]
U6 RNA or miR-328-3p was used as a miRNA internal control in the cell line or plasma, respectively. [score:1]
S1 Fig The Ct values of miR-328-3p in untreated SKG mice and that in ß-glucan -injected SKG mice were quantified. [score:1]
The Ct value of miR-328-3p in untreated SKG mice (n = 5) was 30.7 ± 0.85 (means ± S. E. ), and that in ß-glucan -injected SKG mice (n = 5) was 30.6 ± 1.20 (S1 Fig). [score:1]
We used miR-328-3p as miRNA internal control because the levels of miR-328-3p in untreated SKG mice were almost the same as those in ß-glucan -injected SKG mice. [score:1]
The Ct value of miR-328-3p in untreated SKG mice was 30.7 ± 0.85 and that in ß-glucan -injected SKG mice was 30.6 ± 1.20. are presented as the means ± S. E. for each group (n = 5). [score:1]
The Ct value of miR-328-3p in untreated SKG mice and that in ß-glucan -injected SKG mice. [score:1]
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It is possible that a 3′UTR could harbor multiple sites targeted by the same miRNA, and this has been shown by us in the study demonstrating that CD44 3′UTR is regulated by miR-328 through multiple target sites [20]. [score:6]
Expression of two unrelated miRNAs, miR-17-5p and miR-328, were examined using the same samples. [score:3]
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Recently, a role for seed sequence-independent regulation has emerged for miR-328, which acts through its C-rich region to titrate a translational inhibitor, hnRNP E2 protein, from its target mRNA [40]. [score:8]
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For example, miR-328, a miRNA upregulated by GRA, inhibited cancer cell growth and impaired resistance to chemotherapeutic drugs by decreasing CD44 expression [40, 41]. [score:8]
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As shown in Figure 4, we could not confirm the microarray expression data for the expression levels of miR-328, -341*, -680 or -1224. [score:5]
Additionally, selected miRs that were significantly altered in our microarray, such as miR-26b, miR-27a, miR-143, miR-150, miR-328, miR-341*, miR-680 and miR-1224, were validated. [score:1]
qRT-PCR analysis of miR-328, -341*, -680 and -1224 in exercised and sedentary animals at days 7 and 35 after the start of the study. [score:1]
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Among the targets for differentially expressed miRNAs in the spleen of Wistar rats, miR-3584-5p, miR-328*, miR-3095-3p and miR-3072* have important roles in signal pathway induction (involved in the Wnt, MAPK, mTOR, and neurotrophin signaling pathways) and immune regulation (involved in the chemokine signaling pathway in miR-1895). [score:6]
33rno-miR-19b−1.590.33rno-miR-451−4.370.05rno-miR-196c*−1.660.32Tissue/LungLog2(infected/control)Fold changemmu-miR-32*−2.170.22rno-miR-2062.234.69mmu-miR-328*−2.630.16rno-miR-2231.823.53rno-miR-32*−2.850.14rno-miR-981.22.3mmu-miR-468−3.490.09mmu-miR-4681.192.28mmu-miR-691−4.040.06mmu-miR-669d1.112.16mmu-miR-297a−4.620.04rno-miR-328a*1.12.14mmu-miR-467h−4.960. [score:1]
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[+] score: 7
Other miRNAs from this paper: mmu-mir-155, mmu-mir-21a, mmu-mir-21b, mmu-mir-21c
For example, Barana et al. reported that microRNA-21 participated in AF by inhibiting I [Ca-L] and CACNA1C expression [1], and Lu et al. also showed that microRNA-328 contributed to the adverse atrial electric remo deling in AF through targeting CACNA1C and CACNB1 [40]. [score:7]
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A number of studies have shown that miRNAs, such as miR-34, miR-125, miR-200, miR-205, miR-328, and miR-30, were down-regulated and acted as tumor suppressors in breast cancer [16– 22]. [score:6]
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Mutations in the binding site of miR-328 within 3’-UTR of a myopia-causing gene Pax6 were also shown to be associated with high myopia in a Chinese cohort [54, 55], suggesting that miRNAs play an important role in refractive eye development as well. [score:3]
It was reported that a SNP located within the miR-328 binding site in the 3’-UTR of PAX6 reduced PAX6 protein levels and was significantly associated with extreme myopia in a Chinese cohort [54, 55]. [score:1]
MicroRNA-328 may influence myopia development by mediating the PAX6 gene. [score:1]
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miR-328 was expressed at much higher levels, but a reduced rather than increased expression in maternal HF diet fed offspring was observed (data not shown). [score:5]
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Indeed, several miRNAs target BACE1, including miR-9, miR-29, miR-107, miR-186, miR-188, miR-298, and miR-328, some of which are closely related to synaptic and cognitive function [40, 41]. [score:3]
Previously, several miRNAs have been demonstrated to be involved in post-transcriptional regulation of BACE1, including miR-9, miR-29, miR-107, miR-186, miR-188, miR-298, and miR-328 [40, 41]. [score:2]
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Other miRNAs from this paper: hsa-mir-328, ssc-mir-328
PCBP2 is a poly(C) binding protein known to control translation of specific mRNA through competitive binding of C-rich tracts in target genes 5'UTR and mir-328 [49]. [score:5]
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Ccnd2, a cell-cycle associated gene, is a potential target of miR-322-5p, miR-328-5p, miR-378b, miR-669b-5p and miR–206, whose expression are altered by exposure to ELF-EMFs [40, 41]. [score:5]
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Among the targets for differentially expressed miRNAs in spleen of M. fortis, miR-328*, miR-10a and miR-10b had important roles in the immune response (involved in Toll-like receptor signaling pathway in miR-10a and miR-10b) and signal pathway induction (involved in MAPK signaling pathway and Wnt signaling pathway in miR-328*). [score:5]
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MicroRNA-298 and microRNA-328 regulate expression of mouse beta-amyloid precursor protein-converting enzyme 1. J. Biol. [score:4]
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In our PAH mice mo del, miR-328, miR-210, miR-342, and miR-125 were also downregulated in addition to miR-29b. [score:4]
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MicroRNA-298 and microRNA-328 regulate expression of mouse beta-amyloid precursor protein-converting enzyme 1. J. Biol. [score:4]
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In addition, the downregulation of miR-328-3p by intratracheal administration of antagomirs of miR-328-3p enhanced bacterial killing when mice were infected with non-typeable Haemophilus influenza (89). [score:4]
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As shown in the heat map, 7 of the miRNAs (all except miR-328-3p) were detected in EVs derived from cancer cell lines (Figure 5B). [score:1]
To address these limitations, we developed a predictive algorithm that differentiates early-stage cancers from benign tumors using 7 miRNAs (miR-200a-3p, miR-766-3p, miR-26a-5p, miR-142-3p, let-7d-5p, miR-130b-3p and miR-328-3p). [score:1]
With the addition of CA-125, the conventional serum biomarker for OvCa, performance further improved; the optimal mo del, selected after considering all possible combinations with the 8 miRNAs, included CA-125 and 6 miRNAs (miR-200a-3p, miR-766-3p, miR-26a-5p, miR-142-3p, let-7d-5p and miR-328-3p), and had an AUC of 0.994 (95% CI, 0.988-0.999) (Figure 3B), sensitivity of 0.984, and specificity 0.956 at the optimal cut-off points. [score:1]
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NI MV OpenArray RT-qPCR hsa-miR-328 − 2.5* ± 0.93Not tested [a] hsa-miR-335* − 3.0* ± 1.13Not tested [a] mmu-miR-16* 2.8** ± 0.65Not tested [a] mmu-miR-21* 5.0** ± 0.88Not tested [a] mmu-miR-297a* 5.8* ± 1.60Not tested [a] mmu-miR-685 3.0* ± 1.00Not tested [a] mmu-miR-1949 5.0* ± 1.69Not tested [a] hsa-miR-590-5p Unique to NINot validated [b] rno-miR-450 Unique to CMNot validated [b] mmu-miR-10b 2.7* ± 0.85Not validated [b] hsa-miR-146a 3.2** ± 0.68 7.2* ± 2.74 hsa-miR-150 1.8* ± 0.64 2.7 (ns) ± 2.26 hsa-miR-205 2.3* ± 0.75 − 0.5 (ns) ± 1.89 hsa-miR-486 2.3*** ± 0.18 4.7 (ns) ± 1. 45 mmu-miR-193b − 2.7** ± 0.62 − 7.5* ± 0 62 mmu-miR-215 2.1* ± 0.554.6 (ns) ± 99.39 [c] mmu-miR-467a − 2.0* ± 0.69 − 5.6 (ns) ± 0.96 The list of significantly differentially expressed miRNA in CM vs NI MV from the was compared with the results obtained by. [score:2]
The database was searched with the full names of each murine miRNA as per the ThermoFisher Scientific product information and miRBase version 21: mmu-miR-16-1-3p, mmu-miR-21a-3p, mmu-miR-146a-5p, mmu-miR-150-5p, mmu-miR-193b-3p, mmu-miR-205-5p, mmu-miR-215-5p, mmu-miR-297a-3p, mmu-miR-328-3p, mmu-miR-335-3p, mmu-miR-467a-5p, mmu-miR-486a-5p, mmu-miR-685, mmu-miR-1949, and rno-miR-10b-5p. [score:1]
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Indeed, Eiring et al. have recently reported that miR-328 acts as a decoy factor by binding to a repressor ribonucleoprotein, independently from the seed sequence and RISC, and blocking it from translational repression of mRNA involved in myeloid cell differentiation [23, 24]. [score:3]
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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]
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Mmu-miR-328-3p (2 targets), Bace1 [Luciferase reporter assay//Northern blot//EMSA], Bace2 [Luciferase reporter assay]. [score:1]
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pval miRNA fold change mRNA fold change description mmu-miR-449c-5p Myc −0.89 1.2E-04 1.60E-03 −13.7 7.7 v-myc avian myelocytomatosis viral oncogene homolog mmu-miR-181a-5p Lmo1 −0.73 5.8E-03 1.80E-02 −8.1 5.1 LIM domain only 1 (rhombotin 1) mmu-let-7d-3p Ccnd2 −0.94 6.0E-06 4.00E-04 −77.7 4.3 cyclin D2 mmu-miR-375-3p Specc1 −0.83 7.4E-04 4.40E-03 −7.7 3.8 sperm antigen with calponin homology and coiled-coil domains 1 mmu-miR-92b-5p Notch1 −0.95 3.2E-06 3.10E-04 −108.1 3.5 notch 1 mmu-miR-328-3p Pim1 −0.9 7.6E-05 1.20E-03 −48.1 3.1 Pim-1 proto-oncogene serine/threonine kinase mmu-miR-223-3p Msh2 −0.88 2. 1E-04 2.10E-03 567.7 −3.6 mutS homolog 2 mmu-miR-143-3p Chek2 −0.81 1.3E-03 6.40E-03 6.9 −3.5 checkpoint kinase 2 Due to the similarity of the gene expression patterns, we further investigated whether the bronchial genomic classifier from mice can assist in the diagnosis of lung cancer in humans. [score:1]
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[+] score: 1
Other miRNAs from this paper: mmu-mir-208a, mmu-mir-223, mmu-mir-208b, mmu-mir-664
miR-328. [score:1]
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Other miRNAs from this paper: hsa-mir-328
Antagonism of miR-328 increases the antimicrobial function of macrophages and neutrophils and rapid clearance of non-typeable Haemophilus Influenzae (NTHi) from infected lung. [score:1]
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