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4 publications mentioning mmu-mir-3473e

Open access articles that are associated with the species Mus musculus and mention the gene name mir-3473e. Click the [+] symbols to view sentences that include the gene name, or the word cloud on the right for a summary.

1
[+] score: 182
As Fig.   1d and Fig.   5b shown, Bt can upregulate TNF-α mRNA expression at the late infectious phase (>16 hpi), but it would not change TNF-α expression after treatment of miR-3473 mimics or inhibitors like that in Bp -treated macrophages (Fig.   5b). [score:10]
e qRT-PCR analysis of miR-3473 expression in macrophages transfected with mimic, inhibitor, mimic control or inhibitor control oligonucleotides of miR-3473. [score:7]
This way, we hypothesized that miR-3473 regulated TNF-α expression through targeting TRAF3 rather than direct anchoring. [score:7]
In addition, TargetScan suggested that miR-3473 possibly target TRAF3 (TNF receptor -associated factor 3), a well-known negative regulator of the NF-κB pathway, which was probably involved in the TNF-α induction and apoptosis in cells with Bp infection. [score:6]
Since TRAF3 has been known as a negative regulator of NF-κB pathway, the mechanism for how miR-3473 regulates TNF-α expression is unknown. [score:5]
siRNAs or oligonucleotides (miR-3473 mimics, inhibitors, mimic control and inhibitor control) were purchased from Ribobio Corporation (Guangzhou, China) and suspected oligonucleotide was delivered through aerosol inhalation (15 μg in 50 μL PBS/every dose) [22]. [score:5]
a qRT-PCR analysis of TNF-α mRNA expression in Bp-infected or uninfected macrophages pre -treated with miR-3473 mimic, inhibitor or controls. [score:5]
miR-3473 mimic and inhibitor were used to change the expression level of miR-3473. [score:5]
While, among the list of targets of miR-3473, TNF receptor -associated factor 3 (TRAF3) was included and suggested it should be a potential target of miR-3473 (Fig.   3a). [score:5]
This indicated that miR-3473, as an independent regulation factor, can play a key role in Bp -induced TNF-α expression and cell apoptosis. [score:4]
These results suggested that miR-3473 manipulated TRAF3-NF-κB-TNF-α regulation axis to affect TNF-α expression in Bp-infected macrophages. [score:4]
In addition, miR-3473 inhibitor was administered into mice and its regulation on TNF-α release was equally obvious like that in vitro (Fig.   6c). [score:4]
TRAF3, not TNF-α, was a direct target of miR-3473. [score:4]
After luciferase assay on macrophages which were carrying the 3ˈ-UTR TRAF3 luciferase reporter, it was found that induction of miR-3473 would significantly inhibit the luciferase activities but there was no inhibition in those macrophages transfected with the mutant 3ˈ-UTR TRAF3 luciferase reporter (Fig.   3f). [score:4]
a Protein levels of TRAF3, Phospho-NF-κB p65 and NF-κB p65 in Bp-infected or uninfected macrophages transfected with miR-3473 mimic, inhibitor or controls, as assessed by western blot with Actin as an internal control. [score:3]
A mimic and inhibitor of miR-3473 were transfected into macrophages using Lipofectamine 2000™, and transfection efficiency was confirmed by qRT-PCR (Fig.   3e). [score:3]
In vivo, it was found that miR-3473 expression of total lungs cells from Bp -treated was higher than that from Bt -treated mice. [score:3]
To verify that TRAF3 is a molecular target of miR-3473, a fragment of the 3ˈ-UTR of TRAF3, containing the putative miR-3473 binding site (Fig.   3a) or a mutant miR-3473 binding site (Fig.   3c), was individually cloned into a pMIR-Report luciferase plasmid, with pRL-TK as an internal control. [score:3]
a qRT -PCR analysis of miR-3473 expression in Bp, Bt-infected or uninfected macrophages at different time post infection (8 h, 12 h, 24 h, MOI = 10). [score:3]
d Survival curves of mice infected with Bp, Bt or PBS for 7 days with or without treatment of miR-3473 inhibitor oligonucleotides. [score:3]
And miR-3473 inhibitor was able to decrease the TNF-α release of mice and prolong the survival of mice with Bp infection. [score:3]
Burkholderia pseudomallei (Bp) Burkholderia thailandensis (Bt) TNF-α Apoptosis miR-3473 TRAF3 NF-κB Burkholderia pseudomallei (Bp) is the causative agent of the human disease melioidosis, which is endemic in southeast Asia and northern Australia, with manifestations ranging from fever to pneumonia to life-threatening sepsis. [score:3]
a The putative binding sites of miR-3473 in the TRAF3 3′-UTR are shown (TargetScanMouse 6.2, http://www. [score:3]
We also tested the expression of miR-3473 in TC-1 cell (a type of murine respiratory epithelial cells) treated by Bp, but it did not changed significantly as that in macrophages (Fig.   2d). [score:3]
We found that treatment with miR-3473 mimics markedly enhanced TNF-α mRNA expression in uninfected or Bp-infected macrophages (Fig.   5a). [score:3]
d miR-3473 expression in murine macrophages (RAW264.7 cell line) or epithelial cells (TC-1 cell line) at 12 h post Bp, Bt or no infection (MOI = 10 or 0). [score:3]
c miR-3473 expression of macrophages treated with different pathogens (MOI = 10) for 12 h post infection, including Salmonella typhi, Escherichia coli DH5a, Bt or 3 strains of clinical Bp (BPC006, BPC011, BPC056, all sequenced by MLST and deposited in http://bpseudomallei. [score:3]
To confirm the validity of the microarray, the expression levels of TNF-α, TRAF3 and miR-3473 were detected by qRT-PCR. [score:3]
However, miR-3473 inhibitors had no obvious effect on the intracellular growth of Bp or Bt (Fig.   5d). [score:3]
It suggested that TRAF3 (3ˈ-UTR) should be a probable target of miR-3473. [score:3]
As described in material and method, qRT-PCR was applied to test the expression of miR-3473 in murine lung cells. [score:3]
As described above, miR-3473 expressed significantly and specifically in total lung cells of mice infected with Bp. [score:3]
b miR-3473 expression in Bp, Bt-infected or uninfected macrophages at 12 h post infection with different dose of Bp or Bt (MOI = 1, 10, 100, 10000). [score:3]
c Early apoptosis cells were gated through flow cytometry test in macrophages pre -transfected with miR-3473 inhibitor or control at 12 h after Bp or Bt infection. [score:3]
Conversely, miR-3473 inhibitor oligonucleotides would decrease TNF-α mRNA in Bp-infected macrophages and abrogate the difference of TNF-α mRNA levels between Bp and Bt-infected cells (Fig.   5a). [score:3]
On the contrary, after intravenous administration with miR-3473 inhibitor, the survival period of Bp-infected mice extended although the death rate could not be altered at the end. [score:3]
On the contrary, miR-3473 inhibitor would decrease the activity of NF-κB in Bp-infected macrophages, but not in Bt-infected macrophages (Fig.   4a& b). [score:3]
Based on the above results, we wondered whether miR-3473 alone can influence TNF-α mRNA expression, cell apoptosis and bacterial replication in macrophages. [score:3]
It suggested that there should be a miR-3473-TRAF3-NF-κB regulation axis which would play a vital role in Bp -mediated inflammatory response in macrophages. [score:2]
In sum, miR-3473 plays an important role in the differential pathogenicity of Bp and Bt via miR-3473- TRAF3-TNF-α network, and regulates TNF-α release, cell apoptosis and animal survival after Bp treatment. [score:2]
The fragments of the TRAF3 3ˈ-UTR containing the miR-3473 target site were amplified from genomic DNA (primers details in Table  1) and cloned into the pMIR-Report plasmid downstream of a reporter synthetic Renilla luciferase gene (hRluc) using SpeI and HindIII. [score:2]
In vivo, the miR-3473- TRAF3-TNF-α network was also regulating the TNF-α release and the survival of mice. [score:2]
To generate plasmids with one or more mutations in the binding site for miR-3473, the seed regions were mutated from TCTCTCCA to TGTTTGCA at 1186–1193 of the 3ˈ-UTR and synthesized by Sangon (Shanghai, China) followed by cloning into the pMIR-Report plasmid. [score:2]
It was the same case for the regulation of miR-3473 on cell apoptosis in Bp or Bt-infected macrophages (Fig.   5c). [score:2]
miR-3473 was involved in TRAF3-NF-κB-TNF-α regulation axis. [score:2]
and miR-3473 expression was measured by qRT-PCR described as above. [score:1]
miR-3473 was specifically induced in Bp-infected murine macrophages. [score:1]
Furthermore, miR-3473 had a detrimental impact on the survival period of mice infected with lethal dose of Bp (Fig.   6d). [score:1]
We found that miR-3473 was induced higher in lung cells from Bp-infected mice than that from Bt-infected or uninfected mice (Fig.   6b). [score:1]
These results suggested miR-3473 was indulgent for excessive inflammatory response and associated with acute death of mice after lethal Bp infection. [score:1]
But, miR-3473 specifically increased in Bp-infected murine macrophages, rather than that in Bt -treated macrophages and increased significantly at 12 hpi (Fig.   2a). [score:1]
Moreover, other Gram -negative bacterium, like Salmonella typhi and Escherichia coli DH5α, were not able to induce miR-3473 significantly (Fig.   2c). [score:1]
Analysis of miR-3473 was conducted as described above. [score:1]
c miR-3473 inhibitor oligonucleotide was administrated to mice (i. n., through breathing) on the day before inoculation and TNF-α release was measured at 4 dpi. [score:1]
This indicated that miR-3473 was induced specifically in murine macrophages rather than murine pulmonary cell after Bp infection. [score:1]
Fig. 4Bp infection specifically reduces TRAF3 by miR3473 which activates NF-κB-TNF-α pathway. [score:1]
It suggested that miR-3473 can manipulate bacteria -induced host inflammatory but do not influence the recycle of intracellular Bp or Bt. [score:1]
After transfection of miR-3473 mimics, NF-κB pathway was enhanced significantly (showed by phospho-NF-κB p65 level) with or without Bp infection (Fig.   4a). [score:1]
miR-3473 was induced significantly in lung cells from Bp-infected mice but would not affect murine survival. [score:1]
In addition, miR-3473 increased in a dose -dependent manner after Bp infection, but no alteration of miR-3473 in Bt-infected cells was observed, even at a high MOI (Fig.   2b). [score:1]
miR-3473 was responsible for the differences of TNF-α release and cell apoptosis between Bp and Bt. [score:1]
In addition, we found that miR-3473 was able to affect the TNF-α release, cell apoptosis and inflammatory response via a miR-3473- TRAF3-TNF-α network. [score:1]
d The putative binding sites of miR-3473 in the TRAF3 3′-UTR were mutated as shown. [score:1]
d Intracellular bacteria loads of Bp or Bt-infected macrophages transfected with miR-3473 oligonucleotides were counted at different infectious phase (4 h, 8 h, 12 h, 20 h and 28 h). [score:1]
Among them, miR-3473 was found to be specific to Bp infection and significantly induced along with the infection process both in murine macrophages and pulmonary cell line (TC-1). [score:1]
miR-3473 was one of them specifically induced, but not significantly changed in Bt -treated macrophages. [score:1]
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2
[+] score: 5
The most significantly up- and downregulated miRNAs in scrapie-infected mice were mmu-miR-3473e (9.48 log2) and mmu-miR-141-5p (−7.33 log2) in the 139A group, mmu-miR-3473e (13.18 log2) and mmu-miR-200a-5p (−7.08 log2) in the ME7 group, and mmu-miR-3473e (14.15 log2) and mmu-miR-183-3p (−10.15 log2) in the S15 group. [score:4]
In addition to mmu-miR-3473b, other two family numbers, mmu-miR-3473a and mmu-miR-3473e, are also greatly increased in the brains of the three scrapie-infected mouse mo dels, with average fold-change values of 5.3 and 12.3, respectively. [score:1]
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[+] score: 4
Other miRNAs from this paper: hsa-let-7a-1, hsa-let-7a-2, hsa-let-7a-3, hsa-let-7f-1, hsa-let-7f-2, hsa-mir-16-1, hsa-mir-17, hsa-mir-19a, hsa-mir-19b-1, hsa-mir-19b-2, hsa-mir-23a, hsa-mir-26a-1, hsa-mir-26b, hsa-mir-27a, hsa-mir-29a, hsa-mir-30a, hsa-mir-31, hsa-mir-100, hsa-mir-29b-1, hsa-mir-29b-2, hsa-mir-16-2, mmu-mir-23b, mmu-mir-27b, mmu-mir-29b-1, mmu-mir-30a, mmu-mir-30b, mmu-mir-127, mmu-mir-128-1, mmu-mir-132, mmu-mir-133a-1, mmu-mir-188, mmu-mir-194-1, mmu-mir-195a, mmu-mir-199a-1, hsa-mir-199a-1, mmu-mir-200b, mmu-mir-205, mmu-mir-206, hsa-mir-30c-2, hsa-mir-30d, mmu-mir-122, mmu-mir-30e, hsa-mir-199a-2, hsa-mir-199b, hsa-mir-205, hsa-mir-211, hsa-mir-212, hsa-mir-214, hsa-mir-217, hsa-mir-200b, hsa-mir-23b, hsa-mir-27b, hsa-mir-30b, hsa-mir-122, hsa-mir-128-1, hsa-mir-132, hsa-mir-133a-1, hsa-mir-133a-2, hsa-mir-127, hsa-mir-138-1, hsa-mir-188, hsa-mir-194-1, hsa-mir-195, hsa-mir-206, mmu-mir-19b-2, mmu-mir-30c-1, mmu-mir-30c-2, mmu-mir-30d, mmu-mir-200a, mmu-let-7a-1, mmu-let-7a-2, mmu-let-7f-1, mmu-let-7f-2, mmu-mir-16-1, mmu-mir-16-2, mmu-mir-23a, mmu-mir-26a-1, mmu-mir-26b, mmu-mir-29a, mmu-mir-29c, mmu-mir-27a, mmu-mir-31, mmu-mir-351, hsa-mir-200c, mmu-mir-17, mmu-mir-19a, mmu-mir-100, mmu-mir-200c, mmu-mir-212, mmu-mir-214, mmu-mir-26a-2, mmu-mir-211, mmu-mir-29b-2, mmu-mir-199a-2, mmu-mir-199b, mmu-mir-19b-1, mmu-mir-138-1, mmu-mir-128-2, hsa-mir-128-2, mmu-mir-217, hsa-mir-194-2, mmu-mir-194-2, hsa-mir-29c, hsa-mir-30c-1, hsa-mir-200a, hsa-mir-30e, hsa-mir-26a-2, hsa-mir-379, mmu-mir-379, mmu-mir-133a-2, mmu-mir-133b, hsa-mir-133b, mmu-mir-412, mmu-mir-431, hsa-mir-431, hsa-mir-451a, mmu-mir-451a, mmu-mir-467a-1, hsa-mir-412, hsa-mir-485, hsa-mir-487a, hsa-mir-491, hsa-mir-503, hsa-mir-504, mmu-mir-485, hsa-mir-487b, mmu-mir-487b, mmu-mir-503, hsa-mir-556, hsa-mir-584, mmu-mir-665, mmu-mir-669a-1, mmu-mir-674, mmu-mir-690, mmu-mir-669a-2, mmu-mir-669a-3, mmu-mir-669c, mmu-mir-696, mmu-mir-491, mmu-mir-504, hsa-mir-665, mmu-mir-467e, mmu-mir-669k, mmu-mir-669f, hsa-mir-664a, mmu-mir-1896, mmu-mir-1894, mmu-mir-1943, mmu-mir-1983, mmu-mir-1839, mmu-mir-3064, mmu-mir-3072, mmu-mir-467a-2, mmu-mir-669a-4, mmu-mir-669a-5, mmu-mir-467a-3, mmu-mir-669a-6, mmu-mir-467a-4, mmu-mir-669a-7, mmu-mir-467a-5, mmu-mir-467a-6, mmu-mir-669a-8, mmu-mir-669a-9, mmu-mir-467a-7, mmu-mir-467a-8, mmu-mir-669a-10, mmu-mir-467a-9, mmu-mir-669a-11, mmu-mir-467a-10, mmu-mir-669a-12, mmu-mir-3473a, hsa-mir-23c, hsa-mir-4436a, hsa-mir-4454, mmu-mir-3473b, hsa-mir-4681, hsa-mir-3064, hsa-mir-4436b-1, hsa-mir-4790, hsa-mir-4804, hsa-mir-548ap, mmu-mir-3473c, mmu-mir-5110, mmu-mir-3473d, mmu-mir-5128, hsa-mir-4436b-2, mmu-mir-195b, mmu-mir-133c, mmu-mir-30f, hsa-mir-6825, hsa-mir-6888, mmu-mir-6967-1, mmu-mir-3473f, mmu-mir-3473g, mmu-mir-6967-2, mmu-mir-3473h
Furthermore, the pathway analysis links a group of miRNAs that were differentially expressed in cbs [+/–] retina to oxidative stress pathway such as miR-205, miR-206, miR-217, miR-30, miR-27, miR-214 and miR-3473. [score:3]
Hcy also induces alteration of miRNAs related to tight junctions signaling such as miR-128, miR-132, miR-133, miR-195, miR-3473, miR-19, miR-200, miR-205, miR-214, miR-217, miR-23, miR-26, miR-29, miR-30, miR-31 AND miR-690. [score:1]
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[+] score: 3
miRNA p-value Fold-Change miR-146a 1.15E-09 −4.82 miR-31 9.66E-08 −4.95 miR-155 1.97E-07 −3.82 miR-2134 2.13E-07 −2.05 miR-711 1.63E-06 −4.10 miR-3473 1.95E-06 −5.62 miR-574-3p 3.32E-06 −2.55 miR-1195 6.59E-06 2.26 miR-27a* 6.89E-06 14.92 miR-27b* 7.35E-06 2.92 miR-34c 1.80E-05 −3.43 miR-1931 3.34E-05 −2.30 miR-874 4.07E-05 −2.01 miR-196b 7.99E-05 2.59 miR-181a-1* 8.02E-05 4.15 miR-187 8.11E-05 2. 02List of miRs whose expression is altered, identified from microarray analysis by comparison of levels in TM [+] and TM [−] DCs which change >2 fold with p<0.0001. [score:3]
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