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8 publications mentioning rno-mir-344a-2

Open access articles that are associated with the species Rattus norvegicus and mention the gene name mir-344a-2. Click the [+] symbols to view sentences that include the gene name, or the word cloud on the right for a summary.

[+] score: 200
As shown in Figure 5i, the miR-344a-5p mimic rescued the function of lnc-PCF in lung fibrosis and the expression of E-cadherin expression, which was inhibited by lnc-PCF overexpression, and reduced the expression of α-SMA, vimentin, and Snail, which were promoted by lnc-PCF overexpression. [score:13]
Knockdown or knockin of lnc-PCF could significantly downregulate or upregulate the expression of map3K11, which was rescued by cotransfection with the miR-344a-5p inhibitor or mimic (Figures 6d–g). [score:13]
The miR-344a-5p overexpression (mimic) resulted in decreased lnc-PCF expression, and the suppression of miR-344a-5p (inhibitor) significantly enhanced the lnc-PCF expression as compared with that in the TGF- β1+NC group (Figure 4f). [score:10]
By contrast, miR-344a-5p inhibitor increased the S and G2/M phase proportion, decreased the G0/G1 phase ratio, downregulated cyclin E, and upregulated cyclin B and PCNA, thereby activating epithelial cell proliferation (Figures 5e and h). [score:9]
Data showed that the miR-344a-5p mimic could inhibit map3k11 expression, whereas the miR-344a-5p inhibitor could promote map3k11 expression as compared with that in the TGF- β1-activated group (Figures 6b and c). [score:8]
These results indicated that miR-344a-5p directly binds with map3k11, which consequently downregulates its expression level. [score:7]
analysis showed that the miR-344a-5p overexpression (mimic) could reduce cyclin E expression and increase cyclin B expression (Figure 5b). [score:7]
Test screening and data analysis results showed that miR-344a-5p is one of the directly targeted miRNAs by lnc-PCF, and map3k11 is a target gene of miR-344a-5p. [score:6]
Data showed that due to the upregulated miR-344a-5p (mimic) expression, the cells accumulated in G0/G1, and the percentage of cell accumulation in the S and G2/M phases is lower than that in the control (Figure 5a). [score:6]
The miR-344a-5p mimic and inhibitor were transfected into pulmonary epithelial cells activated with TGF- β1 to further confirm the target relation between map3k11 and miR-344a-5p. [score:5]
Rescue experiments further supported the evidence that miR-344a-5p directly regulates map3k11 expression. [score:5]
In addition, the miR-344a-5p expression levels increased when lnc-PCF was knocked down (Figure 4g) but was reduced by the knockin of lnc-PCF (Figure 4h). [score:5]
Therefore, the miR-344a-5p target genes were predicted based on TargetScan, miRanda data, and miRbase. [score:5]
Among the list of miR-344a-5p target genes, we focused on map3k11 because it has relatively higher affinity than other genes and is an important indicator of the master regulatory factor in cell differentiation, proliferation, and individual development. [score:5]
On the other hand, miR-344a-5p exhibited an opposing expression trend to lnc-PCF in vivo and in vitro (Figures 4a and b), thereby indicating its potential as a target for lnc-PCF. [score:5]
The luciferase genetic testing report showed that miR-344a-5p overexpression suppressed the luciferase activity of the WT reporter vector but not that of the mutant reporter vector (Figure 4c). [score:5]
[30] In the current study, we presented a novel, highly expressed lnc-PCF that can promote the proliferation of activated epithelial cells by competitively binding to miR-344a-5p -targeted map3k11 in pulmonary fibrosis (Figure 8). [score:5]
[45] In general, our study on the regulation of the activated epithelial cell proliferation in pulmonary fibrosis by lnc-PCF and miR-344a-5p -targeted map3k11 introduces a new approach to examine the complex post-transcriptional regulatory networks and present new therapeutic approaches to pulmonary fibrosis. [score:5]
RNA pull down, anti-AGO2 RNA immunoprecipitation (RIP), and rescue experiments were conducted to further verify the direct targeted relationship between lnc-PCF and miR-344a-5p. [score:4]
Given that lnc-PCF was confirmed to directly target miR-344a-5p, experiments were designed to verify whether or not lnc-PCF promotes the proliferation of activated epithelial cells dependent on miR-344a-5p. [score:4]
Identification of target -regulating mechanism in miR-344a-5p, map3k11, and lnc-PCF. [score:4]
All these results revealed the direct targeted association between lnc-PCF and miR-344a-5p. [score:4]
All of these findings revealed that lnc-PCF promotes cell proliferation that is dependent on miR-344a-5p by directly targeting miR-344a-5p. [score:4]
Lnc-PCF can regulate map3k11 by targeting miR-344a-5p to promote the proliferation of activated epithelial cells, which results in pulmonary fibrosis. [score:4]
Lnc-PCF directly targeted miR-344a-5p. [score:4]
The affinity of predicted target genes with miR-344a-5p was also analyzed. [score:3]
The map3k11 levels were inversely correlated with miR-344a-5p expression. [score:3]
The luciferase activity of the WT 3′-UTR–map3k11 was significantly decreased in the cells transfected with miR-344a-5p mimics, whereas the miR-344a-5p mimic could not inhibit the luciferase activities of the MU 3′UTR–map3k11 (Figures 6a, 1–4). [score:3]
The miR-344a-5p mimic and inhibitor were transfected into RLE-6TN cells. [score:3]
This result suggested that miR-344a-5p is a target gene for lnc-PCF. [score:3]
Thus, map3k11 is the target gene of miR-344a-5p. [score:3]
We further used a rescue experiment (lnc-PCF overexpression+miR-344a-5p mimic) to detect whether or not the effect of lnc-PCF is dependent on miR-344a-5p. [score:3]
Moreover, we induced anti-AGO2 RIP and transiently overexpressed miR-344a-5p in RLE-6TN cells. [score:3]
Lnc-PCF smart silencer, miR-344-5p mimic, and miR-344-5p inhibitor were purchased from RiboBio Co. [score:3]
In conclusion, the profibrotic function of lnc-PCF could be mediated by targeting map3K11 via miR-344a-5p. [score:3]
[24]A luciferase assay reporter system was established by amplifying and inserting the 3′ UTR of map3k11 into a vector containing a downstream firefly luciferase to verify map3k11 as a target gene of miR-344a-5p. [score:2]
qPCR analysis revealed that lnc-PCF was significantly enriched in miR-344a-5p as compared with that in non -targeting miR-708-3p (Figure 4d). [score:2]
[24] A luciferase assay reporter system was established by amplifying and inserting the 3′ UTR of map3k11 into a vector containing a downstream firefly luciferase to verify map3k11 as a target gene of miR-344a-5p. [score:2]
miR-344a-5p mimic could reduce the growth of activated epithelial cells (Figure 5c) and PCNA (Figure 5d). [score:1]
was performed to detect the endogenous miR-344a-5p associated with lnc-PCF using transcribed biotin-labeled lnc-PCF in vitro. [score:1]
To investigate whether or not miR-344a-5p is targeted by lnc-PCF, we conducted dual-luciferase report system to construct a plasmid vector with full-length lnc-PCF containing wild-type (WT) and mutant-type (MT) 3′-UTR, which was behind two luciferases, namely, firefly and Renilla. [score:1]
In addition, cells were transfected with lnc-PCF WT/MT to confirm that lnc-PCF could protect map3k11 by competitively binding with miR-344a-5p (Figure 6a, 5–10). [score:1]
MiR-344a-5p transfection reagents were prepared at the final density of 100 nM miRNA and 0.25  μl of transfection regents and incubated for 5 min. [score:1]
This occurrence may imply that lnc-PCF competitively binds with miR-344a-5p to protect map3k11 from being degraded by miR-344a-5p, which results in the promotion of cell proliferation. [score:1]
The endogenous lncRNA-ATB pulled down by AGO2 was specifically enriched in the miR-344a-5p -transfected cells (Figure 4e). [score:1]
Lnc-PCF promoted the proliferation of activated epithelial cells dependent on miR-344a-5p. [score:1]
MiR-344a-5p, miR-138-5p, miR-370-3p, and miR-484 were selected for the study according to their relative high affinity between lnc-PCF and miRNAs (Supplementary Figure 2). [score:1]
About 50  μl of the medium was removed, and 25  μl of lnc-PCF transfection mixture and 25  μl of miR-344a-5p transfection mixture were added to the cultured cells. [score:1]
Thus, miR-344a-5p was selected for further study. [score:1]
Afterward, we mixed lnc-PCF and miR-344a-5p with their transfection reagents and incubated the mixtures for 20 min. [score:1]
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[+] score: 39
Moreover, miR-344a, miR-294, and miR-133b-3p weakened the upregulation of α-SMA and inhibited the downregulation of E-cadherin in HK2 cells induced by TGF-β1 (Figs. 4e- i and 5e- i). [score:9]
In secreted BM-MSC-MVs, the expression of miR-344a, miR-133b-3p, miR-294, miR-423-3p, and miR-872-3p was significantly downregulated in older rats than in younger rats (P < 0.05), and the serum level of these miRNAs exhibited the same patterns. [score:6]
miR-344a, miR-133b-3p, miR-294, miR-423-3p, and miR-872-3p in BM-MSC-MVs from aged rats were downregulated, and the expression of miR-294 and miR-872-3p showed a significant decline (P < 0.05) (Fig.   2c). [score:6]
α-SMA alpha-smooth muscle actin, TGF-β1 transforming growth factor-beta 1 HK2 cells were initially transfected with miR-344a, miR-294, miR-872-3p, miR-133b-3p, and miRNA mimic control and then incubated in a medium containing 8 ng/ml TGF-β1 for 48 h. Compared with non -transfected HK2 cells, the expression level of α-SMA significantly decreased in HK2 cells transfected with miR-344a, miR-294, and miR-133b-3p (P < 0.05), and the expression level of E-cadherin significantly increased in HK2 cells transfected with miR-294 and miR-133b-3p (P < 0.05). [score:4]
a, c of E-cadherin and α-SMA expression in HK2 cells under TGF-β1 stimulation co-cultured with Y-MV /O-MV or pre-transfection with miR-872, miR-344, miR-294, miR-133b-3p, and miR-control mimic. [score:3]
It also indicated the expression of α-SMA in HK2 cells treated with TGF-β1 but pre -transfected with miR-872, miR-344, miR-294, miR-133b-3p, and miR-control mimic (e–i). [score:3]
Lastly, an ABI-Prism 7500 Sequence Detection System (Applied Biosystems, Waltham, MA, USA) and SYBR PrimeScript miRNA RT-PCR Kit (Takara) were used to detect the expression level of specific miRNAs (miR-344a, miR-294, miR-872-3p, miR-133b-3p, and miR-423-3p) and the loading control, miR-191. [score:3]
It also indicated the expression of E-cadherin in HK2 cells treated with TGF-β1 but pre -transfected with miR-872, miR-344, miR-294, miR-133b-3p, and miR-control mimic (e-i). [score:3]
For the miRNA transfection groups, miR-344a, miR-294, miR-872-3p, miR-133b-3p, and miRNA mimic control (GeneCopoeia Inc. [score:1]
MiR-344a, miR-133b-3p, and miR-294 affected TGF-β1 -mediated EMT in HK2 cells. [score:1]
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[+] score: 24
We found that up-regulated miRNAs (miR-346, miR-135b, miR-30ab, miR-344, miR-18a, miR-99a, miR-210, miR-207, miR-18a, and miR-129) in ARDS were inversely correlated with the expression of their predicted targets such as Gabrb1, Mdh1, Eif2ak1, Fbln5, and Tspan8. [score:8]
The down-regulated miRNAs included miR-24, miR-26a, miR-126, and Let-7a, b, c, f. The up-regulated miRNAs were composed of miR-344, miR-346, miR-99a, miR-127, miR-128b, miR-135b, and miR-30a/b. [score:7]
miR-346, miR-135b, miR-30a/b, miR-344, and miR-18a had more than one mRNA target. [score:3]
miR-26a, miR-346, miR-135b, miR-30a/b, miR-344, and miR-18a targeted multiple altered mRNAs. [score:3]
miR-346, miR-135b, miR-30ab, miR-344, and miR-18a were inversely correlated with more than one mRNA targets. [score:3]
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[+] score: 16
Stem-loop RT-PCR was used to confirm the expression levels of four selected miRNAs, in which miR-150 and miR-497 demonstrated upregulation, whereas miR-344-3p and let-7f showed downregulation, confirming the changes detected by the microarray (Fig. 1; P<0.05). [score:9]
Among the miRNAs, miR-214, miR-199a-5p, miR-150, miR-199a-3p, miR-351, miR-145, miR-764, miR-497 and miR-92b were upregulated, whilst miR-7a, miR-325-5p, miR-485, miR-708, miR-344-3p, let-7f, miR-26b, miR-129, miR-29c and let-7a were downregulated. [score:7]
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[+] score: 12
miRNA-344 has not been reported to be associated with renal disease, although miRNA-344 can activate Wnt/ β-catenin signaling and inhibit adipocyte differentiation [47]. [score:5]
In conclusion, triptolide significantly attenuated podocyte injury in rats with adriamycin -induced nephropathy by regulating the expression of miRNA-344-3p and miRNA-30b-3p. [score:4]
It demonstrates that miRNA-344-3p and miRNA-30b-3p might be potential therapeutic targets in the treatment of CKD. [score:3]
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[+] score: 11
miRNA expression profiling of lung tissues demonstrated differential expression of seven miRNAs, with downregulation of miR-344a-3p (−2.36-fold change) and upregulation of miR-103 (4.04-fold change), miR-22 (2.72-fold change), miR-30b-5p (1.51-fold change), miR-347 (1.95-fold change), miR-382 (2.82-fold change), and miR-3573-3p (3.32-fold change) (Figures 3A,B). [score:11]
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[+] score: 4
The majority of the miRNAs identified by microarray as significantly dysregulated were verified as dysregulated by stem loop qPCR, with the exception of Rattus norvegicus (rno)-miR-344a/rno-miR-344a-5p, rno-miR-3572, rno-miR-138-1, rno-miR-3596c, rno-let-7i and rno-miR-465, providing evidence that the microarrays effectively screened dysregulated miRNAs. [score:4]
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[+] 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-15a, hsa-mir-26b, hsa-mir-29a, hsa-mir-30a, hsa-mir-29b-1, hsa-mir-29b-2, hsa-mir-106a, mmu-let-7g, mmu-let-7i, mmu-mir-15b, mmu-mir-29b-1, mmu-mir-30a, mmu-mir-30b, mmu-mir-125a, mmu-mir-125b-2, mmu-mir-130a, mmu-mir-138-2, mmu-mir-181a-2, mmu-mir-182, hsa-mir-30c-2, hsa-mir-30d, mmu-mir-30e, hsa-mir-10a, hsa-mir-34a, hsa-mir-181a-2, hsa-mir-181b-1, hsa-mir-181c, hsa-mir-182, hsa-mir-181a-1, mmu-mir-297a-1, mmu-mir-297a-2, mmu-mir-301a, mmu-mir-34c, mmu-mir-34b, mmu-let-7d, mmu-mir-106a, mmu-mir-106b, hsa-let-7g, hsa-let-7i, hsa-mir-15b, hsa-mir-30b, hsa-mir-125b-1, hsa-mir-130a, hsa-mir-138-2, hsa-mir-125a, hsa-mir-125b-2, hsa-mir-138-1, mmu-mir-30c-1, mmu-mir-30c-2, mmu-mir-30d, 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-26b, mmu-mir-29a, mmu-mir-29c, mmu-mir-34a, rno-mir-301a, rno-let-7d, rno-mir-344a-1, mmu-mir-344-1, rno-mir-346, mmu-mir-346, rno-mir-352, hsa-mir-181b-2, mmu-mir-10a, mmu-mir-181a-1, mmu-mir-29b-2, mmu-mir-138-1, mmu-mir-181b-1, mmu-mir-181c, mmu-mir-125b-1, hsa-mir-106b, hsa-mir-29c, hsa-mir-30c-1, hsa-mir-34b, hsa-mir-34c, hsa-mir-301a, hsa-mir-30e, hsa-mir-362, mmu-mir-362, hsa-mir-369, hsa-mir-374a, mmu-mir-181b-2, hsa-mir-346, 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-10a, rno-mir-15b, rno-mir-26b, rno-mir-29b-2, rno-mir-29a, rno-mir-29b-1, rno-mir-29c-1, rno-mir-30c-1, rno-mir-30e, rno-mir-30b, rno-mir-30d, rno-mir-30a, rno-mir-30c-2, rno-mir-34b, rno-mir-34c, rno-mir-34a, rno-mir-106b, rno-mir-125a, rno-mir-125b-1, rno-mir-125b-2, rno-mir-130a, rno-mir-138-2, rno-mir-138-1, rno-mir-181c, rno-mir-181a-2, rno-mir-181b-1, rno-mir-181b-2, rno-mir-181a-1, hsa-mir-449a, mmu-mir-449a, rno-mir-449a, mmu-mir-463, mmu-mir-466a, hsa-mir-483, hsa-mir-493, hsa-mir-181d, hsa-mir-499a, hsa-mir-504, mmu-mir-483, rno-mir-483, mmu-mir-369, rno-mir-493, rno-mir-369, rno-mir-374, hsa-mir-579, hsa-mir-582, hsa-mir-615, hsa-mir-652, hsa-mir-449b, rno-mir-499, hsa-mir-767, hsa-mir-449c, hsa-mir-762, mmu-mir-301b, mmu-mir-374b, mmu-mir-762, mmu-mir-344d-3, mmu-mir-344d-1, mmu-mir-673, mmu-mir-344d-2, mmu-mir-449c, mmu-mir-692-1, mmu-mir-692-2, mmu-mir-669b, mmu-mir-499, mmu-mir-652, mmu-mir-615, mmu-mir-804, mmu-mir-181d, mmu-mir-879, mmu-mir-297a-3, mmu-mir-297a-4, mmu-mir-344-2, mmu-mir-466b-1, mmu-mir-466b-2, mmu-mir-466b-3, mmu-mir-466c-1, mmu-mir-466e, mmu-mir-466f-1, mmu-mir-466f-2, mmu-mir-466f-3, mmu-mir-466g, mmu-mir-466h, mmu-mir-493, mmu-mir-504, mmu-mir-466d, mmu-mir-449b, hsa-mir-374b, hsa-mir-301b, rno-mir-466b-1, rno-mir-466b-2, rno-mir-466c, rno-mir-879, mmu-mir-582, rno-mir-181d, rno-mir-182, rno-mir-301b, rno-mir-463, rno-mir-673, rno-mir-652, mmu-mir-466l, mmu-mir-669k, mmu-mir-466i, mmu-mir-669i, mmu-mir-669h, mmu-mir-466f-4, mmu-mir-466k, mmu-mir-466j, mmu-mir-1193, mmu-mir-767, rno-mir-362, rno-mir-504, rno-mir-582, rno-mir-615, mmu-mir-3080, mmu-mir-466m, mmu-mir-466o, mmu-mir-466c-2, mmu-mir-466b-4, mmu-mir-466b-5, mmu-mir-466b-6, mmu-mir-466b-7, mmu-mir-466p, mmu-mir-466n, mmu-mir-344e, mmu-mir-344b, mmu-mir-344c, mmu-mir-344g, mmu-mir-344f, mmu-mir-374c, mmu-mir-466b-8, hsa-mir-466, hsa-mir-1193, rno-mir-449c, rno-mir-344b-2, rno-mir-466d, rno-mir-1193, rno-mir-344b-1, hsa-mir-374c, hsa-mir-499b, mmu-mir-466q, mmu-mir-344h-1, mmu-mir-344h-2, mmu-mir-344i, rno-mir-344i, rno-mir-344g, mmu-let-7j, mmu-mir-30f, mmu-let-7k, mmu-mir-692-3, rno-let-7g, rno-mir-15a, rno-mir-762, mmu-mir-466c-3, rno-mir-29c-2, rno-mir-29b-3, rno-mir-344b-3, rno-mir-466b-3, rno-mir-466b-4
1Proliferation, Invasion, Tumor suppression [63– 66] miR-344 ↓2.0 ↓3.2 NA miR-346 ↓2.4Proliferation [67, 68] miR-362 ↓2.3Proliferation, Invasion, Apoptosis [69– 76] miR-369 ↓2.8 ↓2.6 ↓2.1Aerobic glycolysis [77] miR-374 ↑3.0 ↓2.2 NA miR-449 ↑2.7 ↑2.4Proliferation [78– 81] miR-463 ↓2.7 NAmiR-466 [°] ↑2.4 ↑2.1 ↓3.5 NA miR-483 ↓3.2Apoptosis [82] miR-493 ↑2.1 ↓2.2Proliferation [83– 85] miR-499a ↓5.0 ↑2.3Proliferation [86] miR-504 ↓2.6 ↑2.0Proliferation, Apoptosis [87, 88] miR-579 ↑2.8 NAmiR-582 [^] ↑2.4Proliferation [89] miR-615 ↓2.1Proliferation, Invasion [90, 91] miR-652 ↑2.4Proliferation, EMT [92, 93] miR-669b ↓2.1 NA miR-669h ↓3.6 ↑2.3 NA miR-669i ↓2.3 NA miR-669k ↓7.2 ↓5. [score:3]
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