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miRBase |
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![]() 7 publications mentioning hsa-mir-3180-1Open access articles that are associated with the species Homo sapiens and mention the gene name mir-3180-1. Click the [+] symbols to view sentences that include the gene name, or the word cloud on the right for a summary. |
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Other miRNAs from this paper: hsa-mir-17, hsa-mir-106b, hsa-mir-369, hsa-mir-483, hsa-mir-501, hsa-mir-552, hsa-mir-543, hsa-mir-3180-2, hsa-mir-3180-3, hsa-mir-3189, hsa-mir-4323, hsa-mir-4283-1, hsa-mir-4287, hsa-mir-4283-2, hsa-mir-3180-4, hsa-mir-3180-5, hsa-mir-374c
In this study, we demonstrated that hydrostatic pressure upregulated/downregulated multiples in HBSMCs and that the proliferation of HBSMCs could be altered by the overexpression of a single miRNA (miR-3180-5p), which reduces PODN expression, leading to cdk2 -mediated proliferation of HBSMCs.
[score:10]
In samples from patient cells, expression of miR-3180-5p was upregulated under hydrostatic pressure (Fig. 7c,d; p < 0.00001), whereas that of PODN was downregulated (Fig. 7e,f; p < 0.00001).
[score:9]
Our study revealed that the expression of podocan, the functional protein product of the PODN gene, could be suppressed by miR-3180-5p overexpression in HBSMCs (p = 0.041).
[score:7]
Computational prediction of human targets using miRanda and TargetScan indicated that PODN is a potential target of miR-3180-5p.
[score:7]
The upregulateds included miR-3180-5p, miR-3189-3p, miR-369-5p, miR-4283, miR-4287, miR-4323, miR-483-3p, miR-501-5p, and miR-552-3p (Table 1), and the downregulateds included miR-106b-5p, miR-17-3p, miR-374c-5p, and miR-543 (Table 1).
[score:7]
MiR-3180-5p and miR-4323 were significantly upregulated (p = 0.043 and p = 0.027, respectively; Fig. 3a), whereas miR-543 was significantly downregulated (p = 0.048; Fig. 3b).
[score:7]
Overall, our results demonstrated that high hydrostatic pressure leads to an increase in the expression of miR-3180-5p, which promotes HBSMC proliferation by the suppression of PODN, thereby leading to the activation of the pro-proliferative cdk2 pathway.
[score:5]
To our knowledge, the identification of miR-3180-5p as a mechano-sensitive in HBSMCs represents the first evidence linking to cell proliferation in the bladder, and miR-3180-5p may be an important target for treatment of bladder diseases.
[score:5]
The expression levels of ADARB1 and PODN in the HBSMCs were validated by RT-PCR and western blot to investigate the effect of the overexpression of miR-3180-5p on target.
[score:5]
HBSMCs were transfected with miR-3180-5p mimics, a miR-3180-5p inhibitor or a non -targeting control sequence, grown for 48 h, and then washed three times in phosphate-buffered saline (PBS).
[score:5]
PODN expression was suppressed by miR-3180-5p.
[score:5]
Therefore, it was apparent that miR-3180-5p inhibits PODN gene expression, leading to decreased production of its functional protein, podocan.
[score:5]
In addition, miR-3180-5p was the most upregulated in response to hydrostatic pressure (Fig. 3a); thus, it was selected for further validation experiments.
[score:4]
Our data indicated that miR-3180-5p directly affects PODN, as observed by decreased PODN expression levels using RT-PCR and reduced podocan levels in western blots from cells exposed to miR-3180-5p, and this effect was confirmed as a direct effect based on a luciferase reporter assay.
[score:4]
To validate the functional significance of the identifieds, we selected the 3180-5p (miR-3180-5p) because it was found to be upregulated in response to hydrostatic pressure.
[score:4]
We focused on miR-3180-5p because it was the most upregulated by hydrostatic pressure.
[score:4]
PODN was directly inhibited by miR-3180-5p.
[score:4]
To study the clinical relevance of miR-3180-5p and its target gene PODN, the expression levels of miR-3180-5p and PODN were investigated in patient samples by in situ hybridization.
[score:3]
The expression of miR-3180-5p and PODN in patient cells.
[score:3]
Thus, miR-3180-5p may be a novel molecular target for the regeneration of cells in engineering bladder tissue.
[score:3]
This result essentially suggests that when miR-3180-5p is overexpressed, transcription of PODN is limited, and the levels of podocan decrease.
[score:3]
To further validate the inhibitory effect of miR-3180-5p on podocan expression, we investigated the effect of miR-3180-5p on the proteins p21 and cdk2, which function downstream of podocan.
[score:3]
In addition, the changes in PODN, podocan, cdk2 and p21 were confirmed by a complementary approach utilizing a miR-3180-5p inhibitor.
[score:3]
This result demonstrated that overexpression of miR-3180-5p, which is involved in the cell cycle, induced cells to progress from G1 to S phase, thus promoting the proliferation of HBSMCs.
[score:3]
Luciferase constructs were synthesized using ligating oligonucleotides containing wild-type or mutant target sites for miR-3180-5p and were inserted into a psiCHECK-2 vector (Promega, Madison, WI, USA).
[score:3]
HBSMCs were transfected with miR-3180-5p mimics or inhibitor at 100 nM (GenePharma, Shanghai, China) using the transfection reagent Lipofectamine 3000 (Invitrogen, Carlsbad, CA, USA) according to the manufacturer’s instructions.
[score:3]
RNA in situ hybridization of miR-3180-5p and PODNTo study the clinical relevance of miR-3180-5p and its target gene PODN, the expression levels of miR-3180-5p and PODN were investigated in patient samples by in situ hybridization.
[score:3]
Our preliminary gene-chip results showed that there are some lncRNAs that can target miR-3180-5p.
[score:3]
Transfection of HBSMCs with mimics of miR-3180-5p or with a miR-3180-5p inhibitor clearly demonstrated that miR-3180-5p significantly promoted the proliferation of HBSMCs under hydrostatic pressure.
[score:3]
Moreover, the levels of PODN and podocan were demonstrably increased in cells transfected with the miR-3180-5p inhibitor (p = 0.0035; p = 0.025).
[score:3]
Expression of cdk2 is promoted by miR-3180-5p.
[score:3]
Our flow cytometry results confirmed that the percentage of cells in (S + G2/M) increased when podocan levels were reduced by the overexpression of miR-3180-5p.
[score:3]
These results were consistent with a previous study, confirmed the clinical relevance of miR-3180-5p, and demonstrated that a better understanding of the relationship between miR-3180-5p and proliferative signaling pathways may provide important novel targets for engineering bladder tissue.
[score:3]
The above results suggest that the function of cdk2 was affected by miR-3180-5p via the regulation of podocan.
[score:2]
However, when the results are compared with previously published reports of cell proliferation under HP, the increase in cell proliferation is similar to that observed in our miR-3180-5p overexpressing transfected cells 3. Thus, we can conclude that miR-3180-5p is involved in the HP -induced HBSMC proliferation.
[score:2]
For the luciferase assay, 293T cells (human embryonic kidney cells) were co -transfected with wild-type or mutant psiCHECK-PODN reporter vectors and miR-3180-5p mimics or a non -targeting control mimic sequence (as the NC groups) using Lipofectamine 3000 (Invitrogen).
[score:2]
The next important point here is that the factors regulating the miR-3180-5p levels remain unknown.
[score:2]
Thus, miR-3180-5p regulates HBSMC proliferation under hydrostatic pressure.
[score:2]
-induced miR-3180-5p participates in proliferation.
[score:1]
RNA in situ hybridization of miR-3180-5p and PODN.
[score:1]
This finding indicated that miR-3180-5p was likely involved in the process of HBSMC proliferation.
[score:1]
However, adenosine deaminase RNA-specific B1, the functional protein of ADARB1, showed no changes (p = 0.134) in response to miR-3180-5p.
[score:1]
We transfected HBSMCs with miR-3180-5p mimics, and the increased intracellular levels of miR-3180-5p were accompanied by a significant increase (p = 0.002) in the proliferation index (the percentage of cells in (S + G2/M)) of HBSMCs, from 29.32 ± 6.25% in the NC group to 50.50 ± 3.34% in the cells transfected with miR-3180-5p (Fig. 7a,b).
[score:1]
Luciferase activity was decreased by ~41% (p = 0.0022) when wild-type psiCHECK-PODN reporter vectors were co -transfected with miR-3180-5p in 293T cells.
[score:1]
All of these results are presented in Fig. 4. Previous research revealed that miR-3180-5p is involved in HBSMC proliferation.
[score:1]
In cells transfected with miR-3180-5p mimics, the level of PODN was found to be decreased (p = 0.004), whereas that of ADARB1 was found to be increased (p = 0.008).
[score:1]
Further, we determined the functional importance of the most sensitive to hydrostatic pressure, miR-3180-5p.
[score:1]
RNA in situ hybridization for miR-3180-5p and PODN was performed after HBSMCs were subjected to cyclic hydrodynamic pressure.
[score:1]
Next, samples were hybridized overnight with miR-3180-5p probe or PODN probe at 28 °C or 34 °C, respectively.
[score:1]
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Other miRNAs from this paper: hsa-mir-26a-1, hsa-mir-30d, hsa-mir-26a-2, hsa-mir-202, hsa-mir-1468, hsa-mir-1285-1, hsa-mir-1285-2, hsa-mir-1307, hsa-mir-2110, hsa-mir-3127, hsa-mir-378b, hsa-mir-3150a, hsa-mir-3179-1, hsa-mir-3180-2, hsa-mir-3179-2, hsa-mir-3180-3, hsa-mir-3179-3, hsa-mir-3180-4, hsa-mir-3180-5, hsa-mir-4472-1, hsa-mir-4472-2, hsa-mir-3179-4
Remarkably, miR-3180 showed up-regulation of miR-3180-3p (p = 0.007) while miR-3180-5p was significantly down-regulated (p = 0.003).
[score:7]
Clearly, the 3p form is up-regulated while the 5p form is down regulated for miR-3180 (panel a) while miR-202 shows the opposite behavior (panel b).
[score:5]
In this figure, opposite fold changes of the 3p and the 5p mature form of miRNAs is shown for two miRNAs, miR-3180 in panel a and miR-202 in panel b. The right part shows the pileup plots, the sequence in the middle represents the precursor, the two mature forms are highlighted in red (5p) and blue (3p) and with the blue shaded area.
[score:1]
Pileup plots for both miRNAs showing the accurate mapping pattern of reads to the mature miRNAs are presented in Figure 4 (a: miR-3180, b: miR-202).
[score:1]
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DMR Name Gene Association Category DMR Name Gene Association Category DMR2:238198201 ILKAP Signaling DMR1:175491101 TNR ECM DMR5:164501 PLEKHG4B Signaling DMR5:151531101 FAT2 ECM DMR5:55530601 PPAP2A Signaling DMR9:28333101 LINGO2 ECM RNF138P1 Unknown DMR19:43206901 PSG4 ECM DMR5:9122501 SEMA5A Signaling DMR1:12173801 TNFRSF1B Receptor DMR7:158556901 PTPRN2 Signaling DMR9:98644001 GABBR2 Receptor DMR8:99694501 VPS13B Signaling DMR10:123691901 GPR26 Receptor AC018442.1 Unknown DMR6:31814701 HSPA1L Protein Binding DMR13:98815001 DOCK9 Signaling HSPA1A Protein Binding DMR16:2603101 PDPK1 Signaling DMR6:31828001 HSPA1B Protein Binding AC141586.5 Unknown DMR5:134314001 CDKL3 Cell Cycle DMR17:8836901 PIK3R6 Signaling CTD-2410N18.4 Unknown DMR18:8634901 RAB12 Signaling DMR19:756801 MISP Cell Cycle DMR10:73117601 NUDT13 Metabolism DMR18:46969701 KATNAL2 Cytoskeleton DMR11:484301 PTDSS2 Metabolism TCEB3CL Transcription DMR12:81062701 ACSS3 Metabolism DMRX:115191101 LRCH2 Cytoskeleton DMR12:95948901 AMDHD1 Metabolism RBMXL3 Translation DMR14:46935601 MDGA2 Metabolism DMR6:31326001 HLA-C Immune DMR20:2311001 TGM3 Metabolism DMR19:54772001 KIR2DL1 Immune DMR2:2189101 MYT1L Transcription KIR3DL1 Immune DMR2:144492201 ZEB2 Transcription CTB-61M7.1 Unknown DMR10:30846501 ZNF438 Transcription DMR7:87205701 TMEM243 Mitochondria DMR10:32731701 CCDC7 Transcription DMR7:101239401 FIS1 Mitochondria DMR19:52916701 ZNF888 Transcription DMR10:1197701 ADARB2 Translation DMR20:61964901 TAF4 Transcription DMR22:11248401 5_8S_rRNA Translation DMR4:186476501 F11-AS1 Epigenetic AC137488.1 Unknown RP11-215A19.2 Unknown DMR19:48181401 CARD8 Apoptosis DMR4:188443001 LINC01060 Epigenetic ZNF114 Transcription DMR8:27797501 ESCO2 Epigenetic C19orf68 Unknown DMR16:14910901 MIR3180-1 Epigenetic DMR3:55470001 WNT5A Development NPIPA3 Unknown DMR22:48701801 FAM19A5 Growth Factor RP11-958N24.1 Unknown DMR12:130657401 RIMBP2 Misc.
[score:8]
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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-24-1, hsa-mir-24-2, hsa-mir-25, hsa-mir-29a, hsa-mir-32, hsa-mir-92a-1, hsa-mir-92a-2, hsa-mir-93, hsa-mir-101-1, hsa-let-7g, hsa-let-7i, hsa-mir-1-2, hsa-mir-122, hsa-mir-125b-1, hsa-mir-133a-1, hsa-mir-133a-2, hsa-mir-143, hsa-mir-145, hsa-mir-191, hsa-mir-125a, hsa-mir-125b-2, hsa-mir-134, hsa-mir-206, hsa-mir-1-1, hsa-mir-101-2, hsa-mir-99b, hsa-mir-370, hsa-mir-323a, hsa-mir-485, hsa-mir-491, hsa-mir-503, hsa-mir-611, hsa-mir-637, hsa-mir-638, hsa-mir-661, hsa-mir-654, hsa-mir-657, hsa-mir-762, hsa-mir-770, hsa-mir-760, hsa-mir-939, hsa-mir-1236, hsa-mir-1249, hsa-mir-1470, hsa-mir-1538, hsa-mir-2277, hsa-mir-3131, hsa-mir-3151, hsa-mir-323b, hsa-mir-3180-2, hsa-mir-3180-3, hsa-mir-4298, hsa-mir-4259, hsa-mir-4254, hsa-mir-4286, hsa-mir-3622a, hsa-mir-3663, hsa-mir-3677, hsa-mir-3180-4, hsa-mir-3180-5
Start position 530 was targeted by hsa-miR-3131, hsa-miR-4298, and hsa-miR-939 while position 531 was targeted by hsa-miR-134 and hsa-miR-3180-3p.
[score:5]
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Other miRNAs from this paper: hsa-mir-17, hsa-mir-18a, hsa-mir-19a, hsa-mir-19b-1, hsa-mir-20a, hsa-mir-92a-1, hsa-mir-99a, hsa-mir-34a, hsa-mir-190a, hsa-mir-34b, hsa-mir-34c, hsa-mir-99b, hsa-mir-877, hsa-mir-936, hsa-mir-940, hsa-mir-3128, hsa-mir-3180-2, hsa-mir-3180-3, hsa-mir-4276, hsa-mir-4329, hsa-mir-3614, hsa-mir-3180-4, hsa-mir-3180-5, hsa-mir-3928, hsa-mir-4443, hsa-mir-4633, hsa-mir-4693, hsa-mir-4731, hsa-mir-4764
Among all of the TGF-β pathway-related miRNAs, five known miRNAs (miR-3180-3p, miR-34b-5p, miR-877-3p, miR-936, and miR-940) and 10 novel miRNA candidates (seq-915_x4024, seq-5118_x304, seq-6713_x208, seq-14465_x69, seq-18595_x48, seq-19788_x44, seq-38785_x17, seq-38875_x17, seq-48658_x13, and seq-52107_x11) target pathway members that positively regulate the pathway.
[score:4]
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Other miRNAs from this paper: hsa-mir-26b, hsa-mir-196a-1, hsa-mir-197, hsa-mir-129-1, hsa-mir-7-1, hsa-mir-7-2, hsa-mir-7-3, hsa-mir-196a-2, hsa-mir-222, hsa-mir-128-1, hsa-mir-132, hsa-mir-145, hsa-mir-9-1, hsa-mir-9-2, hsa-mir-9-3, hsa-mir-126, hsa-mir-129-2, hsa-mir-149, hsa-mir-128-2, hsa-mir-34c, hsa-mir-130b, hsa-mir-196b, hsa-mir-572, hsa-mir-885, hsa-mir-374b, hsa-mir-3148, hsa-mir-3180-2, hsa-mir-3180-3, hsa-mir-3622a, hsa-mir-3622b, hsa-mir-3646, hsa-mir-3648-1, hsa-mir-3180-4, hsa-mir-3180-5, hsa-mir-4470, hsa-mir-4672, hsa-mir-4690, hsa-mir-3648-2
Using stringent algorithm, we have identified ten miRNAs (miR-129-5p, miR-3148, miR-4470, miR-4672, miR-3646, miR-3180, miR-4690, miR-3622, miR-5096, and miR-885) that can target different genes in innate immune pathway.
[score:3]
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Other miRNAs from this paper: hsa-mir-21, hsa-mir-22, hsa-mir-34a, hsa-mir-182, hsa-mir-183, hsa-mir-132, hsa-mir-144, hsa-mir-150, hsa-mir-194-1, hsa-mir-155, hsa-mir-194-2, hsa-mir-130b, hsa-mir-30e, hsa-mir-342, hsa-mir-409, hsa-mir-181d, hsa-mir-501, hsa-mir-942, hsa-mir-3180-2, hsa-mir-3180-3, hsa-mir-3200, hsa-mir-4318, hsa-mir-3180-4, hsa-mir-3180-5
In whole blood samples of healthy controls we found nine miRNAs (hsa-miR-130b*, hsa-miR-182, hsa-miR-183, hsa-miR-3180-3p, hsa-miR-3200-5p, hsa-miR-409-3p, hsa-miR-4318, hsa-miR-501-5p, hsa-miR-942) that were detected in all whole blood samples but not in any of the separated leukocyte subsets of healthy controls.
[score:1]
For the lung cancer patients five miRNAs (hsa-miR-3180-3p, hsa-miR-3200-5p, hsa-miR-4318, hsa-miR-942, hsa-miR-144*) were detected in all whole blood samples but not in any of the separated leukocyte subsets of lung cancer patients.
[score:1]
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