14 publications mentioning gga-mir-29b-1

Open access articles that are associated with the species Gallus gallus and mention the gene name mir-29b-1. Click the [+] symbols to view sentences that include the gene name, or the word cloud on the right for a summary.

1

miR-29b directly targets DNMT3A and DNMT3B, and indirectly targets DNMT1, thereby leading to downregulation of genes, reduction of global DNA methylation, and re -expression of the DNA hypermethylated and silenced tumor suppressor genes [32].

To validate the downregulation of c DNMT3B at the post-transcription levels, the miRNAs, gga-miR-15c (target score: 74, seed location: 544 and 732), gga-miR-29b (target score: 62, seed location: 1223), gga-miR-383 (target score: 53, seed location: 996), and gga-miR-222 (target score: 50, seed location: 591) were selected for the c DNMT3B 3′-UTR based on an online database miRDB (Fig. 11A).

Regulation of cDNMT3B using 3′UTR target miRNAsTo examine the regulation of c DNMT3B expression, we selected four miRNAs including gga-miR-15c (5′-UAG CAG CAC AUC AUG GUU UGU A-3′), gga-miR-29b (5′-UAG CAC CAU UUG AAA UCA GUG UU-3′), gga-miR-383 (5′-AGA UCA GAA GGU GAU UGU GGC U-3′), and gga-miR-222 (5′-AGC UAC AUC UGG CUA CUG GGU CUC-3′) specific to the 3′UTR region of c DNMT3B from miRDB, a microRNA target prediction and functional annotation database [17].

Expression patterns of miRNA and Regulation of cDNMT3B Expression patterns of miRNAs gga-miR-15c, gga-miR-29b, gga-miR-383 and gga-miR-222 were examined during meiotic stages of germ line development by qRT-PCR.

To examine the regulation of c DNMT3B expression, we selected four miRNAs including gga-miR-15c (5′-UAG CAG CAC AUC AUG GUU UGU A-3′), gga-miR-29b (5′-UAG CAC CAU UUG AAA UCA GUG UU-3′), gga-miR-383 (5′-AGA UCA GAA GGU GAU UGU GGC U-3′), and gga-miR-222 (5′-AGC UAC AUC UGG CUA CUG GGU CUC-3′) specific to the 3′UTR region of c DNMT3B from miRDB, a microRNA target prediction and functional annotation database [17].

During female germ line development, miR-15c, miR-29b and miR-222 showed similar patterns of expression.

Gga-miR-29b is believed to downregulate c DNMT3B in a sex specific manner.

Expression patterns of miRNAs gga-miR-15c, gga-miR-29b, gga-miR-383 and gga-miR-222 were examined during meiotic stages of germ line development by qRT-PCR.

Earlier publications reported the downregulation of DNMT3B by miR-29b or miR-383 particularly in tumor cells [31], [32].

We examined the expression of gga-miR-15c, gga-miR-29b, gga-miR-383 and gga-miR-222 during meiotic stages of germ line development by qRT-PCR.

We performed miRNA to examine the relative quantification of the expression level of gga-miR-15c, gga-miR-29b, gga-miR-383 and gga-miR-222 during germ line development.

Our studies in chickens reinforce that miR-15c, miR-29b, miR-383 and miR-222 may downregulate DNMT3B in PGCs from female embryos after they enter meiosis.

Regulation of c DNMT3B using the c DNMT3B 3′UTR target miRNAs gga-miR-15c, gga-miR-29b, gga-miR-383, and gga-miR-222 is of great interest in this study.

Expression of gga-miR-15c, gga-miR-29b, gga-miR-383 and gga-miR-222 during meiotic stages of germ line development examined by qRT-PCR.

Our dual fluorescent reporter assay suggests that gga-miR-29b, gga-miR-383 and gga-miR-222 may cause maximum (30.01–31.28%) downregulation of c DNMT3B in vitro.

In contrast to other miRNAs, miR-29b expression was detected at a high level on E9.5, and continuously decreased until E15.5.

Compared to each mutants, c DNMT3B 3′UTR eGFP expression was slightly decreased by gga-miR-15c (25.82%), gga-miR-29b (30.01%), gga-miR-383 (30.0%), and gga-miR-222 (31.28%).

miR-29b significantly regulates many collagen genes, matrix metalloproteinase 2 (MMP2), integrin beta1 (ITGB1), progranulin (PGRN), podoplanin (PDPN), and other genes related to the extracellular matrix [33], [34], [35].

c DNMT3B 3′UTR and cDNMT3B 3′UTR mutants for each miRNA binding sites generated by point mutation cloned into a pcDNA3 plasmid encoding eGFP and c DNMT3B 3′UTR-specific miRNAs including gga-miR-15c, gga-miR-29b, gga-miR-383, and gga-miR-222 cloned into a pDsRed2-N1 plasmid, respectively, encoding RFP were cotransfected into 293 FT cells.

miR-15c, miR-29b, miR-383 and miR-222 binding sites in chicken and corresponding human and mouse sequences are shown in red colour.

The expression and functions of miR-29b and miR-222 have been extensively characterized in mammals.

2

Stage-by-stage examinations revealed further expression patterns, such as emergence at specific time-points during embryogenesis and up-regulation of miRNA groups in late embryos (miR-1 and bantam), expression associated with stage transition between instar and molt larval stages (miR-34b), expression associated with silk gland growth and spinning activity (miR-274), continuous high expression from the spinning larval to pupal and adult stages (miR-252 and miR-31a), a coordinate expression trough in day 3 pupae of both sexes (miR-10b and miR-281), up-regulation in pupal metamorphosis of both sexes (miR-29b), and down-regulation in pupal metamorphosis of both sexes (miR-275).

Our results show that miRNAs display a wide variety of expression profiles over the whole life of the silkworm, including continuous expression from embryo to adult (miR-184), up-regulation over the entire life cycle (let-7 and miR-100), down-regulation over the entire life cycle (miR-124), expression associated with embryogenesis (miR-29 and miR-92), up-regulation from early 3 [rd ]instar to pupa (miR-275), and complementary pulses in expression between miR-34b and miR-275.

Four miRNAs (miR-29b, miR-34b, miR-277, and miR-285) were significantly up-regulated from the spinning larvae to adult stages, and nine (miR-305, miR-275, miR-289, miR-307-3p, miR-274, miR-286, miR-87, miR-315, and miR-92) were significantly down-regulated during this time-course (Additional file 12).

miR-29b expression peaked in egg-removed moths, whereas miR-92 expression was maximal in the new pupae of both sexes.

Whereas expression in both sexes fluctuated in a generally similar manner, miR-29b was far more highly expressed in females.

Interestingly, in other organisms, such as the mouse, miR-29b was almost undetectable in the embryo, but extensively expressed in the adult during brain development [33].

In the whole-life test, miR-29b was not present in early female pupae, but was strongly expressed in the early female moth (Additional file 4).

miR-29b was detected at the late embryo and 1 [st ]instar larval stages (Figure 3A), but was not expressed from early 4 [th ]to 5 [th ]instar day 7 larval stages (Additional file 7).

At this time-point, 8 miRNAs were initially expressed (including miR-29b, miR-34b, and miR-124).

In fact, miR-29 was additionally expressed in late 1 [st ]instar, late 2 [nd ]instar, and late 3 [rd ]molt larvae.

The whole-life array revealed that, in contrast to miR-29b, miR-275 expression peaked in early female pupae, but not in the early female moth (Figures 1B, C).

miR-29b displayed the highest expression at the embryo stage, and rapidly decreased in level after the 1 [st ]molt larval stage, but rose significantly once more in fresh female moths carrying eggs in the abdomen (Figure 1A), raising the possibility of an involvement in oogenesis and embryogenesis.

The whole-life array revealed exclusive miR-29 expression at the early 1 [st ]instar and late 1 [st ]molt larval stages.

miR-29b and miR-92 appeared to share similar patterns by whole-life profiling, but the detailed assay revealed evident differences between their expression profiles.

3

gga-miR-451 was too down-regulated by GH in chicken hepatocytes in our study, indicating gga-miR-451 might mediate GH regulation of chicken liver metabolism but gga-miR-29b played different roles in GH regulation of liver metabolism comparing to miR-29b in rat.

In male rat livers, miR-451 and miR-29b are down-regulated by GH [45].

4

Top amongst them were miRs reported to decrease tumor metastasis and invasion (miR-194, miR-103, miR-29) [21, 22], inhibit cell proliferation (let-7 family, miR-215) [23], induce apoptosis (miR-125) [24], and tumor suppressors (let-7 family, miR-125, miR-106) [25, 26] to mention but a few.

Among the top 24 differentially regulated candidates were several miRs, which were known to be deregulated in pancreatic cancer, among them the miR-29 and let-7 families (Figure 1A).

5

Pekarsky Y. Croce C. M. Is miR-29 an oncogene or tumor suppressor in CLL?

Seed sequence homology has also been observed between mdv2-miR-M21 and miR-29, which is known to function both as an oncogene and a tumor suppressor depending on the context [63].

Furthermore, EBV-encoded miR-BART1-3p and RLCV-encoded miR-rL1-6-3p also share seed sequence with miR-29.

BLV-encoded miRNA, blv-miR-B4, has been shown to be a functional ortholog of host miR-29 [11].

6

In other studies, the ability of miR-29 to inhibit the expression of several types of collagen and to stimulate the expression of MMP-2 and -9 has been observed (Chen et al. 2011).

7

All members of the miR-15, miR-181, and miR-29 families were down-regulated in L30 compared with L20, whereas the other families included members that were either up- or down-regulated.

Seven conserved families all were DE with P ≤ 0.05, including let-7 (let-7a, -7b, -7c,-7f, -7g, -7i, -7j, and -7k), miR-130 (miR-130a, and -130b), miR-146 (miR-146a, -146b, and -146c), miR-15 (miR-15a, -15b, and -15c), miR-181 (miR-181a and -181b), miR-29 (miR-29a, -29b and -29c), and miR-30 (miR-30a, -30b, -30c, -30d, and -30e).

8

For instance, miR-29b has been approved to induce global DNA hypomethylation and reactivate tumor suppressor gene P15 and ESR1 in acute myeloid leukemia by targeting DNMT3A and DNMT3B directly and DNMT1 indirectly (18).

9

miR-22 can regulate the PTEN/AKT pathway and target HDAC6 [66– 68]; miR-206 and miR-1a can suppress hepatic lipogenesis [69]; miR-29b and miR-9 are involved in insulin sensitivity and diabetes [70, 71]; miR-31 and miR-32 participate in differentiation of stem cells into adipocyte and lipid metabolism in oligodendrocytes [72, 73].

10

In addition, increased miRNA29 expression in the livers of diet -induced obese mice and Zucker diabetic rats has been demonstrated.

It has been known for several years that the miRNA29 family negatively regulates the insulin signalling pathway in adipocytes [258].

Most interestingly, miRNA29 levels were normalised after treatment with pioglitazone, in both mo dels [259].

11

And interestingly, miR-29 family reverted global gene methylation by targeting DNMT3a and DNMT3b directly in non-small-cell lung cancer (NSCLC) and acute myeloid leukemia cells [15, 16].

12

The reproducibility of these results was tested by Taqman RT-PCR, selecting 18 miRNAs (hsa-let-7a, hsa-miR-141, hsa-miR-143, hsa-miR-145, hsa-miR-17, hsa-miR-182, hsa-miR-191, hsa-miR-199a-5p, hsa-miR-200a, hsa-miR-200b, hsa-miR-222, hsa-miR-29b, hsa-miR-34a, hsa-miR-424, hsa-miR-15a, hsa-miR-199a-3p, hsa-miR-26b, hsa-miR-361-3p) previously showing at least a three-fold modulation in expression in a wide panel of PDAC cell lines 49.

13

In MDV infected CEFs, gga-mir-29b,-196,-133a,-10b,-30d were increased, and gga-mir-let-7a, 7b, 7f and gga-mir-1a, mir-130a were decreased [87]; of these only gga-mir-10b was increased in our data.

14

Several miRNAs previously reported to be involved in immune responses such as miR-155, miR-9, miR-30, miR-126, and miR-29 families were identified.