MiR-18a regulates myoblasts proliferation by targeting Fgf1

Liu, Chuncheng; Chen, Min; Wang, Meng; Pi, Wen-Hui; Li, Ning; Meng, Qingyong

doi:10.1371/journal.pone.0201551

Cited by 12 publications

(10 citation statements)

References 35 publications

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“… 7 A series of in vitro and in vivo studies have demonstrated that miR-18a plays an important role in different cell functions via downregulating FGF1, Smad4, HIF-1α, and other target genes. 12 , 13 , 14 Therefore, elucidation of the underlying mechanisms by which miR-18a regulates the functions of trophoblast cells may provide a better understanding of the pathophysiology of this disorder and uncover new targets for therapeutic intervention.…”

Section: Introductionmentioning

confidence: 99%

miR-18a Contributes to Preeclampsia by Downregulating Smad2 (Full Length) and Reducing TGF-β Signaling

Wang

et al. 2020

Molecular Therapy - Nucleic Acids

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The study investigated the regulation of Smad2 by miR-18a and its role in preeclampsia (PE). Bioinformatics analysis showed that both Smad2 and Smad3 were the predicted targets for miR-18a. Mass spectrum analysis showed that two mature Smad2 isoforms existed in human placenta: full length, Smad2(FL), and that lacking exon3, Smad2(Δexon3). The protein level of Smad2(FL), but not Smad2(Δexon3) or Smad3, was significantly increased in severe PE (sPE) placenta, which was inversely correlated with the level of miR-18a. Elevated Smad2(FL) phosphorylation level appeared in sPE placenta, and Smad2 was colocalized with miR-18a in various subtypes of trophoblasts in human placenta. Smad2(FL) was validated as the direct target of miR-18a in HTR8/SVneo cells. miR-18a enhanced trophoblast cell invasion, which was blocked by the overexpression of Smad2(FL). Furthermore, overexpression of miR-18a repressed Smad2 activation and the inhibition of trophoblast cell invasion by transforming growth factor-β (TGF-β). In conclusion, our results suggest that miR-18a inhibits the expression of Smad2(FL), but not Smad2(Δexon3) or Smad3, which can reduce TGF-β signaling, leading to the enhancement of trophoblast cell invasion. A lack of miR-18a, which results in the upregulation of Smad2(FL), contributes to the development of PE.

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Section: Introductionmentioning

confidence: 99%

miR-18a Contributes to Preeclampsia by Downregulating Smad2 (Full Length) and Reducing TGF-β Signaling

Wang

et al. 2020

Molecular Therapy - Nucleic Acids

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“…These miRNAs have important roles in muscle differentiation, development and atrophy (33–35), and are predicted to participate in the regulatory networks of myogenesis, muscle fiber type composition, muscle growth and homeostasis (33). The miRNAs associated with muscle differentiation, development and muscular atrophy include miR-133a (36,37), miR-133b (38), miR-206 (39,40), miR-186 (41), miR-23a (42,43), miR-27b (44), miR-29b (32), miR-1a (39) and miR-18a (45,46). miR-1 promotes myoblast differentiation and regeneration (36,37,39,47).…”

Section: Introductionmentioning

confidence: 99%

Expression patterns of regulatory lncRNAs and miRNAs in muscular atrophy models induced by starvation in vitro and in vivo

et al. 2019

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Starvation or severe deprivation of nutrients, which is commonly seen in surgical patients, can result in catabolic changes in skeletal muscles, such as muscle atrophy. Therefore, it is important to elucidate the underlying molecular regulatory mechanisms during skeletal muscle atrophy. In the present study, muscular atrophy was induced by starvation and the results demonstrated that myosin heavy chain was decreased, whereas muscle RING finger protein 1 and atrogin-1 were increased, both in vitro and in vivo. The impact of starvation on the expression patterns of long non-coding RNAs (lncRNAs) and microRNAs (miRNAs) was next determined. The expression patterns of miR-23a, miR-206 and miR-27b in the starved mice exhibited similar trends as those in starved C2C12 cells in vitro, whereas the expression patterns of six other miRNAs (miR-18a, miR-133a, miR-133b, miR-186, miR-1a and miR-29b) differed between the in vivo and the in vitro starvation models. The present study indicated that in vitro expression of the selected miRNAs was not completely consistent with that in vivo. By contrast, lncRNAs showed excellent consistency in their expression patterns in both the in vitro and in vivo starvation models; six of the lncRNAs (Atrolnc-1, long intergenic non-protein coding RNA of muscle differentiation 1, Myolinc, lncRNA myogenic differentiation 1, Dum and muscle anabolic regulator 1) were significantly elevated in starved tissues and cells, while lnc-mg was significantly decreased, compared with the control groups. Thus, lncRNAs involved in muscle atrophy have the potential to be developed as diagnostic tools.

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“…Also, in the developing mouse neocortex, the miR-17-92 cluster, which includes miR-18a, has been shown to promote proliferation of neuronal progenitors [50]. Interestingly, however, miR-18a has also been shown to suppress cell proliferation in other contexts such in pancreatic progenitor cells [47] and myoblast cells [51], and even has anti-proliferation/anti-tumor effects in colorectal and breast cancers [52,48,53]. The effects of miR-18a on the cell proliferation are, therefore, dependent on the cell type and injury/disease state of the tissue involved.…”

Section: Discussionmentioning

confidence: 99%

“…Also, in the developing mouse neocortex, the miR-17-92 cluster, which includes miR-18a, has been shown to promote proliferation of neuronal progenitors [50]. Interestingly, however, miR-18a has also been shown to suppress cell proliferation in other contexts such in pancreatic progenitor cells [47] and myoblast cells [51], and even . CC-BY-NC-ND 4.0 International license available under a was not certified by peer review) is the author/funder, who has granted bioRxiv a license to display the preprint in perpetuity.…”

Section: Discussionmentioning

confidence: 99%

Disruption ofmiR-18aalters proliferation, photoreceptor replacement kinetics, inflammatory signaling and microglia/macrophage numbers during retinal regeneration in zebrafish

Magner

Sandoval-Sanchez

Hitchcock

et al. 2021

Preprint

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In mammals, photoreceptor loss causes permanent blindness, but in zebrafish (Danio rerio), Müller glia function as intrinsic stem cells, producing progenitor cells that regenerate photoreceptors and restore vision. MicroRNAs (miRNAs) critically regulate neurogenesis in the brain and retina, but the roles of miRNAs in injury-induced neuronal regeneration are largely unknown. The miRNA miR-18a regulates photoreceptor differentiation in the embryonic retina. The purpose of the current study was to determine the function of miR-18a during injury-induced photoreceptor regeneration. RT-qPCR, in-situ hybridization (ISH) and immunohistochemistry (IHC) showed that miR-18a expression increases throughout the retina by 1-day post-injury (dpi) and continues to increase through 5 dpi. Bromodeoxyuridine (BrdU) labeling showed that at 7 and 10 dpi, when regenerated photoreceptors are normally differentiating, there are more proliferating Müller glia-derived progenitors in homozygous miR-18a mutant (miR-18ami5012) retinas compared with wild type (WT), indicating that miR-18a negatively regulates injury-induced proliferation. At 7 and 10 dpi, miR-18ami5012 retinas have fewer mature photoreceptors than WT, but there is no difference at 14 dpi, revealing that photoreceptor regeneration is delayed. BrdU labeling showed that the excess progenitors in miR-18ami5012 retinas migrate to other retinal layers besides the photoreceptor layer. Inflammation is critical for photoreceptor regeneration and RT-qPCR showed that, in the absence of miR-18a, inflammation is prolonged. Suppressing inflammation with dexamethasone rescues the miR-18ami5012 phenotype. Together, these data show that during injury-induced photoreceptor regeneration, miR-18a regulates proliferation and photoreceptor regeneration by regulating key aspects of the inflammatory response during photoreceptor regeneration in zebrafish.

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MiR-18a regulates myoblasts proliferation by targeting Fgf1

Cited by 12 publications

References 35 publications

miR-18a Contributes to Preeclampsia by Downregulating Smad2 (Full Length) and Reducing TGF-β Signaling

miR-18a Contributes to Preeclampsia by Downregulating Smad2 (Full Length) and Reducing TGF-β Signaling

Expression patterns of regulatory lncRNAs and miRNAs in muscular atrophy models induced by starvation in vitro and in vivo

Disruption ofmiR-18aalters proliferation, photoreceptor replacement kinetics, inflammatory signaling and microglia/macrophage numbers during retinal regeneration in zebrafish

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