miR‐142‐3p Is a Regulator of the TGFβ‐Mediated Vascular Smooth Muscle Cell Phenotype

Kim, Kwang‐Ho; Yang, Dong Kwon; Kim, Sunghwan; Kang, Hyunjin

doi:10.1002/jcb.25183

Cited by 23 publications

(20 citation statements)

References 30 publications

(36 reference statements)

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Recent evidence indicates that the miRNA-142 locus is important for the regulation of macrophage-related processes, as e.g., macrophage and dendritic cell differentiation (Fordham et al, 2015), regulation of cell migration (Kim et al, 2015), control of profibrogenic macrophage program (Su et al, 2015), role in colony-stimulating factor 1-induced monocyte differentiation into macrophages (Lagrange et al, 2013), prevention of macrophage differentiation during cancer-induced myelopoiesis (Sonda et al, 2013). The relevance of these data for the liver of vaccinated mice remains to be shown.…”

Section: Discussionmentioning

confidence: 99%

Differential miRNA Expression in the Liver of Balb/c Mice Protected by Vaccination during Crisis of Plasmodium chabaudi Blood-Stage Malaria

et al. 2017

View full text Add to dashboard Cite

MicroRNAs are increasingly recognized as epigenetic regulators for outcome of diverse infectious diseases and vaccination efficacy, but little information referring to this exists for malaria. This study investigates possible effects of both protective vaccination and P. chabaudi malaria on the miRNome of the liver as an effector against blood-stage malaria using miRNA microarrays and quantitative PCR. Plasmodium chabaudi blood-stage malaria takes a lethal outcome in female Balb/c mice, but a self-healing course after immunization with a non-infectious blood-stage vaccine. The liver robustly expresses 71 miRNA species at varying levels, among which 65 miRNA species respond to malaria evidenced as steadily increasing or decreasing expressions reaching highest or lowest levels toward the end of the crisis phase on day 11 p.i. in lethal malaria. Protective vaccination does not affect constitutive miRNA expression, but leads to significant (p < 0.05) changes in the expression of 41 miRNA species, however evidenced only during crisis. In vaccination-induced self-healing infections, 18 miRNA-species are up- and 14 miRNA-species are down-regulated by more than 50% during crisis in relation to non-vaccinated mice. Vaccination-induced self-healing and survival of otherwise lethal infections of P. chabaudi activate epigenetic miRNA-regulated remodeling processes in the liver manifesting themselves during crisis. Especially, liver regeneration is accelerated as suggested by upregulation of let-7a-5p, let-7b-5p, let-7c-5p, let-7d-5p, let-7f-5p, let-7g-5p, let-7i-5p, miR-26a, miR-122-5p, miR30a, miR27a, and mir-29a, whereas the up-regulated expression of miR-142-3p by more than 100% is compatible with the view of enhanced hepatic erythropoiesis, possibly at expense of megakaryopoiesis, during crisis of P. chabaudi blood-stage malaria.

show abstract

Section: Discussionmentioning

confidence: 99%

Differential miRNA Expression in the Liver of Balb/c Mice Protected by Vaccination during Crisis of Plasmodium chabaudi Blood-Stage Malaria

et al. 2017

View full text Add to dashboard Cite

show abstract

“…In contrast, miR-132 and miR-125b could block VSMC proliferation and neointimal hyperplasia in atherosclerosis [116, 117]. Other miRNAs that inhibit VSMCs proliferation and migration include miR-142-3p [118], miR-145 [119], miR-599 [120], miR-25 [121], miR-23b [122], miR-15b/16 [123], and miR-29b [124]. …”

Section: Mirnas and Vascular Agingmentioning

confidence: 99%

Function, Role, and Clinical Application of MicroRNAs in Vascular Aging

Lin

Zhan

Wang

et al. 2016

BioMed Research International

View full text Add to dashboard Cite

Vascular aging, a specific type of organic aging, is related to age-dependent changes in the vasculature, including atherosclerotic plaques, arterial stiffness, fibrosis, and increased intimal thickening. Vascular aging could influence the threshold, process, and severity of various cardiovascular diseases, thus making it one of the most important risk factors in the high mortality of cardiovascular diseases. As endothelial cells (ECs) and vascular smooth muscle cells (VSMCs) are the main cell biological basis of these pathology changes of the vasculature, the structure and function of ECs and VSMCs play a key role in vascular aging. MicroRNAs (miRNAs), small noncoding RNAs, have been shown to regulate the expression of multiple messenger RNAs (mRNAs) posttranscriptionally, contributing to many crucial aspects of cell biology. Recently, miRNAs with functions associated with aging or aging-related diseases have been studied. In this review, we will summarize the reported role of miRNAs in the process of vascular aging with special emphasis on EC and VSMC functions. In addition, the potential application of miRNAs to clinical practice for the diagnosis and treatment of cardiovascular diseases will also be discussed.

show abstract

“…For example, during region-dependent-chondrogenesis, miR-142-3p was involved in the limb type-specific effect of TGF-β3 on mesenchymal cells by modulating transcription of a disintegrin and metalloprotease (ADAM) [26]. In vascular smooth muscle cells (VSMCs), TGF-β could induce the expression of miR-142-3p, which inhibited cell migration and determined contractile phenotype of VSMCs by targeting at dedicator of cytokinesis 6 (DCK6) [27]. On the other hand, miR-142-3p was revealed to directly bind to 3’-UTR of TβRII and suppress expression of TβRII mRNA and protein, leading to repression of TGF-β-induced growth inhibition in non-small cell lung cancer (NSCLC) [28].…”

Section: Introductionmentioning

confidence: 99%

MiR-142-3p Inhibits TGF-β3-Induced Blood-Testis Barrier Impairment by Targeting Lethal Giant Larvae Homolog 2

Xu¹,

Wu²,

Fan³

et al. 2018

Cell Physiol Biochem

View full text Add to dashboard Cite

Background/Aims: Transforming growth factor-β3 (TGF-β3) has been proved to perturb the blood-testis barrier (BTB) by accelerating junction protein endocytosis in Sertoli cells (SCs) to accommodate the traversing of preleptotene spermatocytes across the BTB around stage VIII in rat. Yet the molecular network underlying the impairment of TGF-β3 on BTB integrity is not fully elucidated. Our study herein was designed to investigate the participation of microRNA-142-3p (miR-142-3p), which has been reported to affect TGF-β3 signaling via different pathways, during BTB dynamics and the corresponding mechanisms. Methods: MiRNA mimic or agomiRNA was co-administered with or without TGF-β3 in the cultured SCs or in the rat testis. The SC permeability barrier function was reflected by measuring the transepithelial resistance (TER) and the permeability of the sodium fluorescein (Na-F). The BTB integrity was detected by the permeation of biotin. A luciferase reporter assay was used to testify the potential target of miR-142-3p, lethal giant larvae 2 (Lgl2). Laser capture microdissection (LCM) was applied to acquire cell components of different stages of seminiferious tubules, followed by detection of the expression levels of miR-142-3p, TGF-β3, and Lgl2 by qPCR. The SC barrier function was also detected as above in the presence of TGF-β3 after Lgl2 knockdown. Results: We revealed a reversion of TGF-β3-induced BTB impairment after miR-142-3p treatment both in vitro and in vivo. Meanwhile, the activation of Cdc42 and reduction in occludin aroused by TGF-β3 were also reversed by miR-142-3p. The predicted binding of miR-142-3p with 3’-untranslated region (3’-UTR) of Lgl2, was verified by the luciferase assay. Moreover, an increased Lgl2 level in TGF-β3-treated SCs was found and correlated stage-specific expressions of TGF-β3, miR-142-3p, and Lgl2 were revealed. Knockdown of Lgl2 in SCs was shown to partially antagonize the BTB disruption mediated by TGF-β3. Conclusions: Collectively, our results suggest a resistance of miR-142-3p on the BTB impairment caused by TGF-β3 during the seminiferous epithelial cycle by targeting Lgl2.

show abstract

miR‐142‐3p Is a Regulator of the TGFβ‐Mediated Vascular Smooth Muscle Cell Phenotype

Cited by 23 publications

References 30 publications

Differential miRNA Expression in the Liver of Balb/c Mice Protected by Vaccination during Crisis of Plasmodium chabaudi Blood-Stage Malaria

Differential miRNA Expression in the Liver of Balb/c Mice Protected by Vaccination during Crisis of Plasmodium chabaudi Blood-Stage Malaria

Function, Role, and Clinical Application of MicroRNAs in Vascular Aging

MiR-142-3p Inhibits TGF-β3-Induced Blood-Testis Barrier Impairment by Targeting Lethal Giant Larvae Homolog 2

Contact Info

Product

Resources

About