MicroRNA-30b-5p promotes the proliferation and migration of human airway smooth muscle cells induced by platelet-derived growth factor by targeting phosphatase and tensin homolog deleted on chromosome ten

Wang, Wentao; Guo, Jun; Wang, Yan

doi:10.1080/21655979.2021.1950401

Cited by 8 publications

(5 citation statements)

References 35 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Phosphatase and tensin homolog deleted on chromosome ten (PTEN) is a popular oncogene that has been studied in recent years and has a close relationship with tumorigenesis. Recent studies have found that it also plays an important regulatory role in the osteogenic differentiation of MSCs [ 17 , 18 ]. This study focuses on the role of miR-144-3p in MSC proliferation, apoptosis, and osteogenic differentiation under tension and its possible mechanisms.…”

Section: Prefacementioning

confidence: 99%

Effect of miR-144-3p-Targeted Regulation of PTEN on Proliferation, Apoptosis, and Osteogenic Differentiation of Bone Marrow Mesenchymal Stem Cells under Stretch

Ling¹,

Luo

Lv³

et al. 2022

Emergency Medicine International

View full text Add to dashboard Cite

Objective. To investigate the effects of miR-144-3p-targeted regulation of phosphatase and tensin homolog deleted on chromosome ten (PTEN) gene on proliferation, apoptosis, and osteogenic differentiation of bone marrow mesenchymal stem cells (BMSCs) under retraction force. Methods. The BMSCs of rats were randomly divided into the tension MSC group with detrusor stimulation and the MSC group without detrusor stimulation, after which osteogenic differentiation of BMSCs was induced in both groups. Alkaline phosphatase (ALP) staining and alizarin red staining were used to detect the osteogenic differentiation ability of the two groups of cells. Real-time quantitative reverse transcription PCR (qRT-PCR) was used to detect the expression of miR-144-3p and PTEN in the two groups of cells after osteogenic differentiation. Bioinformatics website and dual luciferase reporter were used to detect the relationship between miR-144-3p and PTEN. The tension MSC group was used as a control group, and miR-144-3p mimics (miR-144-3p mimic group), mimic controls (mimic-NC group), PTEN interferers (si-PTEN group), and interference controls (si-NC group) were transfected into BMSCs. The BMSCs were then continuously stimulated for 24 h using a Flexercell in vitro cellular mechanics loading device, applying a draft force at a frequency of 1 Hz and a deformation rate of 18%. The cell proliferation was detected by Cell Counting Kit-8 (CCK-8) colorimetric assay; the expression levels of cyclin, cyclin-dependent kinases (CDK), BCL2-associated X (BAX), B-cell lymphoma-2 (BCL-2), and other cell cycle and apoptosis related proteins were detected by western blot (WB); and the osteogenic differentiation ability of MSC cells was detected by ALP staining and alizarin red staining. Results. Compared with the MSC group, the level of miR-144-3p was significantly lower and the level of PTEN was significantly higher in the tension MSC group. ALP staining showed normal activity in the MSC group and decreased ALP activity in the tension MSC group compared to the MSC group. Alizarin red staining in the MSC group showed scattered calcium nodule formation, and alizarin red staining showed red nodules with a more uniform color distribution. Compared to the MSC group, the tension MSC group showed fewer, smaller, and lighter staining mineralized nodules. Compared with the tension group and mimic-NC group (si-NC group), the proliferation rate of cells in the miR-144-3p mimic group (si-PTEN group) was significantly higher; the expression levels of PTEN and BAX were significantly lower; and the expression levels of cyclin, CDK, and BCL-2 protein were significantly higher. ALP staining results revealed that the miR-144-3p mimic group (si-PTEN group) showed significantly higher osteogenic differentiation ability and ALP activity of MSC than the tension group and mimic-NC group (si-NC group). Conclusion. miR-144-3p may inhibit apoptosis and promote proliferation and osteogenic differentiation of BMSCs under tension by targeting and regulating PTEN.

show abstract

Section: Prefacementioning

confidence: 99%

Effect of miR-144-3p-Targeted Regulation of PTEN on Proliferation, Apoptosis, and Osteogenic Differentiation of Bone Marrow Mesenchymal Stem Cells under Stretch

Ling¹,

Luo

Lv³

et al. 2022

Emergency Medicine International

View full text Add to dashboard Cite

show abstract

“… 35 , 49 Thus, in this study, PDGF‐BB‐induced HASMCs mimic airway remodeling in asthma, and the significant enhancement of HASMC proliferation and migration indicated the success of the model. 36 , 50 In this study, we found that lncRNA ANRIL was upregulated and miR‐7‐5p was downregulated in the serumof patients with asthma and PDGF‐BB‐induced HASMCs. In HASMCs, lncRNA ANRIL negatively regulates miR‐7‐5p.…”

Section: Discussionmentioning

confidence: 57%

“…Among them, PDGF‐BB is widely used to induce ASMC proliferation and migration and aggravate airway remodeling 35,49 . Thus, in this study, PDGF‐BB‐induced HASMCs mimic airway remodeling in asthma, and the significant enhancement of HASMC proliferation and migration indicated the success of the model 36,50 . In this study, we found that lncRNA ANRIL was upregulated and miR‐7‐5p was downregulated in the serumof patients with asthma and PDGF‐BB‐induced HASMCs.…”

Section: Discussionmentioning

confidence: 63%

Long noncoding RNA antisense noncoding RNA in the INK4 locus inhibition alleviates airway remodeling in asthma through the regulation of the microRNA‐7‐5p/early growth response factor 3 axis

Wang

Liu

2023

Immunity Inflam & Disease

View full text Add to dashboard Cite

Asthma, a chronic inflammatory disease of the airways, clinically manifests as airway remodeling. The purpose of this study was to probe the potential role of long noncoding RNA (lncRNA) antisense noncoding RNA in the INK4 locus (lncRNA ANRIL) in the proliferation and migration of airway smooth muscle cell (ASMC) and to explore its potential mechanisms in asthma. Serum samples were obtained from 30 healthy volunteers and 30 patients with asthma. Additionally, platelet‐derived growth factor‐BB (PDGF‐BB) was used to induce airway remodeling in ASMCs. The level of lncRNA ANRIL and microRNA (miR)‐7‐5p in serum samples were measured by quantitative reverse transcriptase polymerase chain reaction (qRT‐PCR). TargetScan predicted the binding site of miR‐7‐5p to early growth response factor 3 (EGR3) and validated the results using a dual‐luciferase reporter assay. 3‐(4,5‐dimethylthiazol‐2‐yl)‐2,5‐diphenyl‐2H‐tetrazolium bromide (MTT) and Transwell assays were used to detect cellular proliferation and migration, respectively. Subsequently, changes in proliferation‐ and migration‐related genes were verified using western blot analysis and qRT‐PCR. These results indicate that lncRNA ANRIL was upregulated in the serum and PDGF‐BB‐induced ASMCs of patients with asthma, whereas miR‐7‐5p expression was reduced. EGR3 was a direct target of miR‐7‐5p. LncRNA ANRIL silencing inhibited the proliferation or migration of ASMCs induced by PDGF‐BB through miR‐7‐5p upregulation. Mechanistic studies indicated that miR‐7‐5p inhibits the proliferation or migration of PDGF‐BB‐induced ASMCs by decreasing EGR3 expression. EGR3 upregulation reverses the role of miR‐7‐5p in airway remodeling. Thus, downregulation of lncRNA ANRIL inhibits airway remodeling through inhibiting the proliferation and migration of PDGF‐BB‐induced ASMCs by regulating miR‐7‐5p/EGR3 signaling.

show abstract

“…As an inhibitor, miR-590–5p suppressed platelet-derived growth factor (PDGF)-mediated ASMC proliferation via the negative regulation of signal transducer and activator of transcription (STAT) 3 signalling [ 18 ]. In contrast, miR-30b-5p increased in PDGF-stimulated ASMCs and the overexpression of miR-30b-5p facilitated the proliferation and migration of ASMCs by directly targeting phosphatase and tensin homologue (PTEN) and activating the PI3K/Akt pathway [ 19 ]. C hen et al [ 20 ] found an increase in miR-620 in TGF-β1-stimulated ASMCs.…”

Section: Mirnas In Asthmatic Asmcsmentioning

confidence: 99%

Noncoding RNAs in asthmatic airway smooth muscle cells

Xiao

Dong

et al. 2023

Eur Respir Rev

View full text Add to dashboard Cite

Asthma is a complex and heterogeneous airway disease caused by genetic, environmental and epigenetic factors treated with hormones and biologics. Irreversible pathological changes to airway smooth muscle cells (ASMCs) such as hyperplasia and hypertrophy can occur in asthmatic patients. Determining the mechanisms responsible is vital for preventing such changes. In recent years, noncoding RNAs (ncRNAs), especially microRNAs, long noncoding RNAs and circular RNAs, have been found to be associated with abnormalities of the ASMCs. This review highlights recent ncRNA research into ASMC pathologies. We present a schematic that illustrates the role of ncRNAs in pathophysiological changes to ASMCs that may be useful in future research in diagnostic and treatment strategies for patients with asthma.

show abstract

MicroRNA-30b-5p promotes the proliferation and migration of human airway smooth muscle cells induced by platelet-derived growth factor by targeting phosphatase and tensin homolog deleted on chromosome ten

Cited by 8 publications

References 35 publications

Effect of miR-144-3p-Targeted Regulation of PTEN on Proliferation, Apoptosis, and Osteogenic Differentiation of Bone Marrow Mesenchymal Stem Cells under Stretch

Effect of miR-144-3p-Targeted Regulation of PTEN on Proliferation, Apoptosis, and Osteogenic Differentiation of Bone Marrow Mesenchymal Stem Cells under Stretch

Long noncoding RNA antisense noncoding RNA in the INK4 locus inhibition alleviates airway remodeling in asthma through the regulation of the microRNA‐7‐5p/early growth response factor 3 axis

Noncoding RNAs in asthmatic airway smooth muscle cells

Contact Info

Product

Resources

About