MiR-23b controls TGF-β1 induced airway smooth muscle cell proliferation via direct targeting of Smad3

Chen, Ming; Shi, Jianting; Zhang, Wei; Huang, Lixiang; Lin, Xiaoling; Lv, Zhiqiang; Liang, Ruiyun; Jiang, Shanping

doi:10.1016/j.pupt.2017.01.001

Cited by 31 publications

(14 citation statements)

References 28 publications

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“…Recently, multiple lines of evidence suggest that miRNAs play pivotal roles in the control of ASM phenotypes that are critically involved in asthma pathogenesis (Deshpande, Dileepan, Walseth, Subramanian, & Kannan, ). Thus far, several miRNAs, including miR‐10a, miR‐23b, miR‐143‐3p, miR‐21, and miR‐203, have been implicated in the regulation of ASM cell proliferation and/or migration (M. Chen et al, ; Cheng et al, ; Hu et al, ; Y. Liu et al, ). Further identification of novel miRNAs involved in the regulation of ASMC proliferation and migration will help us develop novel therapeutic strategies for the treatment of asthma.…”

Section: Introductionmentioning

confidence: 99%

MicroRNA‐638 inhibits human airway smooth muscle cell proliferation and migration through targeting cyclin D1 and NOR1

Wang

Yao

et al. 2018

Journal Cellular Physiology

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Abnormal airway smooth muscle cell (ASMC) proliferation and migration contribute significantly to increased ASM mass associated with asthma. MicroRNA (miR)-638 is a primate-specific miRNA that plays important roles in development, DNA damage repair, hematopoiesis, and tumorigenesis. Although it is highly expressed in ASMCs, its function in ASM remodeling remains unknown. In the current study, we found that in response to various mitogenic stimuli, including platelet-derived growth factor-two B chains (PDGF-BB), transforming growth factor β1, and fetal bovine serum, the expression of miR-638, as determined by quantitative real-time polymerase chain reaction (qRT-PCR), was significantly downregulated in the proliferative human ASMCs. Both gain- and loss-of-function studies were performed to study the role of miR-638 in ASMC proliferation and migration. We found that adenovirus-mediated miR-638 overexpression markedly inhibits ASMC proliferation and migration, while ablation of miR-638 by anti-miR-638 markedly increases cell proliferation and migration, as determined by WST-8 proliferation and scratch wound assays. Dual-luciferase reporter assay, qRT-PCR, and immunoblot analysis were used to investigate the effects of miR-638 on the expression of the downstream target genes in ASMCs. Our results demonstrated that miR-638 overexpression significantly reduced the expression of downstream target cyclin D1 and NOR1, both of which have been shown to be essential for cell proliferation and migration. Together, our study provides the first in vitro evidence highlighting the antiproliferative and antimigratory roles of miR-638 in human ASMC remodeling and suggests that targeted overexpression of miR-638 in ASMCs may provide a novel therapeutic strategy for preventing ASM hyperplasia associated with asthma.

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Section: Introductionmentioning

confidence: 99%

MicroRNA‐638 inhibits human airway smooth muscle cell proliferation and migration through targeting cyclin D1 and NOR1

Wang

Yao

et al. 2018

Journal Cellular Physiology

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“…In the case of ISR, we here show that miRNA-23b could be used as a noninvasive biomarker to identify patients with ISR. This miRNA is highly expressed in cell cultures of VSMC, decreasing their proliferation, differentiation, and migration [ 13 ]. In addition, in vitro studies show that miRNA-23b regulates the expression of the Forkhead Box protein (Fox04) [ 24 ], which represses differentiation of smooth muscle cells and activates the migration of VSMC in response to TNF- α and urokinase-type plasminogen activator (uPA) [ 15 , 19 ] through the MEK/ERK signaling pathway [ 25 ] and SMAD3 [ 19 ], a protein important for the proliferation of VSMC [ 26 ].…”

Section: Discussionmentioning

confidence: 99%

“…On the other hand, miRNA-23b plays a critical role in angiogenesis, cardiac ischemia, and homeostasis of endothelial cells [ 12 ]. Moreover, the overexpression of miRNA-23b in balloon-injured arteries by Ad-miRNA-23b markedly decreased neointimal hyperplasia in VSMC, in vitro [ 13 ]. Yet, another relevant and highly attractive feature of miRNAs corresponds to their remarkable extracellular stability, an outcome that has received especial attention due to a promising role as blood-based biomarkers for diagnosis and prognosis of several illnesses [ 14 ].…”

Section: Introductionmentioning

confidence: 99%

Circulating miRNA-23b and miRNA-143 Are Potential Biomarkers for In-Stent Restenosis

Saavedra

Rojas

Herrera

et al. 2020

BioMed Research International

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In-stent restenosis (ISR) is one of the main complications in patients undergoing percutaneous coronary angioplasty, and microRNAs participate in the contractile-to-synthetic phenotypic switch of vascular smooth muscle cells, a hallmark of restenosis development. MicroRNAs (miRNAs) can be released into circulation from injured tissues, enticing a potential role as noninvasive biomarkers. We aimed to evaluate circulating levels of miRNA-23b, miRNA-143, and miRNA-145 as diagnostic markers of ISR. 142 patients with coronary artery disease undergoing successful angioplasty and a follow-up angiography were included. Subjects were classified according to the degree of obstruction at the angioplasty site into cases (≥50%) or controls (<50%). Total RNA was isolated from plasma to quantify circulating miRNAs levels, and the ROC curves were constructed. Among circulating miRNAs assessed, miRNA-23b and miRNA-143 were significantly lower in cases (miRNA-23b: 18.4x10−5 and miRNA-143: 13.7x10−5) than controls (miRNA-23b: 5.2x10−5, p<0.0001; miRNA-143: 4.0x10−5, p<0.0001). Plasma levels of miRNA-145 showed no significant differences. The analysis of the ROC curves showed an area under the curve for miRNA-23b of 0.71 (95% CI: 0.62-0.80, p<0.0001) and 0.69 for miRNA-143 (95% CI: 0.60-0.78; p<0.0001). Our data suggest that plasma levels of miRNA-23b and miRNA-143 could be useful as noninvasive biomarkers of ISR.

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“…Its possible mechanism was regulating the transcription of nuclear factor, and suppressing the transcription of TGF-b downstream Smad2 and Smad3. These genes regulated many cell signals related to proliferation and differentiation; for example, Smad3 promoted apoptosis by promoting the process of P21 and P15 inhibiting cell proliferation [18][19][20]. Therefore, c-Ski may participate in cell proliferation through the abovementioned pathways, affecting cell viability.…”

Section: Discussionmentioning

confidence: 99%

Silencing of c-Ski augments TGF-b1-induced epithelial-mesenchymal transition in cardiomyocyte H9C2 cells

et al. 2019

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Background: The shRNA lentiviral vector was constructed to silence c-Ski expression in cardiac muscle cells, with the aim of exploring the role of c-Ski in transforming growth factor b1 (TGF-b1)-induced epithelial-mesenchymal transitions (EMT) in H9C2 cells. Methods: Real-time polymerase chain reaction (RT-PCR) and western blot were used to detect c- development and progression. (Cardiol J 2019; 26, 1: 66-76)

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MiR-23b controls TGF-β1 induced airway smooth muscle cell proliferation via direct targeting of Smad3

Cited by 31 publications

References 28 publications

MicroRNA‐638 inhibits human airway smooth muscle cell proliferation and migration through targeting cyclin D1 and NOR1

MicroRNA‐638 inhibits human airway smooth muscle cell proliferation and migration through targeting cyclin D1 and NOR1

Circulating miRNA-23b and miRNA-143 Are Potential Biomarkers for In-Stent Restenosis

Silencing of c-Ski augments TGF-b1-induced epithelial-mesenchymal transition in cardiomyocyte H9C2 cells

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