MiR-204-5p Inhibits Transforming Growth Factor-β1-Induced Proliferation and Extracellular Matrix Production of Airway Smooth Muscle Cells by Regulating Six1 in Asthma

Yang, Zhaochuan; Qu, Zhenghai; Man, Yi; Lv, Zhi‐Dong; Wang, Yanxia; Shan, Yanchun; Ni, Ran; Liu, Xinjie

doi:10.1159/000505064

Cited by 25 publications

(18 citation statements)

References 27 publications

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“…In ASM cells from asthmatic patients, a number of miRNAs are downregulated compared to control subjects, leading to elevated ECM expression. The expression of miR-19 is decreased in ASM cells from asthmatic patients and induces elevated expression of collagen I, fibronectin and arginine methyltransferase activity through the ERK1/MAPK signalling pathway [ 100 ]. miR-204-5p has also been shown to be down-regulated in ASM cells from asthmatic patients and promotes the expressions of fibronectin and collagen III via the Six1 gene (a TGF-β1 inducible gene) [ 101 ].…”

Section: The Ecm In Lung Remodeling and Diseasementioning

confidence: 99%

The Role of miRNAs in Extracellular Matrix Repair and Chronic Fibrotic Lung Diseases

Usman

Hackett

2021

Cells

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The lung extracellular matrix (ECM) plays a key role in the normal architecture of the lung, from embryonic lung development to mechanical stability and elastic recoil of the breathing adult lung. The lung ECM can modulate the biophysical environment of cells through ECM stiffness, porosity, topography and insolubility. In a reciprocal interaction, lung ECM dynamics result from the synthesis, degradation and organization of ECM components by the surrounding structural and immune cells. Repeated lung injury and repair can trigger a vicious cycle of aberrant ECM protein deposition, accompanied by elevated ECM stiffness, which has a lasting effect on cell and tissue function. The processes governing the resolution of injury repair are regulated by several pathways; however, in chronic lung diseases such as asthma, chronic obstructive pulmonary disease (COPD) and idiopathic pulmonary disease (IPF) these processes are compromised, resulting in impaired cell function and ECM remodeling. Current estimates show that more than 60% of the human coding transcripts are regulated by miRNAs. miRNAs are small non-coding RNAs that regulate gene expressions and modulate cellular functions. This review is focused on the current knowledge of miRNAs in regulating ECM synthesis, degradation and topography by cells and their dysregulation in asthma, COPD and IPF.

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Section: The Ecm In Lung Remodeling and Diseasementioning

confidence: 99%

The Role of miRNAs in Extracellular Matrix Repair and Chronic Fibrotic Lung Diseases

Usman

Hackett

2021

Cells

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“…The stimulation of ASM cells with TGF‐β1 induces hyperproliferation and ECM production, which contribute to airway remodeling 33,34 . TGF‐β1‐stimulated ASM cells have been widely used as an in vitro model with which to study airway remodeling 35–37 . In this study, we found that AMOTL2 expression was decreased in ASM cells in response to TGF‐β1 stimulation.…”

Section: Discussionmentioning

confidence: 75%

AMOTL2 restrains transforming growth factor‐β1‐induced proliferation and extracellular matrix deposition of airway smooth muscle cells via the down‐regulation of YAP1 activation

Fang

Deng

Fan

et al. 2021

Environmental Toxicology

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Angiomotin‐like 2 (AMOTL2) is a key modulator of signaling transduction and participates in the regulation of various cellular progresses under diverse physiological and pathological conditions. However, whether AMOTL2 participates in asthma pathogenesis has not been fully studied. In the present work, we studied the possible role and mechanism of AMOTL2 in regulating transforming growth factor‐β1 (TGF‐β1)‐induced proliferation and extracellular matrix (ECM) deposition of airway smooth muscle (ASM) cells. Our results showed marked reductions in the abundance of AMOTL2 in TGF‐β1‐stimulated ASM cells. Cellular functional investigations confirmed that the up‐regulation of AMOTL2 dramatically decreased the proliferation and ECM deposition induced by TGF‐β1 in ASM cells. In contrast, the depletion of AMOTL2 exacerbated TGF‐β1‐induced ASM cell proliferation and ECM deposition. Further research revealed that the overexpression of AMOTL2 restrained the activation of Yes‐associated protein 1 (YAP1) in TGF‐β1‐stimulated ASM cells. Moreover, the reactivation of YAP1 markedly reversed AMOTL2‐mediated suppression of TGF‐β1‐induced ASM cell proliferation and ECM deposition. Together, these findings suggest that AMOTL2 restrains TGF‐β1‐induced proliferation and ECM deposition of ASM cells by down‐regulating YAP1 activation.

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“…Three miRNAs are interesting-miR-1, miR-155 and miR-204. These miRNAs are connected with proliferation, apoptosis, and cardiac injury [25] as well as transforming growth factor-β1 (TGF-β1) and glial cell line-derived neurotrophic factor (GDNF) regulation during glaucoma, asthma and obesity [26][27][28][29]. However, what is even more interesting is that it has been also shown that these miRNAs regulate brain-derived neurotrophic factor (BDNF) [30][31][32].…”

Section: Discussionmentioning

confidence: 99%

Serum Level of miR-1 and miR-155 as Potential Biomarkers of Stress-Resilience of NET-KO and SWR/J Mice

Solich

Kuśmider

Faron-Górecka

et al. 2020

Cells

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In the present study, we used three strains of mice with various susceptibility to stress: mice with knock-out of the gene encoding norepinephrine transporter (NET-KO), which are well characterized as displaying a stress-resistant phenotype, as well as two strains of mice displaying two different stress-coping strategies, i.e., C57BL/6J (WT in the present study) and SWR/J. The procedure of restraint stress (RS, 4 h) was applied, and the following behavioral experiments (the forced swim test and sucrose preference test) indicated that NET-KO and SWR/J mice were less sensitive to RS than WT mice. Then, we aimed to find the miRNAs which changed in similar ways in the serum of NET-KO and SWR/J mice subjected to RS, being at the same time different from the miRNAs found in the serum of WT mice. Using Custom TaqMan Array MicroRNA Cards, with primers for majority of miRNAs expressed in the serum (based on a preliminary experiment using the TaqMan Array Rodent MicroRNA A + B Cards Set v3.0, Thermo Fisher Scientific, Waltham, MA, USA) allowed the identification of 21 such miRNAs. Our further analysis focused on miR-1 and miR-155 and their targets-these two miRNAs are involved in the regulation of BDNF expression and can be regarded as biomarkers of stress-resilience.Cells 2020, 9, 917 2 of 17 are regarded as endogenous "hubs" (as Issler and Chen have put it) for the fine tuning of target gene expression or an "expression switch", and can provide deeper insight into complex biological processes underlying stress response.In the present study, we used three strains of mice differentially reacting to stress: mice with knock-out of the gene encoding norepinephrine transporter (NET-KO), which are well characterized as displaying a stress-resistant phenotype [7-9], as well as two other strains of mice displaying different stress-coping strategies, i.e., C57BL/6J (WT in the present study) and swiss SWR/J, described extensively by Szklarczyk and co-workers [10]. The different reaction to stress of these strains of mice has been confirmed by measuring corticosterone level. The NET-KO mice display a slower increase in corticosterone level after stress compared with WT animals, while corticosterone level was not changed at 2 h after restraint stress in the blood of SWR/J mice [8,10]. We applied the procedure of restraint stress (RS), which has been shown to induce an uncontrollable aversive situation that produces both physical and psychological consequences leading to neuronal and behavioral alterations [11]. The aim of following molecular studies was to find biomarkers for different behavioral responses to RS among miRNAs expressed in the serum of three genotypes under study. This goal was achieved, as we were able to identify a group of miRNAs differentiating the stress response of NET-KO and SWR/J mice from WT animals. The most interesting were the alterations in the miR-1 and miR-155 levels, which are involved in regulation of BDNF expression, which in turn affects important biochemical processes. Materials and Methods AnimalsH...

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MiR-204-5p Inhibits Transforming Growth Factor-β1-Induced Proliferation and Extracellular Matrix Production of Airway Smooth Muscle Cells by Regulating Six1 in Asthma

Cited by 25 publications

References 27 publications

The Role of miRNAs in Extracellular Matrix Repair and Chronic Fibrotic Lung Diseases

The Role of miRNAs in Extracellular Matrix Repair and Chronic Fibrotic Lung Diseases

AMOTL2 restrains transforming growth factor‐β1‐induced proliferation and extracellular matrix deposition of airway smooth muscle cells via the down‐regulation of YAP1 activation

Serum Level of miR-1 and miR-155 as Potential Biomarkers of Stress-Resilience of NET-KO and SWR/J Mice

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