MiR-23b controls TGF-β1 induced airway smooth muscle cell proliferation via TGFβR2/p-Smad3 signals

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

doi:10.1016/j.molimm.2015.12.012

Cited by 26 publications

(15 citation statements)

References 22 publications

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“…In addition, the dual-luciferase reporter gene assay in our study also confirmed Smurf2 as the target gene of miR-485. Similarly, miR-23b was found to suppress ASMC proliferation through inhibiting the GFβR2/p-Smad3 pathway [48]. Thus, overexpressed miR-485 suppresses cell proliferation and promotes cell apoptosis of ASMCs in mice with chronic asthma.…”

Section: Discussionmentioning

confidence: 91%

MicroRNA-485 Modulates the TGF-β/ Smads Signaling Pathway in Chronic Asthmatic Mice by Targeting Smurf2

Wang

et al. 2018

Cell Physiol Biochem

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Background/Aims: Chronic respiratory conditions continue to plague millions of people worldwide. We aimed to elucidate the detailed mechanisms of microRNA-485 (miR-485) in airway smooth muscle cell (ASMC) proliferation and apoptosis in chronic asthmatic mice. Methods: A mouse model of chronic asthma was established. Ovalbumin was used to induce chronic asthma in the mice. The levels of transforming growth factor β (TGF-β), interleukin (IL)-4, IL-5, IL-13 and IL-17 in bronchoalveolar lavage fluid in mice were measured by enzyme-linked immunoassays (ELISAs). ASMCs were transfected with miR-485 mimic, miR-485 inhibitor and siRNA-Smurf2. The reverse transcription quantitative polymerase chain reaction (RT-qPCR) and western blot analyses were applied to detect the mRNA and protein levels of Smurf2, α-SMA, TGF-β1 and decapentaplegic homolog (Smads). The MTT assay was utilized for cell proliferation, while flow cytometry was conducted to assess cell cycle distribution and apoptosis. Results: Lower expression of miR-485 and higher expression levels of TGF-β1, IL-4, IL-5, IL-13 and IL-17 were detected in mice with chronic asthma. Smurf2 was identified as the target gene of miR-485. Upregulation of miR-485 mimic and downregulation of Smurf2 decreased expression levels of Smurf2, α-SMA, TGF-β1 and Smad3, inhibited cell proliferation and increased apoptosis, while contrary results were observed in ASMCs transfected with miR-485 inhibitor. Conclusion: Overexpressed miR-485 inhibits cell proliferation and promotes apoptosis of ASMCs through the Smurf2-mediated TGF-β/Smads signaling pathway in mice with chronic asthma.

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Section: Discussionmentioning

confidence: 91%

MicroRNA-485 Modulates the TGF-β/ Smads Signaling Pathway in Chronic Asthmatic Mice by Targeting Smurf2

Wang

et al. 2018

Cell Physiol Biochem

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“…Finally, we found that miR-23b-3p was downregulated in females exposed to O 3 in non-proestrus stages (i.e., when estrogen levels are low) but not in females exposed in proestrus. To this end, studies have shown that miR-23b inhibits TGF-β1-induced airway smooth muscle proliferation and promotes apoptosis, indicating a potential role of this miRNA in lung functions and diseases that are affected by the menstrual cycle [ 74 – 77 ].…”

Section: Discussionmentioning

confidence: 99%

Sex-specific microRNA expression networks in an acute mouse model of ozone-induced lung inflammation

et al. 2018

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BackgroundSex differences in the incidence and prognosis of respiratory diseases have been reported. Studies have shown that women are at increased risk of adverse health outcomes from air pollution than men, but sex-specific immune gene expression patterns and regulatory networks have not been well studied in the lung. MicroRNAs (miRNAs) are environmentally sensitive posttranscriptional regulators of gene expression that may mediate the damaging effects of inhaled pollutants in the lung, by altering the expression of innate immunity molecules.MethodsMale and female mice of the C57BL/6 background were exposed to 2 ppm of ozone or filtered air (control) for 3 h. Female mice were also exposed at different stages of the estrous cycle. Following exposure, lungs were harvested and total RNA was extracted. We used PCR arrays to study sex differences in the expression of 84 miRNAs predicted to target inflammatory and immune genes.ResultsWe identified differentially expressed miRNA signatures in the lungs of male vs. female exposed to ozone. In silico pathway analyses identified sex-specific biological networks affected by exposure to ozone that ranged from direct predicted gene targeting to complex interactions with multiple intermediates. We also identified differences in miRNA expression and predicted regulatory networks in females exposed to ozone at different estrous cycle stages.ConclusionOur results indicate that both sex and hormonal status can influence lung miRNA expression in response to ozone exposure, indicating that sex-specific miRNA regulation of inflammatory gene expression could mediate differential pollution-induced health outcomes in men and women.Electronic supplementary materialThe online version of this article (10.1186/s13293-018-0177-7) contains supplementary material, which is available to authorized users.

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“…Under the induction of mechanical elongation, miR-26a causes ASM hypertrophy by attenuating GSK3β [96]. However, ASM proliferation appears to be driven by multiple miRNAs, including miR-10a [97], miR-23b [98], miR-138 [99], miR-145 [100], and miR-203 [101]. In general, we have found many miRNA pathways in ASM, but many problems remain unresolved, and miRNAs will be a focus for targeted asthma therapy in the future.…”

Section: Asm Mirna and Asthmamentioning

confidence: 99%

Role of Airway Smooth Muscle Cells in Asthma Pathology

Tang¹

2019

Asthma - Biological Evidences

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Airway smooth muscle (ASM) cells have been shown to play an important role in bronchial asthma. As the research progresses, the mechanism becomes more and more complex. This chapter reviews the role of ASM in asthma pathological mechanisms including inflammatory reaction, extracellular matrix proteins, cell contraction, cell structure, neuromodulation, airway remodeling, apoptosis, autophagy, miRNA, mitochondria, etc. In brief, ASM is similar to a "processing station." It is not only affected by various signals in the body to produce biological effects and secrete various signals to act on downstream target cells but also feeds back to the upstream pathways or receives feedback from downstream pathways to form a complex network. The results summarized in this chapter are expected to provide new targets for the clinical treatment of asthma.

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MiR-23b controls TGF-β1 induced airway smooth muscle cell proliferation via TGFβR2/p-Smad3 signals

Cited by 26 publications

References 22 publications

MicroRNA-485 Modulates the TGF-β/ Smads Signaling Pathway in Chronic Asthmatic Mice by Targeting Smurf2

MicroRNA-485 Modulates the TGF-β/ Smads Signaling Pathway in Chronic Asthmatic Mice by Targeting Smurf2

Sex-specific microRNA expression networks in an acute mouse model of ozone-induced lung inflammation

Role of Airway Smooth Muscle Cells in Asthma Pathology

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