MicroRNA-98-5p Inhibits IL-13-Induced Proliferation and Migration of Human Airway Smooth Muscle Cells by Targeting RAC1

Zeng, Shaolin; Cui, Juan; Zhang, Yunting; Zheng, Zhong

doi:10.1007/s10753-022-01640-1

Cited by 4 publications

(2 citation statements)

References 34 publications

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“…Quantitative RT‑PCR (qRT‑PCR) was performed following the protocols described in a previous study 29 . Total RNA in ASMCs was isolated with TRIzol, which was reverse‐transcribed into complementary DNA with a reverse transcription kit (ThermoFisher Scientific).…”

Section: Methodsmentioning

confidence: 99%

“…Quantitative RT-PCR (qRT-PCR) was performed following the protocols described in a previous study. 29 Total RNA in ASMCs was isolated with TRIzol, which was reverse-transcribed into complementary DNA with a reverse transcription kit (ThermoFisher Scientific). The complementary DNA was mixed with SYBR Green Master Mix (ThermoFisher Scientific) and specific primers for amplification via RT-PCR, following the thermal cycling programs: 95℃, 20 s and 40 cycles of 95℃, 3 s and 60℃, 30 s. The primers The primer sequences used for qRT-PCR were as follows: Csrp2 forward: 5'-GTCTGGGGC GGTGGAAATAAG-3′ and reverse: 5′-GCAAACCATGCACAGGAAG C-3′; GAPDH forward: 5′-CCAGTTGGTAACAATGCCATGT-3′ and reverse: 5′-CTTCCCATTCTCGGCCTTG-3′.…”

Section: Quantitative Real Time-pcr (Rt-pcr)mentioning

confidence: 99%

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Cysteine and glycine‐rich protein 2 retards platelet‐derived growth factor‐BB‐evoked phenotypic transition of airway smooth muscle cells by decreasing YAP/TAZ activity

Wang,

Zhang,

Zhong

et al. 2023

Cell Biochemistry & Function

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Cysteine and glycine‐rich protein 2 (Csrp2) has emerged as a key factor in controlling the phenotypic modulation of smooth muscle cells. The phenotypic transition of airway smooth muscle cells (ASMCs) is a pivotal step in developing airway remodeling during the onset of asthma. However, whether Csrp2 mediates the phenotypic transition of ASMCs in airway remodeling during asthma onset is undetermined. This work aimed to address the link between Csrp2 and the phenotypic transition of ASMCs evoked by platelet‐derived growth factor (PDGF)‐BB in vitro. The overexpression or silencing of Csrp2 in ASMCs was achieved through adenovirus‐mediated gene transfer. The expression of mRNA was measured by quantitative real‐time‑PCR. Protein levels were determined through Western blot analysis. Cell proliferation was detected by EdU assay and Calcein AM assays. Cell cycle distribution was assessed via fluorescence‐activated cell sorting assay. Cell migration was evaluated using the scratch‐wound assay. The transcriptional activity of Yes‐associated protein (YAP)/transcriptional coactivator with PDZ‐binding motif (TAZ) was measured using the luciferase reporter assay. A decline in Csrp2 level occurred in PDGF‐BB‐stimulated ASMCs. Increasing Csrp2 expression repressed the PDGF‐BB‐evoked proliferation and migration of ASMCs. Moreover, increasing Csrp2 expression impeded the phenotypic change of PDGF‐BB‐stimulated ASMCs from a contractile phenotype into a synthetic/proliferative phenotype. On the contrary, the opposite effects were observed in Csrp2‐silenced ASMCs. The activity of YAP/TAZ was elevated in PDGF‐BB‐stimulated ASMCs, which was weakened by Csrp2 overexpression or enhanced by Csrp2 silencing. The YAP/TAZ activator could reverse Csrp2‐overexpression‐mediated suppression of the PDGF‐BB‐evoked phenotypic switching of ASMCs, while the YAP/TAZ suppressor could dimmish Csrp2‐silencing‐mediated enhancement on PDGF‐BB‐evoked phenotypic switching of ASMCs. In summary, Csrp2 serves as a determinant for the phenotypic switching of ASMCs. Increasing Csrp2 is able to impede PDGF‐BB‐evoked phenotypic change of ASMCs from a synthetic phenotype into a synthetic/proliferative phenotype through the effects on YAP/TAZ. This work implies that Csrp2 may be a key player in airway remodeling during the onset of asthma.

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Section: Methodsmentioning

confidence: 99%

Section: Quantitative Real Time-pcr (Rt-pcr)mentioning

confidence: 99%

Cysteine and glycine‐rich protein 2 retards platelet‐derived growth factor‐BB‐evoked phenotypic transition of airway smooth muscle cells by decreasing YAP/TAZ activity

Wang,

Zhang,

Zhong

et al. 2023

Cell Biochemistry & Function

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CLDN1 silencing suppresses the proliferation and migration of airway smooth muscle cells by modulating MMP14

Li,

Liu,

Duanqing

et al. 2023

Autoimmunity

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Noncoding RNAs in asthmatic airway smooth muscle cells

Xiao

Dong

et al. 2023

Eur Respir Rev

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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.

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MicroRNA-98-5p Inhibits IL-13-Induced Proliferation and Migration of Human Airway Smooth Muscle Cells by Targeting RAC1

Cited by 4 publications

References 34 publications

Cysteine and glycine‐rich protein 2 retards platelet‐derived growth factor‐BB‐evoked phenotypic transition of airway smooth muscle cells by decreasing YAP/TAZ activity

Cysteine and glycine‐rich protein 2 retards platelet‐derived growth factor‐BB‐evoked phenotypic transition of airway smooth muscle cells by decreasing YAP/TAZ activity

CLDN1 silencing suppresses the proliferation and migration of airway smooth muscle cells by modulating MMP14

Noncoding RNAs in asthmatic airway smooth muscle cells

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