Calpain-activated mTORC2/Akt pathway mediates airway smooth muscle remodelling in asthma

2016 ◽  
Vol 47 (2) ◽  
pp. 176-189 ◽  
Author(s):  
S.-S. Rao ◽  
Q. Mu ◽  
Y. Zeng ◽  
P.-C. Cai ◽  
F. Liu ◽  
...  
Keyword(s):  
Smooth Muscle ◽  
Airway Smooth Muscle ◽  
Akt Pathway ◽  
Muscle Remodelling

Acetylcholine: a novel regulator of airway smooth muscle remodelling?

2004 ◽  
Vol 500 (1-3) ◽  
pp. 193-201 ◽  
Author(s):  
Reinoud Gosens ◽  
Johan Zaagsma ◽  
Mechteld Grootte Bromhaar ◽  
Adriaan Nelemans ◽  
Herman Meurs
Keyword(s):  
Smooth Muscle ◽  
Airway Smooth Muscle ◽  
Muscle Remodelling

scholarly journals Distribution of airway smooth muscle remodelling in asthma: Relation to airway inflammation

Respirology ◽  
2014 ◽  
Vol 20 (1) ◽  
pp. 66-72 ◽  
Author(s):  
John G. Elliot ◽  
Robyn L. Jones ◽  
Michael J. Abramson ◽  
Francis H. Green ◽  
Thais Mauad ◽  
...  
Keyword(s):  
Smooth Muscle ◽  
Airway Inflammation ◽  
Airway Smooth Muscle ◽  
Muscle Remodelling

scholarly journals Mitochondrial ATP-Sensitive K+ Channel Opening Increased the Airway Smooth Muscle Cell Proliferation by Activating the PI3K/AKT Signaling Pathway in a Rat Model of Asthma

2021 ◽  
Vol 2021 ◽  
pp. 1-7
Author(s):  
Min Gao ◽  
Qinran Sun ◽  
Qingfa Liu
Keyword(s):  
Smooth Muscle ◽  
Signaling Pathway ◽  
Airway Smooth Muscle ◽  
Rat Model ◽  
Akt Signaling ◽  
Akt Pathway ◽  
Airway Smooth Muscle Cells ◽  
Akt Signaling Pathway ◽  
Channel Opening ◽  
Mitokatp Channel

Abnormal proliferation of airway smooth muscle cells (ASMCs) leads to airway remodeling and the development of asthma. This study aimed to assess whether mitochondrial ATP-sensitive K+ (mitoKATP) channels regulated the proliferation of ASMCs by regulating the phosphoinositide 3-kinase/protein kinase B (PI3K/AKT) pathway in asthmatic rats. Forty-eight Sprague Dawley rats were immunized with ovalbumin-containing alum to establish the asthma models. The ASMCs were isolated and identified by phase-contrast microscopic images and immunohistochemical staining for α-smooth muscle actin. The ASMCs were treated with a potent activator of mitoKATP, diazoxide, or an inhibitor of mitoKATP, 5-hydroxydecanoate (5-HD). Rhodamine-123 (R-123) was used for detecting the mitochondrial membrane potential (Δψm). The proliferation of ASMCs was examined by the MTT (3-[4,5-dimethylthiazol-2-yl]-2,5 diphenyl tetrazolium bromide) assay. The protein and mRNA expressions of AKT and p-AKT were detected using western blotting and quantitative real-time PCR. The results showed that diazoxide enhanced the mitoKATP channel opening in ASMCs in the rat model of asthma, while 5-HD impeded it. Diazoxide also increased ASMC proliferation in the rat model of asthma, whereas 5-HD alleviated it. However, LY294002, a PI3K/AKT pathway inhibitor, reversed the functional roles of diazoxide in the proliferation ability of ASMCs in the rat model of asthma. Furthermore, treatment with diazoxide induced the phosphorylation of AKT, and treatment with 5-HD decreased the phosphorylation of AKT in ASMCs in the rat model of asthma. In conclusion, the mitoKATP channel opening increased the proliferation of ASMCs by activating the PI3K/AKT signaling pathway in a rat model of asthma.

scholarly journals MiR-18a Inhibits PI3K/AKT Signaling Pathway to Regulate PDGF BB-Induced Airway Smooth Muscle Cell Proliferation and Phenotypic Transformation

2021 ◽  
pp. 883-892
Author(s):  
W. Yang ◽  
Y. Chen ◽  
C. Huang ◽  
W. Wang ◽  
C. Huang ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Smooth Muscle ◽  
Airway Smooth Muscle ◽  
Airway Remodeling ◽  
Akt Pathway ◽  
Airway Smooth Muscle Cells ◽  
Migration Ability ◽  
Phenotypic Transformation ◽  
And Migration ◽  
Proliferation And Migration

The increased proliferation and migration of airway smooth muscle cells (ASMCs) is a key process in the formation of airway remodeling in asthma. In this study, we focused on the expression of mircoRNA-18a (miR-18a) in airway remodeling in bronchial asthma and its related mechanisms. ASMCs are induced by platelet-derived growth factor BB (PDGF-BB) for in vitro airway remodeling. The expression of miR-18a in sputum of asthmatic patients and healthy volunteers was detected by qRT-PCR. The expression of miR-18a was over-expressed or interfered with in PDGF-BB-treated ASMCs. Cell proliferation, apoptosis and migration were detected by MTT, flow cytometry and Transwell, respectively; the expression of contractile phenotype marker proteins (SM-22α, α-SM-actin, calponin) and key molecules of the phosphatidylinositol 3-kinase (PI3K)/AKT pathway (PI3K, p-PI3K, AKT and p-AKT) in ASMCs were detected by Western blot. The expression of miR-18a was down-regulated in the sputum and PDGF-BB-treated ASMCs of asthma patients. PDGF-BB could promote the proliferation and migration of ASMCs and inhibit their apoptosis; it could also promote the phenotypic transformation of ASMCs and activate the PI3K/AKT pathway. MiR-18a could inhibit the proliferation, migration ability and phenotypic transformation of ASMCs induced by PDGF-BB to a certain extent and alleviate the effect of PDGF-BB in supressing apoptosis, while miR-18a could inhibit the activation of the PI3K/AKT pathway. MiR-18a inhibits PDGF-BB-induced proliferation, migration and phenotypic conversion of ASMCs by inhibiting the PI3K/AKT pathway, thus attenuating airway remodeling in asthma.

Animal models of airway inflammation and airway smooth muscle remodelling in asthma

2009 ◽  
Vol 22 (5) ◽  
pp. 455-465 ◽  
Author(s):  
Judith E. Allen ◽  
Robert J. Bischof ◽  
Herng-Yu Sucie Chang ◽  
Jeremy A. Hirota ◽  
Stuart J. Hirst ◽  
...  
Keyword(s):  
Smooth Muscle ◽  
Animal Models ◽  
Airway Inflammation ◽  
Airway Smooth Muscle ◽  
Muscle Remodelling

scholarly journals HMGB1 amplifies ILC2-induced type-2 inflammation and airway smooth muscle remodelling

2020 ◽  
Vol 16 (7) ◽  
pp. e1008651 ◽  
Author(s):  
Zhixuan Loh ◽  
Jennifer Simpson ◽  
Ashik Ullah ◽  
Vivian Zhang ◽  
Wan J. Gan ◽  
...  
Keyword(s):  
Smooth Muscle ◽  
Airway Smooth Muscle ◽  
Muscle Remodelling ◽  
Type 2 Inflammation
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