scholarly journals Recellularization of bronchial extracellular matrix with primary bronchial smooth muscle cells

2019 ◽  
Author(s):  
Selma Ben Hamouda ◽  
Amandine Vargas ◽  
Roxane Boivin ◽  
Maria Angelica Miglino ◽  
Renata Kelly da Palma ◽  
...  
Keyword(s):  
Extracellular Matrix ◽  
Smooth Muscle ◽  
Three Dimensional ◽  
Sodium Deoxycholate ◽  
Current Therapy ◽  
Bronchial Smooth Muscle ◽  
Matrix Layer ◽  
Quantitative Score ◽  
Bronchial Smooth Muscle Cells ◽  
Chemotactic Effect

AbstractSevere asthma is associated with an increased airway smooth muscle (ASM) mass and an altered composition of the extracellular matrix (ECM). Studies have indicated that ECM-ASM cell interactions contribute to this remodeling and its limited reversibility with current therapy. Three-dimensional matrices allow the study of complex cellular responses to different stimuli in an almost natural environment. Our goal was to obtain acellular bronchial matrices and then develop a recellularization protocol with ASM cells. We studied equine bronchi as horses spontaneously develop a human asthma-like disease. The bronchi were decellularized using Triton/Sodium Deoxycholate. The obtained scaffolds retained their anatomical and histological properties. Using immunohistochemistry and a semi-quantitative score to compare native bronchi to scaffolds revealed no significant variation for matrixial proteins. A DNA quantification and electrophoresis indicated that most of DNA was 29.6 ng/mg of tissue ± 5.6 with remaining fragments of less than 100 bp. Primary ASM cells were seeded on the scaffolds. Histological analysis after recellularization showed that ASM cells migrated and proliferated primarily in the decellularized smooth muscle matrix, suggesting a chemotactic effect of the scaffolds. This is the first report of primary ASM cells preferentially repopulating the smooth muscle matrix layer in bronchial matrices. This protocol is now being used to study the molecular interactions occurring between the asthmatic ECMs and ASM to identify effectors of asthmatic bronchial remodeling.

scholarly journals Recellularization of Bronchial Extracellular Matrix With Primary Bronchial Smooth Muscle Cells

2021 ◽  
Vol 96 ◽  
pp. 103313
Author(s):  
Selma Ben Hamouda ◽  
Amandine Vargas ◽  
Roxane Boivin ◽  
Maria Angelica Miglino ◽  
Renata Kelly da Palma ◽  
...  
Keyword(s):  
Extracellular Matrix ◽  
Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Muscle Cells ◽  
Bronchial Smooth Muscle ◽  
Bronchial Smooth Muscle Cells

scholarly journals Endothelin generating pathway through endothelin1-31 in human cultured bronchial smooth muscle cells

1999 ◽  
Vol 127 (6) ◽  
pp. 1415-1421 ◽  
Author(s):  
Yoko Hayasaki-Kajiwara ◽  
Noriyuki Naya ◽  
Toshitake Shimamura ◽  
Takanori Iwasaki ◽  
Masatoshi Nakajima
Keyword(s):  
Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Muscle Cells ◽  
Bronchial Smooth Muscle ◽  
Bronchial Smooth Muscle Cells

scholarly journals Functional KCa3.1 Channels Regulate Steroid Insensitivity in Bronchial Smooth Muscle Cells

2013 ◽  
Vol 191 (5) ◽  
pp. 2624-2636 ◽  
Author(s):  
Latifa Chachi ◽  
Aarti Shikotra ◽  
S. Mark Duffy ◽  
Omar Tliba ◽  
Christopher Brightling ◽  
...  
Keyword(s):  
Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Muscle Cells ◽  
Bronchial Smooth Muscle ◽  
Bronchial Smooth Muscle Cells

scholarly journals TLR3/TAK1 signalling regulates rhinovirus-induced interleukin-33 in bronchial smooth muscle cells

2020 ◽  
Vol 6 (4) ◽  
pp. 00147-2020
Author(s):  
Sangeetha Ramu ◽  
Jenny Calvén ◽  
Charalambos Michaeloudes ◽  
Mandy Menzel ◽  
Hamid Akbarshahi ◽  
...  
Keyword(s):  
Smooth Muscle ◽  
Severe Asthma ◽  
Poly I:C ◽  
Healthy Controls ◽  
Bronchial Smooth Muscle ◽  
Interleukin 33 ◽  
Asthma Exacerbations ◽  
Gene And Protein Expression ◽  
Bronchial Smooth Muscle Cells

BackgroundAsthma exacerbations are commonly associated with rhinovirus (RV) infection. Interleukin-33 (IL-33) plays an important role during exacerbation by enhancing Type 2 inflammation. Recently we showed that RV infects bronchial smooth muscle cells (BSMCs) triggering production of interferons and IL-33. Here we compared levels of RV-induced IL-33 in BSMCs from healthy and asthmatic subjects, and explored the involvement of pattern-recognition receptors (PRRs) and downstream signalling pathways in IL-33 expression.MethodBSMCs from healthy and severe and non-severe asthmatic patients were infected with RV1B or stimulated with the PRR agonists poly(I:C) (Toll-like receptor 3 (TLR3)), imiquimod (TLR7) and poly(I:C)/LyoVec (retinoic acid-inducible gene 1 (RIG-I)/melanoma differentiation-associated protein 5 (MDA5)). Knockdown of TLR3, RIG-I and MDA5 was performed, and inhibitors targeting TBK1, nuclear factor-κB (NF-κB) and transforming growth factor (TGF)-β-activated kinase 1 (TAK1) were used. Gene and protein expression were assessed.ResultsRV triggered IL-33 gene and protein expression in BSMCs. BSMCs from patients with non-severe asthma showed higher baseline and RV-induced IL-33 gene expression compared to cells from patients with severe asthma and healthy controls. Furthermore, RV-induced IL-33 expression in BSMCs from healthy and asthmatic individuals was attenuated by knockdown of TLR3. Inhibition of TAK1, but not NF-κB or TBK1, limited RV-induced IL-33. The cytokine secretion profile showed higher production of IL-33 in BSMCs from patients with non-severe asthma compared to healthy controls upon RV infection. In addition, BSMCs from patients with non-severe asthma had higher levels of RV-induced IL-8, TNF-α, IL-1β, IL-17A, IL-5 and IL-13.ConclusionRV infection caused higher levels of IL-33 and increased pro-inflammatory and Type 2 cytokine release in BSMCs from patients with non-severe asthma. RV-induced IL-33 expression was mainly regulated by TLR3 and downstream via TAK1. These signalling molecules represent potential therapeutic targets for treating asthma exacerbations.

Membrane currents in canine bronchial artery and their regulation by excitatory agonists

2002 ◽  
Vol 282 (6) ◽  
pp. L1358-L1365 ◽  
Author(s):  
Q. J. Li ◽  
L. J. Janssen
Keyword(s):  
Smooth Muscle ◽  
Bronchial Artery ◽  
Similar Degree ◽  
Ion Currents ◽  
Significant Suppression ◽  
Bronchial Smooth Muscle ◽  
Voltage Dependent ◽  
Inward Currents ◽  
Bronchial Smooth Muscle Cells ◽  
Airway Physiology

The bronchial vasculature plays an important role in airway physiology and pathophysiology. We investigated the ion currents in canine bronchial smooth muscle cells using patch-clamp techniques. Sustained outward K+current evoked by step depolarizations was significantly inhibited by tetraethylamonium (1 and 10 mM) or by charybdotoxin (10−6M) but was not significantly affected by 4-aminopyridine (1 or 5 mM), suggesting that it was primarily a Ca2+-activated K+current. Consistent with this, the K+current was markedly increased by raising external Ca2+to 4 mM but was decreased by nifedipine (10−6M) or by removing external Ca2+. When K+currents were blocked (by Cs+in the pipette), step depolarizations evoked transient inward currents with characteristics of L-type Ca2+current as follows: 1) activation that was voltage dependent (threshold and maximal at −50 and −10 mV, respectively); 2) inactivation that was time dependent and voltage dependent (voltage causing 50% maximal inactivation of −26 ± 22 mV); and 3) blockade by nifedipine (10−6M). The thromboxane mimetic U-46619 (10−6M) caused a marked augmentation of outward K+current (as did 10 mM caffeine) lasting only 10–20 s; this was followed by significant suppression of the K+current lasting several minutes. Phenylephrine (10−4M) also suppressed the K+current to a similar degree but did not cause the initial transient augmentation. None of these three agonists elicited inward current of any kind. We conclude that bronchial arterial smooth muscle expresses Ca2+-dependent K+channels and voltage-dependent Ca2+channels and that its excitation does not involve activation of Cl−channels.

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