Acetylcholine beyond bronchoconstriction: roles in inflammation and remodeling

Kistemaker, Loes; Gosens, Reinoud

doi:10.1016/j.tips.2014.11.005

Cited by 130 publications

(133 citation statements)

References 84 publications

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“…Acetylcholine is the most important parasympathetic neurotransmitter in the airways (11). It induces airway smooth muscle contraction and for this reason, anticholinergics are usually used as bronchodilators in obstructive airway diseases (11)(12)(13).…”

Section: Accepted Articlementioning

confidence: 99%

“…It induces airway smooth muscle contraction and for this reason, anticholinergics are usually used as bronchodilators in obstructive airway diseases (11)(12)(13). Interestingly, recent studies reveal that ACh not only induces bronchoconstriction but also promotes changes in the airways associated to Th2 responses such as eosinophilia, mucus overproduction and airway remodeling (11,14,15).…”

Section: Accepted Articlementioning

confidence: 99%

Section: Accepted Articlementioning

confidence: 99%

“…Because ACh induces airway smooth muscle contraction, anticholinergics are used as bronchodilators in obstructive airway diseases such as chronic pulmonary obstructive disease and asthma (11,13,28). However, it is increasingly accepted that anticholinergics not only prevent bronchoconstriction but also reduce mucus secretion, neutrophil infiltration, and airway remodeling (11,15,29).…”

Section: Accepted Articlementioning

confidence: 99%

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Acetylcholine polarizes dendritic cells toward a Th2-promoting profile

Gori

Vermeulen

Remes-Lenicov

et al. 2016

Allergy

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Section: Accepted Articlementioning

confidence: 99%

Section: Accepted Articlementioning

confidence: 99%

Section: Accepted Articlementioning

confidence: 99%

Section: Accepted Articlementioning

confidence: 99%

See 2 more Smart Citations

Acetylcholine polarizes dendritic cells toward a Th2-promoting profile

Gori

Vermeulen

Remes-Lenicov

et al. 2016

Allergy

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“…Ос новными структурными аномалиями бронхолегоч ного аппарата при ХОБЛ, формирующими необра тимый компонент обструктивных нарушений, являются ремоделирование дыхательных путей, эмфизема и сосудистое ремоделирование, ведущее к развитию легочной гипертензии. Нейрональный и ненейрональный АцХ и М холинорецепторы игра ют существенно более важную роль в процессе ремо делинга дыхательных путей и патофизиологии обструктивных заболеваний легких, чем считалось ранее [16,20,39]. АцХ регулирует пролиферативные и профибротические реакции эпителия бронхов по ауто , паракринному механизму [20].…”

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Multiple effects of tiotropium in chronic obstructive pulmonary disease

Кузубова¹,

Лебедева²,

Titova³

2015

Pulʹmonologiâ (Mosk.)

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Резюме М холинолитик длительного действия тиотропия бромид относится к лекарственным средствам первого выбора для пациентов с хро нической обструктивной болезнью легких (ХОБЛ). Высокая эффективность тиотропия бромида в лечении больных ХОБЛ основана не только на блокировании парасимпатической холинергической бронхоконстрикции, но связана с его полимодальными эффектами не нейрональной природы. По результатам исследований последних лет доказана полимодальность тиотропия бромида, обусловленная его влиянием на М рецептор опосредованные внутриклеточные сигнальные системы, участвующие в регуляции клеточно молекулярных взаимодействий, вовлеченных в процессы воспаления, пролиферации и ремоделинга легочных структур. Противовоспалительный, ан типролиферативный, антиремоделирующий, противовирусный, антиоксидантный эффекты тиотропия бромида в сочетании с новым усовершенствованным устройством для его доставки (Респимат) определяют его преимущества перед другими длительно действующи ми антихонергическими препаратами и делают терапию пациентов с ХОБЛ более эффективной и безопасной. Ключевые слова: хроническая обструктивная болезнь легких, тиотропия бромид, мускариновый рецептор, ацетилхолин, ванилоидный рецептор, воспаление, ремоделинг. SummaryTiotropium is a long acting anticholinergic drug and the first line therapy in patients with chronic obstructive pulmonary disease (COPD). High efficacy of tiotropium in COPD is based not only on inhibition of parasympathetic cholinergic bronchoconstriction, but also is associated with mul tiple non neuronal effects. Recent studies demonstrated polymodality of tiotropium due to influence on M receptor mediated intracellular signal ing pathways participating in regulation of cell molecular interactions involved in inflammation, proliferation, and remodeling of pulmonary struc tures. Anti inflammatory, anti proliferative, anti remodeling, antiviral, and antioxidant effects of tiotropium delivered via the new improved device Respimat determine advantages of this drug over other long acting anticholinergics and increase efficacy and safety of therapy in patients with COPD.

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M₃ receptor modulates extracellular matrix synthesis via ERK1/2 signaling pathway in human bladder smooth muscle cells

Chen

Liao

Jin

et al. 2020

J of Cellular Biochemistry

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Extracellular matrix (ECM) accumulation plays a key role in the progression of bladder outlet obstruction (BOO). Muscarinic receptors have been widely reported to serve as pivotal regulators in lung tissue remodeling. However, the influence of them on human bladder smooth muscle cells (HBSMCs) and the underlying molecular mechanisms have not yet been evaluated. The purposes of the present study are to investigate the effect of muscarinic receptors on the synthesis of ECM in HBSMCs and the involvement of intracellular signal transducers. The results indicated that M1‐M5 muscarinic receptors were all encoded in HBSMCs. The expression rank order was M2 > M1 > M5 > M3 > M4. The gene and protein expression of collagen I (COL1), TIMP‐1, and TIMP‐2 was carbachol (CCH) concentration‐dependently enhanced. The synthesis of COL1 in the supernatant of cell culture medium was significantly elevated by exposure to CCH. The CCH‐induced protein expression of COL1, TIMP‐1, and TIMP‐2, however, was obviously reduced by the pretreatment of muscarinic receptor antagonists, atropine, and M3‐preferring antagonist (1,1‐dimethyl‐4‐diphenyl‐acetoxypiperidinium iodide [4‐DAMP]). Furthermore, ERK1/2 was activated by 100 µM CCH when compared with the control group and the pretreatment of ERK1/2 inhibitor significantly suppressed the synthesis of COL1 induced by 100 µM CCH. Besides, CCH‐induced phosphorylation of ERK1/2 was remarkably restrained by the pretreatment of 4‐DAMP. All in all, these findings demonstrated that M3 receptor can modulate extracellular matrix synthesis via the ERK1/2 signaling pathway, which may provide potential novel therapeutic targets for BOO.

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Acetylcholine beyond bronchoconstriction: roles in inflammation and remodeling

Cited by 130 publications

References 84 publications

Acetylcholine polarizes dendritic cells toward a Th2-promoting profile

Acetylcholine polarizes dendritic cells toward a Th2-promoting profile

Multiple effects of tiotropium in chronic obstructive pulmonary disease

M₃ receptor modulates extracellular matrix synthesis via ERK1/2 signaling pathway in human bladder smooth muscle cells

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Acetylcholine beyond bronchoconstriction: roles in inflammation and remodeling

Cited by 130 publications

References 84 publications

Acetylcholine polarizes dendritic cells toward a Th2-promoting profile

Acetylcholine polarizes dendritic cells toward a Th2-promoting profile

Multiple effects of tiotropium in chronic obstructive pulmonary disease

M3 receptor modulates extracellular matrix synthesis via ERK1/2 signaling pathway in human bladder smooth muscle cells

Contact Info

Product

Resources

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M₃ receptor modulates extracellular matrix synthesis via ERK1/2 signaling pathway in human bladder smooth muscle cells