TRPC6 mediates goblet cell differentiation in COPD
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Le résumé fourni par la source
BACKGROUND: Goblet cell metaplasia is a pathological feature of airway remodelling in chronic obstructive pulmonary disease (COPD). Basal cell clones with goblet cell metaplasia demonstrate high transient receptor potential cation channel subfamily C member 6 (TRPC6) expression, but its biological function remains unclear. METHODS: TRPC6 expression was analysed by immunostaining in lung tissues and airway basal cells from patients with COPD, and in the airways of mice exposed to cigarette smoke or interleukin-13. In vitro, the role of TRPC6 was assessed by TRPC6 overexpression and depletion in air–liquid interface cultures of human bronchial epithelial cells. In vivo, TRPC6 function was tested by airway TRPC6 depletion and TRPC6 inhibition in mice exposed to interleukin-13. NOTCH signalling was confirmed as a downstream pathway of TRPC6 by performing rescue experiments. RESULTS: TRPC6 expression was increased in the airway epithelium of patients with COPD and in interleukin-13-exposed mice. TRPC6 overexpression in basal cells from patients without COPD promoted their differentiation into goblet cells, while TRPC6 depletion in basal cells from patients with COPD suppressed goblet cell metaplasia in air–liquid interface cultures. TRPC6 function in suppressed goblet cell metaplasia was confirmed in TRPC6 depletion mice and TRPC6 inhibitor-treated mice. NOTCH signalling increased in interleukin-13-exposed control mice and human bronchial epithelial cell air–liquid interface cultures and decreased after TRPC6 inhibition. CONCLUSIONS: TRPC6 regulated basal cell differentiation, underscoring its potential as a therapeutic target in COPD. The in vivo experiments used mice exposed to interleukin-13, so its clinical potential requires clarification.
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Le contrôle bibliographique ouvert
DOI retrouvé dans Crossref DOI retrouvé ; titre concordant.
- Titre Crossref
- TRPC6 mediates goblet cell differentiation in COPD
- Date Crossref
- 06/04/2026
- Éditeur
- Springer Science and Business Media LLC
- Type
- journal-article
Ce recoupement confirme des métadonnées liées au DOI. Il ne confirme ni la méthode ni les conclusions de l’étude, et il ne compte pas comme une seconde source scientifique indépendante.
Où se fait cette recherche
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First Affiliated Hospital of Guangzhou Medical University State Key Laboratory of Respiratory Disease & National Clinical Research Center for Respiratory Disease & National Center for Respiratory Medicine & pays non établi dans la noticeÉtablissement de santé
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Guangzhou Medical University Department of Pulmonary and Critical Care Medicine pays non établi dans la noticeUniversité ou école supérieure
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Third Affiliated Hospital of Guangzhou Medical University pays non établi dans la noticeÉtablissement de santé
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Shenzhen Bao'an District People's Hospital pays non établi dans la noticeÉtablissement de santé
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First Affiliated Hospital of Jinan University Department of Thoracic Surgery pays non établi dans la noticeÉtablissement de santé
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Shanxi Medical University Department of Pulmonary and Critical Care Medicine pays non établi dans la noticeUniversité ou école supérieure
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Shanxi Academy of Medical Sciences pays non établi dans la noticeÉtablissement de santé
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the Peoples's Hospital of Baoan Shenzhen Department of Thoracic Surgery pays non établi dans la noticeÉtablissement de santé
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Guangzhou National Laboratory pays non établi dans la noticeStructure de recherche
State Key Laboratory of Respiratory Disease & National Clinical Research Center for Respiratory Disease & National Center for Respiratory Medicine & — First Affiliated Hospital of Guangzhou Medical University, Department of Pulmonary and Critical Care Medicine — Guangzhou Medical University et Third Affiliated Hospital of Guangzhou Medical University, avec 6 autres affiliations.
Une affiliation ne permet pas de déduire la nationalité d’un auteur.