Identification of early genes in the ...
Document type :
Article dans une revue scientifique: Article original
Permalink :
Title :
Identification of early genes in the pathophysiology of fibrotic interstitial lung disease in a new model of pulmonary fibrosis
Author(s) :
Hennion, Nathan [Auteur]
Institute for Translational Research in Inflammation - U 1286 [INFINITE]
BEDART, Corentin [Auteur]
Institute for Translational Research in Inflammation - U 1286 [INFINITE]
Vandomber, Leonie [Auteur]
Institute for Translational Research in Inflammation - U 1286 [INFINITE]
Gottrand, fréderic [Auteur]
Institute for Translational Research in Inflammation - U 1286 [INFINITE]
Humez, Sarah [Auteur]
Hétérogénéité, Plasticité et Résistance aux Thérapies des Cancers = Cancer Heterogeneity, Plasticity and Resistance to Therapies - UMR 9020 - U 1277 [CANTHER]
Service de pathologie [CHU Lille]
Chenivesse, Cecile [Auteur]
Centre d’Infection et d’Immunité de Lille - INSERM U 1019 - UMR 9017 - UMR 8204 [CIIL]
Desseyn, Jean-Luc [Auteur]
Lille Inflammation Research International Center - U 995 [LIRIC]
Gouyer, Valerie [Auteur]
Lille Inflammation Research International Center - U 995 [LIRIC]
Institute for Translational Research in Inflammation - U 1286 [INFINITE]
BEDART, Corentin [Auteur]

Institute for Translational Research in Inflammation - U 1286 [INFINITE]
Vandomber, Leonie [Auteur]
Institute for Translational Research in Inflammation - U 1286 [INFINITE]
Gottrand, fréderic [Auteur]

Institute for Translational Research in Inflammation - U 1286 [INFINITE]
Humez, Sarah [Auteur]
Hétérogénéité, Plasticité et Résistance aux Thérapies des Cancers = Cancer Heterogeneity, Plasticity and Resistance to Therapies - UMR 9020 - U 1277 [CANTHER]
Service de pathologie [CHU Lille]
Chenivesse, Cecile [Auteur]

Centre d’Infection et d’Immunité de Lille - INSERM U 1019 - UMR 9017 - UMR 8204 [CIIL]
Desseyn, Jean-Luc [Auteur]

Lille Inflammation Research International Center - U 995 [LIRIC]
Gouyer, Valerie [Auteur]
Lille Inflammation Research International Center - U 995 [LIRIC]
Journal title :
Cellular and Molecular Life Sciences
Pages :
115
Publisher :
Springer Verlag
Publication date :
2025-03-13
ISSN :
1420-682X
English keyword(s) :
Mouse
Embryo
Lung
Explant
Single-cell RNA-sequencing
Embryo
Lung
Explant
Single-cell RNA-sequencing
HAL domain(s) :
Sciences du Vivant [q-bio]
English abstract : [en]
Some interstitial lung diseases involve pulmonary fibrosis, which is a process that is characterized by the excessive and abnormal accumulation of extracellular matrix in the pulmonary interalveolar space. Although the ...
Show more >Some interstitial lung diseases involve pulmonary fibrosis, which is a process that is characterized by the excessive and abnormal accumulation of extracellular matrix in the pulmonary interalveolar space. Although the current anti-fibrotic therapy aims at slowing down the progression of pulmonary fibrosis, it does not reverse it, and many of the drugs that were identified in basic-research studies failed in clinical phases, mainly because of the lack of a model that can recapitulate the pathophysiological mechanisms of human pulmonary fibrosis. We developed a novel experimental model of pulmonary fibrosis induced by a cocktail of molecules on an air/liquid interface culture of mouse embryonic lung explants. Histological analyses revealed a pattern of usual interstitial pneumonia, the worst-prognosis form of pulmonary fibrosis. We performed a transcriptomics analysis at the single-cell level after the induction of fibrosis and before any histological signs of fibrosis could be observed. The results revealed increased expression of several gene families that are involved in early inflammation, fibrosis and iron homeostasis, as well as potential new genetic targets.Show less >
Show more >Some interstitial lung diseases involve pulmonary fibrosis, which is a process that is characterized by the excessive and abnormal accumulation of extracellular matrix in the pulmonary interalveolar space. Although the current anti-fibrotic therapy aims at slowing down the progression of pulmonary fibrosis, it does not reverse it, and many of the drugs that were identified in basic-research studies failed in clinical phases, mainly because of the lack of a model that can recapitulate the pathophysiological mechanisms of human pulmonary fibrosis. We developed a novel experimental model of pulmonary fibrosis induced by a cocktail of molecules on an air/liquid interface culture of mouse embryonic lung explants. Histological analyses revealed a pattern of usual interstitial pneumonia, the worst-prognosis form of pulmonary fibrosis. We performed a transcriptomics analysis at the single-cell level after the induction of fibrosis and before any histological signs of fibrosis could be observed. The results revealed increased expression of several gene families that are involved in early inflammation, fibrosis and iron homeostasis, as well as potential new genetic targets.Show less >
Language :
Anglais
Peer reviewed article :
Oui
Audience :
Internationale
Popular science :
Non
Source :
Submission date :
2025-03-19T03:20:00Z
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