MassIVE MSV000097369

Partial Public PXD062012

Epithelial-fibroblast crosstalk initiates protective mechanisms in epithelial cells upon acute injury

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Description

Idiopathic pulmonary fibrosis (IPF) is a progressive and lethal lung disease characterized by excessive fibrotic scar tissue accumulation, compromising lung function. While the precise etiology of IPF remains elusive, emerging evidence suggests that sustained lung epithelial injury is a key driver in the disease's development and progression. This persistent injury, unlike normal wound healing, maintains a pro-fibrotic niche that continually fuels the fibrotic process. Consequently, the question remains whether there is a way to alter this niche signaling, counteract the pro-fibrotic signals, and restore physiological wound healing. By approaching an epithelial-fibroblast coculture model, we investigated in the intercellular communication in chronic and acute injury situations. We identified that epithelial cells and fibroblasts together, create a protective niche signaling preventing further damage in acute injuries. Within epithelial cells, we observed that a switch of the metabolic state towards increased aerobic fatty acid metabolism initiates regenerative processes. While delineating secreted regulators responsible for inducing these positive responses, we identified pentraxin 3 (PTX3) as a top hit harboring antifibrotic characteristics. Modifying the niche by addition of PTX3 on chronically injured epithelial cells causes an amelioration of the pro-fibrotic phenotype and maintained the epithelial barrier integrity. These findings offer valuable insights in key differences of acute and chronic injuries and underscore the importance of understanding the complex interplay between epithelial cells and fibroblasts in lung injury and repair. [doi:10.25345/C5RF5KT4F] [dataset license: CC0 1.0 Universal (CC0 1.0)]

Keywords: Pulmonary fibrosis ; Epithelial-fibroblast crosstalk ; Fatty acid metabolism ; PTX3 ; DatasetType:Proteomics

Contact

Principal Investigators:
(in alphabetical order) 		Matthew J. Thomas, Boehringer Ingelheim Pharma GmbH, Germany
Submitting User: alexcampos

Publications

Marie-Therese Bammert, Ines Kollak, Jan Hoffmann, Eva Peter, Meshal Ansari, Holger Schlüter, Jun Li, Alexandre R. Campos, Coralie Viollet, Florian Gantner, Muriel Lizé, Matthew J. Thomas, Huy Q. Le.
Dual roles of fibroblast-epithelial crosstalk in acute and chronic lung injury.
Journal of Biological Chemistry (in press).

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