Publications by authors named "Megane Lebel"

Article Synopsis
  • Lung parenchymal hypoxia is a key characteristic of idiopathic pulmonary fibrosis (IPF), which enhances cancer cell invasion and promotes lung fibrogenesis through LPA-dependent signaling.
  • Research shows that lung fibroblasts from IPF patients create invadosomes—structures that degrade the matrix—more effectively, suggesting a correlation between invadosome formation and fibrosis severity.
  • The study finds that hypoxia boosts invadosome formation through LPA and PDGFR-Akt signaling pathways, indicating potential therapeutic targets for reducing lung fibrosis.
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Idiopathic pulmonary fibrosis (IPF) is characterized by abnormal fibroblast accumulation in the lung leading to extracellular matrix deposition and remodeling that compromise lung function. However, the mechanisms of interstitial invasion and remodeling by lung fibroblasts remain poorly understood. The invadosomes, initially described in cancer cells, consist of actin-based adhesive structures that coordinate with numerous other proteins to form a membrane protrusion capable of degrading the extracellular matrix to promote their invasive phenotype.

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Idiopathic pulmonary fibrosis (IPF) is a progressive and fatal lung disease with no curative pharmacological treatment. Current preclinical models fail to accurately reproduce human pathophysiology and are therefore poor predictors of clinical outcomes. Here, we investigated whether the chick embryo chorioallantoic membrane (CAM) assay supports the implantation of xenografts derived from IPF lung tissue and primary IPF lung fibroblasts and can be used to evaluate the efficacy of antifibrotic drugs.

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The importance of the intracellular Ca concentration ([Ca]) in neutrophil function has been intensely studied. However, the role of the intracellular Na concentration ([Na]) which is closely linked to the intracellular Ca regulation has been largely overlooked. The [Na] is regulated by Na transport proteins such as the Na/Ca-exchanger (NCX1), Na/K-ATPase, and Na-permeable, transient receptor potential melastatin 2 (TRPM2) channel.

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