Publications by authors named "L DeMaio"
Claudin 4 knockout mice: normal physiological phenotype with increased susceptibility to lung injury.
Am J Physiol Lung Cell Mol Physiol
October 2014
Claudins are tight junction proteins that regulate paracellular ion permeability of epithelium and endothelium. Claudin 4 has been reported to function as a paracellular sodium barrier and is one of three major claudins expressed in lung alveolar epithelial cells (AEC). To directly assess the role of claudin 4 in regulation of alveolar epithelial barrier function and fluid homeostasis in vivo, we generated claudin 4 knockout (Cldn4 KO) mice.
View Article and Find Full Text PDFKnockout mice reveal key roles for claudin 18 in alveolar barrier properties and fluid homeostasis.
Am J Respir Cell Mol Biol
August 2014
Claudin proteins are major constituents of epithelial and endothelial tight junctions (TJs) that regulate paracellular permeability to ions and solutes. Claudin 18, a member of the large claudin family, is highly expressed in lung alveolar epithelium. To elucidate the role of claudin 18 in alveolar epithelial barrier function, we generated claudin 18 knockout (C18 KO) mice.
View Article and Find Full Text PDFPeroxisome proliferator activated receptor γ (PPARγ) agonists are effective antifibrotic agents in a number of tissues. Effects of these agents on epithelial-mesenchymal transition (EMT) of primary alveolar epithelial cells (AEC) and potential mechanisms underlying effects on EMT have not been well delineated. We examined effects of troglitazone, a synthetic PPARγ agonist, on transforming growth factor (TGF)-β1-induced EMT in primary rat AEC and an alveolar epithelial type II (AT2) cell line (RLE-6TN).
View Article and Find Full Text PDFArticle Synopsis
- Researchers found that a process called epithelial-mesenchymal transition (EMT) may help create a type of cell called fibroblasts in a lung disease known as idiopathic pulmonary fibrosis.
- They used special mice that have cells that glow green to study how lung cells change after injury and what materials in the environment affect these changes.
- The study showed that when lung cells were exposed to type I collagen, they changed shape and began to act more like fibroblasts, which is linked to a specific signaling pathway that helps regulate these changes.
Article Synopsis
- Scientists found that stress in a part of cells called the endoplasmic reticulum (ER) can cause a certain type of lung cell, called AT2 cells, to die and change into another type of cell, which is not good for lung health.
- They did tests using chemicals that caused ER stress and saw that this led to changes in important proteins that help cells stick together, showing that some cells turned into a different type that can make scar tissue in the lungs.
- The researchers also discovered that they could stop these changes by using a special drug, and they found similar signs of cell stress in mouse lungs after injury, which helps show that ER stress can be harmful in lung diseases.