Publications by authors named "C Magaud"
Extracellular aggregates of wild-type human transthyretin are associated with heart diseases such as wild-type transthyretin (TTR)-derived amyloidosis (ATTR-wt). Due to their strategic location, cardiac fibroblasts act as sentinel cells that sense injury and activate the inflammasome. No studies of the effects of TTR amyloid aggregation on the secretion of inflammatory factors by primary human cardiac fibroblasts (hCFs) have been reported yet.
View Article and Find Full Text PDFBackground: Human cardiac stem cells expressing the W8B2 marker (W8B2 CSCs) were recently identified and proposed as a new model of multipotent CSCs capable of differentiating into smooth muscle cells, endothelial cells and immature myocytes. Nevertheless, no characterization of ion channel or calcium activity during the differentiation of these stem cells has been reported.
Methods: The objectives of this study were thus to analyze (using the TaqMan Low-Density Array technique) the gene profile of W8B2 CSCs pertaining to the regulation of ion channels, transporters and other players involved in the calcium homeostasis of these cells.
Article Synopsis
- Cardiac fibroblasts are crucial for maintaining the heart's structure and contribute to heart disease by promoting fibrosis.
- The study focuses on the TRPM4 calcium-activated channel's role in atrial fibroblast behavior, using human cells and mice with a disrupted Trpm4 gene.
- Key findings include TRPM4's influence on fibroblast growth and the expression of fibroblast markers, suggesting that TRPM4 contributes to cardiac fibrosis development.
Anomalies in constitutive calcium entry (CCE) have been commonly attributed to cell dysfunction in pathological conditions such as cancer. Calcium influxes of this type rely on channels, such as transient receptor potential (TRP) channels, to be constitutively opened and strongly depend on membrane potential and a calcium driving force. We developed an optogenetic approach based on the expression of the halorhodopsin chloride pump to study CCE in non-excitable cells.
View Article and Find Full Text PDFArticle Synopsis
- Chronic myeloid leukemia (CML) is driven by a specific oncogene that leads to increased tyrosine kinase activity, prompting research into additional treatments beyond existing tyrosine kinase inhibitors (TKIs) like Imatinib.
- The study found that calcium entry mechanisms, specifically Store-Operated Calcium Entry (SOCE), are disrupted in leukemia cells with the Bcr-Abl oncogene, which correlates with changes in key proteins that regulate calcium levels and reduced cell proliferation.
- Targeting the abnormal calcium entry in these leukemia cells could provide a new therapeutic approach when combined with TKIs, as the alterations in calcium signaling pathways involve changes in Protein Kinase C (PKC) activity.