Publications by authors named "R Braeuer"
Genetic deficiency of the transcription factor NFAT1 confers protection against fibrogenic responses independent of immune influx.
Am J Physiol Lung Cell Mol Physiol
January 2024
Article Synopsis
- Idiopathic pulmonary fibrosis (IPF) is characterized by ongoing tissue damage and scarring in the lungs, driven by persistent activation of mesenchymal cells related to various signaling pathways.
- The study focuses on the role of the transcription factor NFAT1, which controls a key profibrotic mediator (autotaxin) in lung mesenchymal cells, finding that mice lacking NFAT1 have improved survival and less lung fibrosis after injury.
- The research indicates that NFAT1 activates profibrotic processes in IPF and suggests it could be a potential target for therapeutic intervention in treating the disease.
In this study, we demonstrate that forkhead box F1 (FOXF1), a mesenchymal transcriptional factor essential for lung development, was retained in a topographically distinct mesenchymal stromal cell population along the bronchovascular space in an adult lung and identify this distinct subset of collagen-expressing cells as key players in lung allograft remodeling and fibrosis. Using Foxf1-tdTomato BAC (Foxf1-tdTomato) and Foxf1-tdTomato Col1a1-GFP mice, we show that Lin-Foxf1+ cells encompassed the stem cell antigen 1+CD34+ (Sca1+CD34+) subset of collagen 1-expressing mesenchymal cells (MCs) with a capacity to generate CFU and lung epithelial organoids. Histologically, FOXF1-expressing MCs formed a 3D network along the conducting airways; FOXF1 was noted to be conspicuously absent in MCs in the alveolar compartment.
View Article and Find Full Text PDFImmunoglobulins and antibodies to immunoglobulins (autoimmunoglobulins) have been identified to be implicated in the pathogenesis of rheumatoid arthritis (RA). Immunoglobulin deficiencies have been suggested to account for the increased risk of infections in RA patients. This study was carried out to determine the prevalence of immunoglobulin deficiencies in patients with RA and the identification of putative contributing factors.
View Article and Find Full Text PDFArticle Synopsis
- FOXF1 is a transcription factor that helps regulate lung mesenchymal stromal cells (LR-MSCs) and is found in lower levels in fibrotic cells compared to non-fibrotic ones.
- Silencing FOXF1 increases the migratory ability of LR-MSCs by upregulating genes involved in proliferation and inflammation, as well as enhancing the activity of Autotaxin (ATX).
- FOXF1 represses ATX through specific binding sites in its promoter, and the promotion of LR-MSC migration due to FOXF1 loss can be counteracted by inhibiting ATX and its receptor, LPA1.
Article Synopsis
- Understanding the mechanisms behind allograft fibrosis and chronic graft failure is crucial for improving transplant outcomes, particularly in cases of restrictive allograft syndrome (RAS).
- Researchers used a specific lung transplant model to show that humoral immune responses, especially involving B cells, play a significant role in developing RAS.
- Findings indicated that blocking B cell activity reduced fibrosis in lung allografts, suggesting targeted therapies could improve management of different types of chronic lung allograft dysfunction.