Abstract
Pleural fibrosis (PF) is characterized by thickening of the pleura around the lungs due to mesothelial cells transitioning into myofibroblasts. Our research delved into the role of Myocardin (MYOCD) in this transition, revealing Twinfilin 1 (TWF1) and Leiomodin 1 (LMOD1) as significant genes influenced by MYOCD. In our investigation, we explored how TWF1 and LMOD1 impact cytoskeletal changes in human pleural mesothelial cells (HPMCs) induced by Transforming growth factor beta (TGF-β). Knocking down TWF1 resulted in reduced expression of Calponin 1 and alpha-Smooth Muscle Actin (α-SMA), while LMOD1 knock-down suppressed α-SMA expression. Inhibition of TWF1 hindered stress fiber formation but enhanced cortical actin structure, whereas LMOD1 overexpression facilitated stress fiber formation. Knocking down either genos significantly diminished cell contractility and affected myofibroblast differentiation, suggesting their pivotal role in regulating actin cytoskeletal remodeling in HPMCs.
Date of publication
2024
Document Type
Thesis
Language
english
Persistent identifier
http://hdl.handle.net/10950/4712
Recommended Citation
Sato, Kasumi, "Role of Myocardin Effector Genes on the Progression of Cytoskeletal Remodeling and Phenotype Switching of HPMCs" (2024). Biotechnology Theses. Paper 18.
http://hdl.handle.net/10950/4712