Presentation Information
[8p-P02-13]Exploring the elastic properties of beating dilated cardiomyopathy cells with the Q353R mutation using nanoendoscopy-AFM
〇ALEXIS BOROWIAK1,2, TAKEHIKO ICHIKAWA1,2, YOHEI KONO1,2, TAKESHI SHIMI1,2, MASAMICHI ITO3, RYO NITTA4, TAKESHI FUKUMA1,2 (1.Kanazawa Univ., 2.NanoLSI, 3.The Univ. of Tokyo, 4.Kobe Univ.)
Keywords:
Nanoendoscopy-AFM,hiPSC derived-cardiomyocytes,Nuclear membrane
Researchers are currently extensively investigating laminopathies to understand the underlying mechanisms and ultimately find a potential cure. Laminopathies are genetic disorders in humans caused by mutations in the LMNA gene. This gene encodes lamins A and C, which are components of the nuclear lamina that underlie the inner nuclear membrane. One hypothesis regarding the origin of laminopathies is the structural hypothesis: LMNA mutations weaken the lamina's structure, leading to misshapen and softened nuclei that cause local DNA damage due to mechanical stress. Understanding the mechanical properties of these diseases presents a key challenge, as there is no specific treatment for laminopathies. Nanoendoscopy-AFM is a newly developed technique that can directly image 3D structures inside a cell using a nano-needle-like AFM tip. In this communication, we propose to expand this technique by comparing the elasticity of the nucleus in human-induced Pluripotent Stem Cells -cardiomyocytes with the Q353R mutation and without a laminopathy mutation (Wild Type and Rescue cells), using a new approach called Direct Nuclear Elasticity Measurements (DNEM) through nanoendoscopy-AFM, to find evidence supporting the structural hypothesis of laminopathies.