Control of cell phenotype via epigenetic modification through micro-patterning and nano-structuring of cell incubation substrate

• Main Authors: Chia-Liang Yen, 顏嘉良
• Other Authors: Szu-yuan Chen
• Format: Others
• Language: zh-TW
• Published: 2017
• Online Access: http://ndltd.ncl.edu.tw/handle/6vrkna

碩士 === 國立中央大學 === 生物物理研究所 === 105 === It is known that during morphogenesis, totipotent stem cells become the various pluripotent cell lines of the embryo, which in turn become fully differentiated cells, by activating some genes while inhibiting the expression of others. However, the mechanisms underlying the cell type commitment and the cells’ spatial organization in an organism are still largely unknown. On the other hand, cellular behaviors can be modulated not only by biochemical signals but also by biophysical cues, especially those from extracellular matrix (ECM). It is well known that cell ECM is actually made of most importantly collagen microfibrils, which possess specific molecular identity and structural characteristics that may be crucial for controlling cell behaviors such as cell phenotype and coordinating organism morphogenesis. In particular, it has been reported that the characteristic 67-nm-period D-banding of collagen. Microfibrils is required in order to observe the elongation and motional directionality of cells on a collagen substrate. Based on these observations, we hypothesize that the cell phenotype could be controlled by spatial modulation of the chromatin in the cell nucleus through mechanical action from actin filament bundles, which in turn could be controlled by integrin clustering and activation triggered by a micropatterned collagen substrate/scaffold with D-banding. We propose that this could be what dominate cell type commitment in morphogenesis and tumorigenesis. Our result indicated that collagen microfibril could make stem cell differentiate into neuron cell, moreover, collagen microfibril with 67 nm D-banding could enhance the ability of stem cell differentiate into neuron cell.