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Mitochondrial dysfunction and calcium deregulation by the RanBP9-cofilin pathway
Roh, Seung-Eon,Woo, Jung A.,Lakshmana, Madepalli K.,Uhlar, Courtney,Ankala, Vinishaa,Boggess, Taylor,Liu, Tian,Hong, Yun-Hwa,Mook-Jung, Inhee,Kim, Sang Jeong,Kang, David E. The Federation of American Societies for Experimen 2013 The FASEB Journal Vol.27 No.12
<P>Mitochondrial dysfunction and synaptic damage are important features of Alzheimer's disease (AD) associated with amyloid β (Aβ) and tau. We reported previously that the scaffolding protein RanBP9, which is overall increased in brains of patients with AD and in mutant APP transgenic mice, simultaneously promotes Aβ generation and focal adhesion disruption by accelerating the endocytosis of APP and β1-integrin, respectively. Moreover, RanBP9 induces neurodegeneration <I>in vitro</I> and <I>in vivo</I> and mediates Aβ-induced neurotoxicity. Here we show in primary hippocampal neurons that RanBP9 potentiates Aβ-induced reactive oxygen species (ROS) overproduction, apoptosis, and calcium deregulation. Analyses of calcium-handling measures demonstrate that RanBP9 selectively delays the clearance of cytosolic Ca<SUP>2+</SUP> mediated by the mitochondrial calcium uniporter through a process involving the translocation of cofilin into mitochondria and oxidative mechanisms. Further, RanBP9 retards the anterograde axonal transport of mitochondria in primary neurons and decreases synaptic mitochondrial activity in brain. These data indicate that RanBP9, cofilin, and Aβ mimic and potentiate each other to produce mitochondrial dysfunction, ROS overproduction, and calcium deregulation, which leads to neurodegenerative changes reminiscent of those seen in AD.—Roh. S.-E., Woo, J. A., Lakshmana, M. K., Uhlar, C., Ankala, V., Boggess, T., Liu, T., Hong, Y.-H., Mook-Jung, I., Kim, S. J., Kang, D. E. Mitochondrial dysfunction and calcium deregulation by the RanBP9-cofilin pathway.</P>
3차원 마이크로 파이버 플랫폼 구현을 통한 심장세포 수축력 변이 모델링
구상모(Sangmo Koo),Zhen Ma,Nathaniel Huebsch,Mohammad A. Mandegar,Brian Siemons,Steven Boggess,Bruce R. Conklin,Costas P. Grigoropoulos,Kevin E. Healy 대한기계학회 2018 대한기계학회 춘추학술대회 Vol.2018 No.12
The integration of 3D artificial fibrous platform by advanced laser-based direct writing (two-photon polymerization), and human induced pluripotent stem cells (hiPSCs) allows us to measure the physiolocal phenotypes and recapitulation of diverse cardiac diseases. And additional genome editing technologies also make it possible to mimic the realistic disease pathologies. Based on those techniques, it was possible to create the patient-customized 3D platform by fabricating the 3D microscale fibrous structure which has similar mechanical properties such as stiffness for cardiac disease research. 3D cardiac tissues are anchored between two flexible cantilevers, contraction (and relaxation) force was measured by measuring fiber deflection. It is served as force sensor, and showed the tissue mechanical resistance to contraction can regulated by external microenvironments.