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Mol. Cells 2013; 36(3): 245-251

Published online August 7, 2013

https://doi.org/10.1007/s10059-013-0137-3

© The Korean Society for Molecular and Cellular Biology

Involvement of CD137 Ligand Signaling in Neural Stem Cell Death

Chang Ho Yun, Hye Myeong Lee, Sang Chul Lee, Byung Sam Kim, Jeong Woo Park, and Byung Ju Lee

Department of Biological Sciences, College of Natural Sciences, University of Ulsan, Ulsan 680-749, Korea, 1Personalized Medicine System R&D Center, Bio-support Co., Ltd, Anyang 431-810, Korea

Received: May 2, 2013; Revised: June 25, 2013; Accepted: June 26, 2013

Abstract

CD137 is a member of the tumor necrosis factor/nerve growth factor receptor superfamily. Interaction of CD137 with its ligand (CD137L) affects the apoptosis, proliferation and differentiation of immune cells. Interestingly, the CD137 receptor/ligand system involves the bi-directional transduction of signals. The expression of CD137 and its ligand is not restricted to immune organs, but can also be detected in a wide variety of tissues such as the brain, kidney, lung and heart. However, its role in brain is largely unknown. This study was performed to determine the role of CD137L reverse signaling in the apoptosis of neural stem cells. We identified the expression of CD137 and its ligand in C17.2 neural stem cells derived from mouse embryonic cerebellum. We found that the activation of CD137L reverse signaling by CD137 resulted in a decrease in cell adhesion to the fibronectin-coated culture basement, thus causing detachment-induced cell death. Furthermore, we showed that the cell death induced by CD137 was completely ameliorated by integrin activators and caspase inhibitors. Therefore we suggest that CD137L reverse signaling exerts a pro-apoptotic effect by suppressing integrinmediated survival signals in neural stem cells.

Keywords anoikis, CD137L reverse signal, cell adhesion, integrin-fibronectin interaction, neural stem cells

Article

Research Article

Mol. Cells 2013; 36(3): 245-251

Published online September 30, 2013 https://doi.org/10.1007/s10059-013-0137-3

Copyright © The Korean Society for Molecular and Cellular Biology.

Involvement of CD137 Ligand Signaling in Neural Stem Cell Death

Chang Ho Yun, Hye Myeong Lee, Sang Chul Lee, Byung Sam Kim, Jeong Woo Park, and Byung Ju Lee

Department of Biological Sciences, College of Natural Sciences, University of Ulsan, Ulsan 680-749, Korea, 1Personalized Medicine System R&D Center, Bio-support Co., Ltd, Anyang 431-810, Korea

Received: May 2, 2013; Revised: June 25, 2013; Accepted: June 26, 2013

Abstract

CD137 is a member of the tumor necrosis factor/nerve growth factor receptor superfamily. Interaction of CD137 with its ligand (CD137L) affects the apoptosis, proliferation and differentiation of immune cells. Interestingly, the CD137 receptor/ligand system involves the bi-directional transduction of signals. The expression of CD137 and its ligand is not restricted to immune organs, but can also be detected in a wide variety of tissues such as the brain, kidney, lung and heart. However, its role in brain is largely unknown. This study was performed to determine the role of CD137L reverse signaling in the apoptosis of neural stem cells. We identified the expression of CD137 and its ligand in C17.2 neural stem cells derived from mouse embryonic cerebellum. We found that the activation of CD137L reverse signaling by CD137 resulted in a decrease in cell adhesion to the fibronectin-coated culture basement, thus causing detachment-induced cell death. Furthermore, we showed that the cell death induced by CD137 was completely ameliorated by integrin activators and caspase inhibitors. Therefore we suggest that CD137L reverse signaling exerts a pro-apoptotic effect by suppressing integrinmediated survival signals in neural stem cells.

Keywords: anoikis, CD137L reverse signal, cell adhesion, integrin-fibronectin interaction, neural stem cells

Mol. Cells
Nov 30, 2023 Vol.46 No.11, pp. 655~725
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Kim et al. (pp. 710-724) demonstrated that a pathogen-derived Ralstonia pseudosolanacearum type III effector RipL delays flowering time and enhances susceptibility to bacterial infection in Arabidopsis thaliana. Shown is the RipL-expressing Arabidopsis plant, which displays general dampening of the transcriptional program during pathogen infection, grown in long-day conditions.

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