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ß1-integrin-dependent migration of microglia in response to neuron-released α-synuclein.
Kim, Changyoun; Cho, Eun-Deok; Kim, Hyung-Koo; You, Sungyong; Lee, He-Jin; Hwang, Daehee; Lee, Seung-Jae.
Afiliación
  • Kim C; 1] Department of Biomedical Science and Technology, Konkuk University, Seoul, Korea [2] IBST, Konkuk University, Seoul, Korea.
  • Cho ED; Department of Anatomy, School of Medicine, Konkuk University, Seoul, Korea.
  • Kim HK; IBST, Konkuk University, Seoul, Korea.
  • You S; Samuel Oschin Comprehensive Cancer Institute, Cedars-Sinai Medical Center, Los Angeles, CA, USA.
  • Lee HJ; 1] IBST, Konkuk University, Seoul, Korea [2] Department of Anatomy, School of Medicine, Konkuk University, Seoul, Korea.
  • Hwang D; School of Interdisciplinary Bioscience and Bioengineering and Department of Chemical Engineering, POSTECH, Pohang, Kyoungbuk, Korea.
  • Lee SJ; 1] Department of Biomedical Science and Technology, Konkuk University, Seoul, Korea [2] IBST, Konkuk University, Seoul, Korea.
Exp Mol Med ; 46: e91, 2014 Apr 18.
Article en En | MEDLINE | ID: mdl-24743837
Chronic neuroinflammation is an integral pathological feature of major neurodegenerative diseases. The recruitment of microglia to affected brain regions and the activation of these cells are the major events leading to disease-associated neuroinflammation. In a previous study, we showed that neuron-released α-synuclein can activate microglia through activating the Toll-like receptor 2 (TLR2) pathway, resulting in proinflammatory responses. However, it is not clear whether other signaling pathways are involved in the migration and activation of microglia in response to neuron-released α-synuclein. In the current study, we demonstrated that TLR2 activation is not sufficient for all of the changes manifested by microglia in response to neuron-released α-synuclein. Specifically, the migration of and morphological changes in microglia, triggered by neuron-released α-synuclein, did not require the activation of TLR2, whereas increased proliferation and production of cytokines were strictly under the control of TLR2. Construction of a hypothetical signaling network using computational tools and experimental validation with various peptide inhibitors showed that ß1-integrin was necessary for both the morphological changes and the migration. However, neither proliferation nor cytokine production by microglia was dependent on the activation of ß1-integrin. These results suggest that ß1-integrin signaling is specifically responsible for the recruitment of microglia to the disease-affected brain regions, where neurons most likely release relatively high levels of α-synuclein.
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Texto completo: 1 Colección: 01-internacional Base de datos: MEDLINE Asunto principal: Movimiento Celular / Medios de Cultivo Condicionados / Microglía / Integrina beta1 / Alfa-Sinucleína / Neuronas Límite: Animals / Humans Idioma: En Revista: Exp Mol Med Asunto de la revista: BIOLOGIA MOLECULAR / BIOQUIMICA Año: 2014 Tipo del documento: Article Pais de publicación: Estados Unidos
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Texto completo: 1 Colección: 01-internacional Base de datos: MEDLINE Asunto principal: Movimiento Celular / Medios de Cultivo Condicionados / Microglía / Integrina beta1 / Alfa-Sinucleína / Neuronas Límite: Animals / Humans Idioma: En Revista: Exp Mol Med Asunto de la revista: BIOLOGIA MOLECULAR / BIOQUIMICA Año: 2014 Tipo del documento: Article Pais de publicación: Estados Unidos