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Synthetic Prion Peptide 106-126 Resulted in an Increase Matrix Metalloproteinases and Inflammatory Cytokines from Rat Astrocytes and Microglial Cells
It has been shown that the accumulation of prion in the cytoplasm can result in neurodegenerative disorders. Synthetic prion peptide 106-126 (PrP) is a glycoprotein that is expressed predominantly by neurons and other cells, including glial cells. Prion-induced chronic neurodegeneration has a substa...
Autores principales: | , , , , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
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The Korean Society of Toxicology
2012
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3834397/ https://www.ncbi.nlm.nih.gov/pubmed/24278583 http://dx.doi.org/10.5487/TR.2012.28.1.005 |
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author | Song, Kibbeum Na, Ji-Young Oh, Myung-Hoon Kim, Sokho Kim, Young-Ha Park, Byung-Yong Shin, Gi-Wook Kim, Bumseok You, Myungjo Kwon, Jungkee |
author_facet | Song, Kibbeum Na, Ji-Young Oh, Myung-Hoon Kim, Sokho Kim, Young-Ha Park, Byung-Yong Shin, Gi-Wook Kim, Bumseok You, Myungjo Kwon, Jungkee |
author_sort | Song, Kibbeum |
collection | PubMed |
description | It has been shown that the accumulation of prion in the cytoplasm can result in neurodegenerative disorders. Synthetic prion peptide 106-126 (PrP) is a glycoprotein that is expressed predominantly by neurons and other cells, including glial cells. Prion-induced chronic neurodegeneration has a substantial inflammatory component, and an increase in the levels of matrix metalloproteinases (MMPs) may play an important role in neurodegenerative development and progression. However, the expression of MMPs in PrP induced rat astrocytes and microglia has not yet been compared. Thus, in this study, we examined the fluorescence intensity of CD11b positive microglia and Glial Fibrillary Acidic Protein (GFAP) positive astrocytes and found that the fluorescent intensity was increased following incubation with PrP at 24 hours in a dose-dependent manner. We also observed an increase in interleukin-1 beta (IL-1β) and tumor necrosis factor alpha (TNF-α) protein expression, which are initial inflammatory cytokines, in both PrP induced astrocytes and microglia. Furthermore, an increase MMP-1, 3 and 11 expressions in PrP induced astrocytes and microglia was observed by real time PCR. Our results demonstrated PrP induced activation of astrocytes and microglia respectively, which resulted in an increase in inflammatory cytokines and MMPs expression. These results provide the insight into the different sensitivities of glial cells to PrP. |
format | Online Article Text |
id | pubmed-3834397 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2012 |
publisher | The Korean Society of Toxicology |
record_format | MEDLINE/PubMed |
spelling | pubmed-38343972013-11-25 Synthetic Prion Peptide 106-126 Resulted in an Increase Matrix Metalloproteinases and Inflammatory Cytokines from Rat Astrocytes and Microglial Cells Song, Kibbeum Na, Ji-Young Oh, Myung-Hoon Kim, Sokho Kim, Young-Ha Park, Byung-Yong Shin, Gi-Wook Kim, Bumseok You, Myungjo Kwon, Jungkee Toxicol Res Articles It has been shown that the accumulation of prion in the cytoplasm can result in neurodegenerative disorders. Synthetic prion peptide 106-126 (PrP) is a glycoprotein that is expressed predominantly by neurons and other cells, including glial cells. Prion-induced chronic neurodegeneration has a substantial inflammatory component, and an increase in the levels of matrix metalloproteinases (MMPs) may play an important role in neurodegenerative development and progression. However, the expression of MMPs in PrP induced rat astrocytes and microglia has not yet been compared. Thus, in this study, we examined the fluorescence intensity of CD11b positive microglia and Glial Fibrillary Acidic Protein (GFAP) positive astrocytes and found that the fluorescent intensity was increased following incubation with PrP at 24 hours in a dose-dependent manner. We also observed an increase in interleukin-1 beta (IL-1β) and tumor necrosis factor alpha (TNF-α) protein expression, which are initial inflammatory cytokines, in both PrP induced astrocytes and microglia. Furthermore, an increase MMP-1, 3 and 11 expressions in PrP induced astrocytes and microglia was observed by real time PCR. Our results demonstrated PrP induced activation of astrocytes and microglia respectively, which resulted in an increase in inflammatory cytokines and MMPs expression. These results provide the insight into the different sensitivities of glial cells to PrP. The Korean Society of Toxicology 2012-03 /pmc/articles/PMC3834397/ /pubmed/24278583 http://dx.doi.org/10.5487/TR.2012.28.1.005 Text en Copyright ©2012, The Korean Society of Toxicology |
spellingShingle | Articles Song, Kibbeum Na, Ji-Young Oh, Myung-Hoon Kim, Sokho Kim, Young-Ha Park, Byung-Yong Shin, Gi-Wook Kim, Bumseok You, Myungjo Kwon, Jungkee Synthetic Prion Peptide 106-126 Resulted in an Increase Matrix Metalloproteinases and Inflammatory Cytokines from Rat Astrocytes and Microglial Cells |
title | Synthetic Prion Peptide 106-126 Resulted in an Increase Matrix Metalloproteinases and Inflammatory Cytokines from Rat Astrocytes and Microglial Cells |
title_full | Synthetic Prion Peptide 106-126 Resulted in an Increase Matrix Metalloproteinases and Inflammatory Cytokines from Rat Astrocytes and Microglial Cells |
title_fullStr | Synthetic Prion Peptide 106-126 Resulted in an Increase Matrix Metalloproteinases and Inflammatory Cytokines from Rat Astrocytes and Microglial Cells |
title_full_unstemmed | Synthetic Prion Peptide 106-126 Resulted in an Increase Matrix Metalloproteinases and Inflammatory Cytokines from Rat Astrocytes and Microglial Cells |
title_short | Synthetic Prion Peptide 106-126 Resulted in an Increase Matrix Metalloproteinases and Inflammatory Cytokines from Rat Astrocytes and Microglial Cells |
title_sort | synthetic prion peptide 106-126 resulted in an increase matrix metalloproteinases and inflammatory cytokines from rat astrocytes and microglial cells |
topic | Articles |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3834397/ https://www.ncbi.nlm.nih.gov/pubmed/24278583 http://dx.doi.org/10.5487/TR.2012.28.1.005 |
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