Prion diseases are infectious and fatal neurodegenerative diseases.The pathogenic agent is an abnormal prion protein aggregate.Microglial activation in the centre nervous system is a characteristic feature of prion di...Prion diseases are infectious and fatal neurodegenerative diseases.The pathogenic agent is an abnormal prion protein aggregate.Microglial activation in the centre nervous system is a characteristic feature of prion disease.In this study,we examined the effect of PrP 106-126 on PrP mRNA gene expression in Mouse microglia cells BV-2 by real-time quantitative PCR.PrP mRNA expression level was found to be significantly increased after 18 h exposure of BV-2 cells to PrP 106-126,with 3-fold increase after 18 h and 4.5-fold increase after 24 h and BV-2 cells proliferating occurred correspondingly.Our results provide the first in vitro evidence of the increase of PrP mRNA levels in microglial cells exposed to PrP 106-126,and indicate that microglial cells might play a critical role in prion pathogenesis.展开更多
Astrogliosis is a hallmark of prion disease, but the metabolic alterations of astrocytes remain poorly documented. A synthetic peptide corresponding to amino acid 106―126 of the human prion protein (PrP) has been sho...Astrogliosis is a hallmark of prion disease, but the metabolic alterations of astrocytes remain poorly documented. A synthetic peptide corresponding to amino acid 106―126 of the human prion protein (PrP) has been shown to be toxic to neurons. In this study, the effects of PrP 106―126 on astrocytes were investigated in vitro. The proliferation of astrocytes was significantly (P < 0.05) increased when grown in media conditioned with PrP 106―126 (80 μmol/L) from microglia. The expression of laminin (LN) and fibronectin (FN) was examined at both mRNA and protein levels. The results showed that ex- posure of astrocytes to PrP 106―126 enhanced the expression of LN and FN. The increase of FN in astrocyte cultures required cytokines previously released by activated microglia. This study reveals the expression of LN and FN affected by PrP106―126.展开更多
基金National Natural Science Foundations ofChina (30871854)National Science and Technology Supporting Program of China (2006BAD06A13)
文摘Prion diseases are infectious and fatal neurodegenerative diseases.The pathogenic agent is an abnormal prion protein aggregate.Microglial activation in the centre nervous system is a characteristic feature of prion disease.In this study,we examined the effect of PrP 106-126 on PrP mRNA gene expression in Mouse microglia cells BV-2 by real-time quantitative PCR.PrP mRNA expression level was found to be significantly increased after 18 h exposure of BV-2 cells to PrP 106-126,with 3-fold increase after 18 h and 4.5-fold increase after 24 h and BV-2 cells proliferating occurred correspondingly.Our results provide the first in vitro evidence of the increase of PrP mRNA levels in microglial cells exposed to PrP 106-126,and indicate that microglial cells might play a critical role in prion pathogenesis.
基金Supported by the National Natural Science Foundation of China (Grant No. 30571399)the National Basic Research Program of China (Grant No. 2005CB523000)
文摘Astrogliosis is a hallmark of prion disease, but the metabolic alterations of astrocytes remain poorly documented. A synthetic peptide corresponding to amino acid 106―126 of the human prion protein (PrP) has been shown to be toxic to neurons. In this study, the effects of PrP 106―126 on astrocytes were investigated in vitro. The proliferation of astrocytes was significantly (P < 0.05) increased when grown in media conditioned with PrP 106―126 (80 μmol/L) from microglia. The expression of laminin (LN) and fibronectin (FN) was examined at both mRNA and protein levels. The results showed that ex- posure of astrocytes to PrP 106―126 enhanced the expression of LN and FN. The increase of FN in astrocyte cultures required cytokines previously released by activated microglia. This study reveals the expression of LN and FN affected by PrP106―126.
