星形胶质细胞增生是朊病毒病早期的主要病理学特征。PrP106-126(prion protein peptide106-126)具神经毒性,导致星形胶质细胞增生。层黏连蛋白(laminin,LN)和纤黏连蛋白(fibronectin,FN)是星形胶质细胞胞外基质的主要成分。利用PrP106-...星形胶质细胞增生是朊病毒病早期的主要病理学特征。PrP106-126(prion protein peptide106-126)具神经毒性,导致星形胶质细胞增生。层黏连蛋白(laminin,LN)和纤黏连蛋白(fibronectin,FN)是星形胶质细胞胞外基质的主要成分。利用PrP106-126和PrP106-126制备的小胶质条件培养基(conditioned medium from microglia,MiCM)分别作用于体外培养的星形胶质细胞,应用RT-PCR和Westernblot技术探讨PrP106-126对星形胶质细胞的增殖及其胞内LN、FN表达的影响。试验分为5个处理(空白对照、Scr对照、PrP106-126、MiCM、MiCMPrP106-126)。结果表明,PrP106-126可促进星形胶质细胞增殖、LN和FN的表达,但促增殖和FN表达作用有赖于活化小胶质细胞细胞因子的共同参与。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
文摘星形胶质细胞增生是朊病毒病早期的主要病理学特征。PrP106-126(prion protein peptide106-126)具神经毒性,导致星形胶质细胞增生。层黏连蛋白(laminin,LN)和纤黏连蛋白(fibronectin,FN)是星形胶质细胞胞外基质的主要成分。利用PrP106-126和PrP106-126制备的小胶质条件培养基(conditioned medium from microglia,MiCM)分别作用于体外培养的星形胶质细胞,应用RT-PCR和Westernblot技术探讨PrP106-126对星形胶质细胞的增殖及其胞内LN、FN表达的影响。试验分为5个处理(空白对照、Scr对照、PrP106-126、MiCM、MiCMPrP106-126)。结果表明,PrP106-126可促进星形胶质细胞增殖、LN和FN的表达,但促增殖和FN表达作用有赖于活化小胶质细胞细胞因子的共同参与。
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.