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首页> 外文期刊>Journal of Cellular Physiology >Activation of Prn-p gene and stable transfection of Prn-p cDNA in leukemia MEL and neuroblastoma N2a cells increased production of PrP(C) but not prevented DNA fragmentation initiated by serum deprivation.
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Activation of Prn-p gene and stable transfection of Prn-p cDNA in leukemia MEL and neuroblastoma N2a cells increased production of PrP(C) but not prevented DNA fragmentation initiated by serum deprivation.

机译：激活Prn-p基因转染和稳定白血病的Prn-p cDNA梅尔和神经母细胞瘤N2a细胞生产PrP (C)但不增加阻止DNA碎片由血清剥夺。

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摘要

Prion protein (PrP(C)) via its isoform PrP(SC) is involved in the pathogenesis of transmissible spongiform encephalopathies (TSEs). We observed that murine erythroleukemia (MEL) cells arrested in phase G(1) undergo transcriptional activation of Prn-p gene. Here, we explored the potential role of activation of Prn-p gene and cytosolic accumulation of PrP(C) in growth arrest, differentiation, and apoptotic DNA fragmentation by stably transfecting MEL and N2a cells with Prn-p cDNA. Stably transfected MEL cells (clones # 6, 12, 20, 38, and 42) were assessed for growth and differentiation, while clones N2a13 and N2a8 of N2a cells for growth and apoptosis by flow cytometry using Annexin V and propidium iodide (PI). Our results indicate that (a) Induction of terminal differentiation of stably transfected MEL cells led to growth arrest, activation of Prn-p gene, concomitant expression of transfected Prn-p cDNA, suppression of bax gene, cytosolic accumulation of PrP(C), and DNA fragmentation. The latter was also induced in non-differentiated MEL cells growing under serum-free conditions; (b) similarly, serum deprivation promoted growth arrest, apoptosis/necrosis associated with DNA fragmentation in parental N2a and N2a13 cells that produced relative high level of PrP(C) and not PrP(SC). These data indicate that activation of Prn-p gene and expression of transfected Prn-p cDNA in cells of both hematopoietic and neuronal origin occurred concomitantly, and led to cytosolic accumulation of PrP(C) and DNA damage induced by serum deprivation. PrP(C) production failed to protect DNA fragmentation induced by serum deprivation. The question how does PrP(C) contribute to growth arrest and DNA fragmentation is discussed.
机译：朊蛋白(PrP (C))通过其同种型PrP (SC)参与传播的发病机制海绵状脑病(tse)。(MEL)小鼠红白血病细胞被捕在阶段G(1)进行转录激活Prn-p基因。角色Prn-p基因的激活和胞质积累的PrP (C)增长逮捕,分化和凋亡DNA碎片通过稳定使转染梅尔和N2a细胞Prn-p互补脱氧核糖核酸。# 6、12、20、38和增长42)进行了评估和分化,而克隆N2a13 N2a8N2a细胞生长和凋亡的流使用膜联蛋白V和碘化propidium血细胞计数(π)。稳定转染的终端分化梅尔·细胞导致生长逮捕、激活Prn-p基因,相伴的转染表达Prn-p cDNA、伯灵顿基因的抑制,胞质积累的PrP (C)和DNA碎片。后者也在non-differentiated诱导梅尔在无血清条件下细胞生长;(b)同样,血清剥夺促进增长逮捕,细胞凋亡/坏死与DNA相关联在父母的N2a和N2a13细胞分裂产生相对高水平的PrP (C)不是PrP (SC)。转染Prn-p Prn-p基因和表达互补脱氧核糖核酸在细胞的造血和神经起源与此同时发生,并导致胞质积累PrP (C)和DNA损伤引起血清剥夺。未能保护DNA碎片引起的血清剥夺。有助于增长逮捕和DNA碎片进行了探讨。

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