Institute of Immunology and Microbiology, First Faculty of Medicine, Charles University in Prague, Prague, Czech Republic.
PLoS One. 2011;6(9):e24599. doi: 10.1371/journal.pone.0024599. Epub 2011 Sep 2.
Prion diseases have been observed to deregulate the transcription of erythroid genes, and prion protein knockout mice have demonstrated a diminished response to experimental anemia. To investigate the role of the cellular prion protein (PrP(C)) in erythropoiesis, we studied the protein's expression on mouse erythroid precursors in vivo and utilized an in vitro model of the erythroid differentiation of murine erythroleukemia cells (MEL) to evaluate the effect of silencing PrP(C) through RNA interference.The expression of PrP(C) and selected differentiation markers was analyzed by quantitative multicolor flow cytometry, western blot analysis and quantitative RT-PCR. The silencing of PrP(C) expression in MEL cells was achieved by expression of shRNAmir from an integrated retroviral vector genome. The initial upregulation of PrP(C) expression in differentiating erythroid precursors was detected both in vivo and in vitro, suggesting PrP(C)'s importance to the early stages of differentiation. The upregulation was highest on early erythroblasts (16200±3700 PrP(C) / cell) and was followed by the gradual decrease of PrP(C) level with the precursor's maturation reaching 470±230 PrP(C) / cell on most mature CD71(-)Ter119(+) small precursors. Interestingly, the downregulation of PrP(C) protein with maturation of MEL cells was not accompanied by the decrease of PrP mRNA. The stable expression of anti-Prnp shRNAmir in MEL cells led to the efficient (>80%) silencing of PrP(C) levels. Cell growth, viability, hemoglobin production and the transcription of selected differentiation markers were not affected by the downregulation of PrP(C).In conclusion, the regulation of PrP(C) expression in differentiating MEL cells mimics the pattern detected on mouse erythroid precursors in vivo. Decrease of PrP(C) protein expression during MEL cell maturation is not regulated on transcriptional level. The efficient silencing of PrP(C) levels, despite not affecting MEL cell differentiation, enables created MEL lines to be used for studies of PrP(C) cellular function.
朊病毒疾病已被观察到会使红细胞基因的转录失调,而朊病毒蛋白敲除小鼠表现出对实验性贫血的反应减弱。为了研究细胞朊病毒蛋白(PrP(C)) 在红细胞生成中的作用,我们研究了体内小鼠红细胞前体中该蛋白的表达,并利用体外小鼠红白血病细胞(MEL)的红细胞分化模型来评估通过 RNA 干扰沉默 PrP(C) 的效果。通过定量多色流式细胞术、western blot 分析和定量 RT-PCR 分析 PrP(C) 和选定的分化标志物的表达。通过整合逆转录病毒载体基因组中的 shRNAmir 表达来实现 MEL 细胞中 PrP(C) 表达的沉默。在体内和体外均检测到分化中的红细胞前体中 PrP(C) 表达的初始上调,表明 PrP(C) 对分化的早期阶段很重要。在早期红细胞(16200±3700 PrP(C) / 细胞)中检测到上调最高,随后随着前体的成熟,PrP(C) 水平逐渐降低,在大多数成熟的 CD71(-)Ter119(+)小前体上达到 470±230 PrP(C) / 细胞。有趣的是,MEL 细胞成熟时 PrP(C) 蛋白的下调并没有伴随着 PrP mRNA 的减少。MEL 细胞中抗 Prnp shRNAmir 的稳定表达导致 PrP(C) 水平的有效(>80%)沉默。下调 PrP(C) 不会影响细胞生长、活力、血红蛋白生成和选定分化标志物的转录。总之,MEL 细胞分化过程中 PrP(C) 表达的调节模式与体内小鼠红细胞前体中检测到的模式相似。MEL 细胞成熟过程中 PrP(C) 蛋白表达的减少不受转录水平的调节。尽管下调 PrP(C) 水平不会影响 MEL 细胞分化,但能够使创建的 MEL 系用于研究 PrP(C) 细胞功能。