Gajavelli Shyam, Castellanos Daniel A, Furmanski Orion, Schiller Paul C, Sagen Jacqueline
The Miami Project to Cure Paralysis, University of Miami Miller School of Medicine, Miami, FL 33136, USA.
Cell Transplant. 2008;17(4):445-55.
Cell-based therapy for neuropathic pain could provide analgesics to local pain modulatory regions in a sustained, renewable fashion. In order to provide enhanced analgesic efficacy, transplantable cells may be engineered to produce complementary or increased levels of analgesic peptides. In addition, genetic labeling of modified cells is desirable for identification and tracking, but it should be retained intracellularly as desired analgesic peptides are secreted. Usually constructs encode proteins destined for either extra- or intracellular compartments, as these pathways do not cross. However, interactions between intracellular destinations provide a window of opportunity to overcome this limitation. In this report, we have explored this approach using a potential supplementary analgesic peptide, [Ser1]-histogranin (SHG), the stable synthetic derivative of a naturally occurring peptide with N-methyl D-aspartate (NMDA) antagonistic properties. A synthetic SHG gene was combined with (i) nerve growth factor-beta (NGF-beta) amino-terminal signal peptide to enable secretion, and (ii) a fluorescent cellular label (mRFP) with intervening cathepsin L cleavage site, and subcloned into a lentiviral vector. In addition, an endoplasmic retention signal, KDEL, was added to enable retrieval of mRFP. Using immunocytochemistry and confocal microscopic profile analysis, cells transduced by such lentiviruses were shown to synthesize a single SHG-mRFP polypeptide that was processed, targeted to expected subcellular destinations in several cell types. Dot blot and Western analysis revealed stable transduction and long-term secretion of SHG from PC12 cells in vitro. Transplantation of such cells provided modest analgesia in a rodent pain model consistent with low levels of SHG peptide in the cerebrospinal fluid (CSF). These results suggest that it is possible to deliver proteins with different final destinations from a single construct, such as pharmacologically active peptide for secretion and intracellular label for identifying transplantable cells.
基于细胞的神经性疼痛治疗方法能够以持续、可再生的方式为局部疼痛调节区域提供镇痛药物。为了提高镇痛效果,可对可移植细胞进行改造,使其产生互补或更高水平的镇痛肽。此外,对改造后的细胞进行基因标记有助于识别和追踪,但由于所需的镇痛肽会分泌出来,因此该标记应保留在细胞内。通常构建体编码的蛋白质 destined for either extra- or intracellular compartments,因为这些途径不会交叉。然而,细胞内目的地之间的相互作用提供了一个克服这一限制的机会窗口。在本报告中,我们使用一种潜在的补充镇痛肽[Ser1]-组织颗粒蛋白(SHG)探索了这种方法,SHG 是一种具有 N-甲基-D-天冬氨酸(NMDA)拮抗特性的天然肽的稳定合成衍生物。将合成的 SHG 基因与(i)神经生长因子-β(NGF-β)氨基末端信号肽结合以实现分泌,以及(ii)带有中间组织蛋白酶 L 切割位点的荧光细胞标记(mRFP),并亚克隆到慢病毒载体中。此外,添加了内质网保留信号 KDEL 以实现 mRFP 的回收。使用免疫细胞化学和共聚焦显微镜轮廓分析,显示由这种慢病毒转导的细胞合成了一种单一的 SHG-mRFP 多肽,该多肽经过加工,靶向几种细胞类型中预期的亚细胞目的地。斑点印迹和 Western 分析显示体外 PC12 细胞中 SHG 的稳定转导和长期分泌。在啮齿动物疼痛模型中,移植此类细胞可提供适度的镇痛作用,这与脑脊液(CSF)中低水平的 SHG 肽一致。这些结果表明,从单个构建体中递送具有不同最终目的地的蛋白质是可能的,例如用于分泌的药理活性肽和用于识别可移植细胞的细胞内标记。