Department of Physiology and Pennsylvania Muscle Institute, University of Pennsylvania School of Medicine, A-601 Richards Building, 3700 Hamilton Walk, Philadelphia, Pennsylvania 19104-6085, USA.
Brain Pathol. 2010 Mar;20(2):323-42. doi: 10.1111/j.1750-3639.2009.00275.x. Epub 2009 May 22.
Utrophin (Utrn) is the autosomal homolog of dystrophin, the Duchene Muscular Dystrophy (DMD) locus product and of therapeutic interest, as its overexpression can compensate dystrophin's absence. Utrn is transcribed by Utrn-A and -B promoters with mRNAs differing at their 5' ends. However, previous central nervous system (CNS) studies used C-terminal antibodies recognizing both isoforms. As this distinction may impact upregulation strategies, we generated Utrn-A and -B promoter-specific antibodies, Taqman Polymerase chain reaction (PCR)-based absolute copy number assays, and luciferase-reporter constructs to study CNS of normal and dystrophic mdx mice. Differential expression of Utrn-A and -B was noted in microdissected and capillary-enriched fractions. At the protein level, Utrn-B was predominantly expressed in vasculature and ependymal lining, whereas Utrn-A was expressed in neurons, astrocytes, choroid plexus and pia mater. mRNA quantification demonstrated matching patterns of differential expression; however, transcription-translation mismatch was noted for Utrn-B in caudal brain regions. Utrn-A and Utrn-B proteins were significantly upregulated in olfactory bulb and cerebellum of mdx brain. Differential promoter activity, mRNA and protein expressions were studied in cultured C2C12, bEnd3, neurons and astrocytes. Promoter activity ranking for Utrn-A and -B was neurons > astrocytes > C2C12 > bEnd3 and bEnd3 > astrocytes > neurons > C2C12, respectively. Our results identify promoter usage patterns for therapeutic targeting and define promoter-specific differential distribution of Utrn isoforms in normal and dystrophic CNS.
肌萎缩侧索硬化症(DMD)基因产物肌营养不良蛋白(dystrophin)的常染色体同源物 utrophin(Utrn)是治疗的靶点,因为其过表达可以补偿肌营养不良蛋白的缺失。Utrn 由 Utrn-A 和 -B 启动子转录,其 mRNAs 在 5' 端不同。然而,之前的中枢神经系统(CNS)研究使用识别两种同工型的 C 末端抗体。由于这种区别可能会影响上调策略,我们生成了 Utrn-A 和 -B 启动子特异性抗体、Taqman 聚合酶链反应(PCR)基于绝对拷贝数测定法、以及荧光素酶报告基因构建体,以研究正常和肌营养不良症 mdx 小鼠的 CNS。在微切割和毛细血管富集的部分中观察到 Utrn-A 和 -B 的差异表达。在蛋白质水平上,Utrn-B 主要在血管和室管膜衬里中表达,而 Utrn-A 则在神经元、星形胶质细胞、脉络丛和软脑膜中表达。mRNA 定量显示出匹配的差异表达模式;然而,在尾状核脑区观察到 Utrn-B 的转录-翻译不匹配。Utrn-A 和 Utrn-B 蛋白在 mdx 脑的嗅球和小脑显著上调。在培养的 C2C12、bEnd3、神经元和星形胶质细胞中研究了差异启动子活性、mRNA 和蛋白质表达。Utrn-A 和 -B 的启动子活性排名分别为神经元>星形胶质细胞>C2C12>bEnd3 和 bEnd3>星形胶质细胞>神经元>C2C12。我们的结果确定了治疗靶向的启动子使用模式,并定义了正常和肌营养不良性 CNS 中 Utrn 同工型的启动子特异性差异分布。