Mishra Manjari, Paunesku Tatjana, Woloschak Gayle E, Siddique Teepu, Zhu Lihua Julie, Lin Simon, Greco Kristin, Bigio Eileen H
Cognitive Neurology and Alzheimer Disease Center, Northwestern University, Feinberg School of Medicine, 320 East Superior St, Chicago, IL, 60611, USA.
Acta Neuropathol. 2007 Jul;114(1):81-94. doi: 10.1007/s00401-007-0240-7. Epub 2007 Jun 14.
Neurodegenerative disorders share a process of aggregation of insoluble protein. Frontotemporal lobar degeneration with ubiquitinated inclusions (FTLD-U) is characterized by the presence of ubiquitin and TDP-43 positive aggregates which are likely related to specific gene expression profiles. We carried out gene expression microarray analysis on post-mortem brain tissue from FTLD-U, FTLD-MND, and controls. Using total RNA from carefully dissected frontal cortical layer II, we obtained gene expression profiles showing that FTLD-U and controls differ in over 100 networks, including those involved in synapse formation, the ubiquitin-proteasome system, endosomal sorting, and apoptosis. We performed qRT-PCR validation for three genes, representative of three different networks. Dynein axonemal light intermediate chain 1 (DNALI1) (microtubule/cytoskeleton network associated) expression was 3-fold higher and myeloid differentiation primary response gene 88 (MYD88) (signal transduction network) was 3.3 times higher in FTLD-U than FTLD-MND and controls; annexin A2 (ANXA2) (endosomal sorting) expression was 11.3-fold higher in FTLD-U than FTLD-MND and 2.3-fold higher than controls. The identification of progranulin (PGRN) gene mutations and TDP-43 as the major protein component of the ubiquitinated inclusions, are two recent landmark discoveries in the field of FTLD-U. We found 1.5-fold increase in TDP-43 in both FTLD-MND and FTLD-U while progranulin showed no gene expression differences between controls and FTLD-MND. However, one of the FTLD-U cases tested by Affymetrix microarray showed "absence call" of this transcript, suggesting absent or decreased gene expression. Our findings point to specific gene-linked-pathways which may be influenced by neurodegenerative disease process and may be targeted for further exploration.
神经退行性疾病具有不溶性蛋白质聚集的过程。伴有泛素化包涵体的额颞叶变性(FTLD-U)的特征是存在泛素和TDP-43阳性聚集物,这可能与特定的基因表达谱有关。我们对FTLD-U、FTLD-MND患者的死后脑组织以及对照组进行了基因表达微阵列分析。使用从仔细解剖的额叶皮质第二层获得的总RNA,我们得到了基因表达谱,显示FTLD-U与对照组在100多个网络中存在差异,包括那些参与突触形成、泛素-蛋白酶体系统、内体分选和细胞凋亡的网络。我们对代表三个不同网络的三个基因进行了qRT-PCR验证。动力蛋白轴丝轻中间链1(DNALI1)(与微管/细胞骨架网络相关)在FTLD-U中的表达比FTLD-MND和对照组高3倍,髓样分化初级反应基因88(MYD88)(信号转导网络)在FTLD-U中的表达比FTLD-MND和对照组高3.3倍;膜联蛋白A2(ANXA2)(内体分选)在FTLD-U中的表达比FTLD-MND高11.3倍,比对照组高2.3倍。原颗粒蛋白(PGRN)基因突变的鉴定以及TDP-43作为泛素化包涵体的主要蛋白质成分,是FTLD-U领域最近的两项标志性发现。我们发现FTLD-MND和FTLD-U中的TDP-43均增加了1.5倍,而原颗粒蛋白在对照组和FTLD-MND之间未显示出基因表达差异。然而,通过Affymetrix微阵列检测的一个FTLD-U病例显示该转录本“缺失信号”,表明基因表达缺失或降低。我们的研究结果指出了特定的基因相关途径,这些途径可能受到神经退行性疾病过程的影响,可能成为进一步探索的目标。