MTA-ELTE Laboratory of Molecular and Systems Neurobiology, Department of Physiology and Neurobiology, Hungarian Academy of Sciences and Eotvos Lorand University, Budapest, 1117, Hungary.
Department of Anatomy, Histology and Embryology, Semmelweis University, Budapest, 1094, Hungary.
Brain Struct Funct. 2020 Mar;225(2):639-667. doi: 10.1007/s00429-020-02026-5. Epub 2020 Jan 25.
The ketoglutarate dehydrogenase complex (KGDHC) consists of three different subunits encoded by OGDH (or OGDHL), DLST, and DLD, combined in different stoichiometries. DLD subunit is shared between KGDHC and pyruvate dehydrogenase complex, branched-chain alpha-keto acid dehydrogenase complex, and the glycine cleavage system. Despite KGDHC's implication in neurodegenerative diseases, cell-specific localization of its subunits in the adult human brain has never been investigated. Here, we show that immunoreactivity of all known isoforms of OGDHL, OGDH, and DLST was detected exclusively in neurons of surgical human cortical tissue samples identified by their morphology and visualized by double labeling with fluorescent Nissl, while being absent from glia expressing GFAP, Aldhl1, myelin basic protein, Olig2, or IBA1. In contrast, DLD immunoreactivity was evident in both neurons and glia. Specificity of anti-KGDHC subunits antisera was verified by a decrease in staining of siRNA-treated human cancer cell lines directed against the respective coding gene products; furthermore, immunoreactivity of KGDHC subunits in human fibroblasts co-localized > 99% with mitotracker orange, while western blotting of 63 post-mortem brain samples and purified recombinant proteins afforded further assurance regarding antisera monospecificity. KGDHC subunit immunoreactivity correlated with data from the Human Protein Atlas as well as RNA-Seq data from the Allen Brain Atlas corresponding to genes coding for KGDHC components. Protein lysine succinylation, however, was immunohistochemically evident in all cortical cells; this was unexpected, because this posttranslational modification requires succinyl-CoA, the product of KGDHC. In view of the fact that glia of the human brain cortex lack succinate-CoA ligase, an enzyme producing succinyl-CoA when operating in reverse, protein lysine succinylation in these cells must exclusively rely on propionate and/or ketone body metabolism or some other yet to be discovered pathway encompassing succinyl-CoA.
酮戊二酸脱氢酶复合物(KGDHC)由三个不同的亚基组成,分别由 OGDH(或 OGDHL)、DLST 和 DLD 编码,以不同的化学计量组合。DLD 亚基在 KGDHC 和丙酮酸脱氢酶复合物、支链α-酮酸脱氢酶复合物和甘氨酸裂解系统中共享。尽管 KGDHC 与神经退行性疾病有关,但它的亚基在成人大脑中的细胞特异性定位从未被研究过。在这里,我们显示所有已知的 OGDHL、OGDH 和 DLST 同工型的免疫反应性仅在手术人类皮质组织样本的神经元中被检测到,这些神经元通过其形态学进行识别,并通过与荧光 Nissl 双重标记进行可视化,而在表达 GFAP、Aldhl1、髓鞘碱性蛋白、Olig2 或 IBA1 的神经胶质中不存在。相比之下,DLD 免疫反应性在神经元和神经胶质中都很明显。抗 KGDHC 亚基抗血清的特异性通过针对各自编码基因产物的 siRNA 处理的人类癌细胞系染色减少得到验证;此外,人类成纤维细胞中 KGDHC 亚基的免疫反应性与 mitotracker orange 共定位 > 99%,而 63 个死后大脑样本和纯化的重组蛋白的 Western blot进一步保证了抗血清的单特异性。KGDHC 亚基免疫反应性与人类蛋白质图谱的数据以及与 KGDHC 成分编码基因相对应的艾伦大脑图谱的 RNA-Seq 数据相关。然而,蛋白质赖氨酸琥珀酰化在所有皮质细胞中都通过免疫组织化学得到证实;这是出乎意料的,因为这种翻译后修饰需要琥珀酰辅酶 A,而琥珀酰辅酶 A 是 KGDHC 的产物。鉴于人类大脑皮层的神经胶质缺乏琥珀酰辅酶 A 连接酶,当该酶在反转时产生琥珀酰辅酶 A,这些细胞中的蛋白质赖氨酸琥珀酰化必须完全依赖于丙酸盐和/或酮体代谢或其他尚未发现的包含琥珀酰辅酶 A 的途径。