Gruber H E, Koenker R, Luchtman L A, Willis R C, Seegmiller J E
Proc Natl Acad Sci U S A. 1985 Oct;82(19):6662-6. doi: 10.1073/pnas.82.19.6662.
Immunofluorescently labeled glial cells are shown by radioautography to metabolically cooperate with hypoxanthine phosphoribosyltransferase-deficient fibroblasts. The observations of cooperation without cell contact and of incorporation gradients around the glial cells suggest that cooperation occurs through extracellular transport of radiolabeled purine compounds. The transfer of radiolabeled adenine, adenosine, or methylthioadeninosine is supported by the quantitative loss of cooperation when the recipient cell is also deficient in enzymes required for adenine or adenosine salvage. The demonstration of glial cell cooperation provides impetus for current research toward gene replacement therapy for the neurologic symptoms of the Lesch-Nyhan syndrome.
放射自显影显示，免疫荧光标记的神经胶质细胞与次黄嘌呤磷酸核糖基转移酶缺陷的成纤维细胞在代谢上存在协作。无细胞接触时的协作观察以及神经胶质细胞周围的掺入梯度表明，协作是通过放射性标记嘌呤化合物的细胞外转运发生的。当受体细胞也缺乏腺嘌呤或腺苷补救所需的酶时，协作定量减少，这支持了放射性标记腺嘌呤、腺苷或甲硫基腺苷的转移。神经胶质细胞协作的证明为目前针对莱施-奈恩综合征神经症状的基因替代疗法的研究提供了动力。
