| In 1993 GDNF was purified and cloned as one of neurotrophic factors and it can specially promote the survival of midbrain dopaminerigic neurons. After finding GDNF, which is structurally a new distant member of transforming growth factor ?(TGF- {3 )family, quantities of experiments were carried on mostly concentrated in the upregulations of it to a variety of neurons, and have achieved a lot. By now the molecular structure, genie location, genie expression, biological activity and receptors about GDNF have been studied deeply, and experiments using animal models have disclosed treatment of the diseases related to degradation, injury of neurons. Some researchers investigated on the relations between GDNF some tumors, such as Wilms tumor, pancreatic cancer, leukemia, thyroid carcinoma,as well as the research on expression of GDNF in humangliomas, but all did not refer the variation of GDNF in tumors which were different in malignancy. The study on its receptor GDNFRa-1 was a little later than GDNF. Many scholars found GDNF produced a marked effect through binding the special receptor compoud (GDNFRa-l and RET protein) and activating a certain signal transmission pathway. But it is unknown what mechanism GDNF binds these two different receptors by and then what signal transmission pathway is activated. To make sure these problems the research of receptor is important. With the factor GDNF the experiments of receptor was carried out gradually and deeply. By now, we have achieved a lot about this kind of factor which was found as a special neurotrophic of dopaminergic neuron, and have extended beyond the affection only to neurons at the first. We respectively examined the expression of GDNF and GDNFRa-1 in normal human brain and different-grade gliomas tissue using three methods: in situ hybridization, immuohistochmistry, flow cytometry. We found there were significant relations between the two factors and provided new valuable cues to study them more deeply.In the first experiment we examined GDNFmRNA and GDNFRa-1 mRNA using in situ hybridization. We have known that gene was first tanscripted into messengerribonucleicacid(mRNA ) and then translated into a certain protein during the course of gene expression. We designed the experiment to initially deduce the relation between the two biological proteins and human brain gliomas by observing expressions of GDNFmRNA and GDNFRa-1 mRNA from the translation level and cued how GDNF and its receptor GDNFRa-1functioned. First using the specific probe to bind GDNFmRNA and GDNFRa-1 mRNA existing in normal brain tissues (NBT) and gliomas, then the hybridized body were colored by immunoenzyme method in order to observe the distributions of positive hybridization signals in NBT(20 cases ) and gliomas(59 . cases ). It was shown that positive signals were detected out in both NBT and gliomas, but the positive rate in tumors were remarkably higher than NBT and that will heighten with increasing malignancy of gliomas (The differentiation is not evident between I and III5.) .The variant expressions of GDNFmRNA and GDNFRa-1 mRN A reflected the differentiation of gliomas malignancy. We can suspect the same expression tendency for the protein GDNF and GDNFRa-1. The course from a certain gene into a certain protein was influenced by a lot of events, messenger RNA were not always translated into proteins, and messenger RNA may not parallel with their proteins. Then do expressions of GDNF and GDNFRa-1 reflect this changement, too? We will proceed with the next two parts to find more evidences to confirm it by examining them directly.In the second experiment, according to the immunology principle, using SABC method and specific anti-human GDNF and anti-human GDNFRa-1 to*bind the protein GDNF and GDNFRa-1 probably existing in gliomas cells, then using the sensitive labeling antibody(the second antibody) to bind the first antibody and coloring the antigen-antibody complex by same immunoenzyme method, we detected these two factors in NBT and tumor tissues the same to experimen...
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