Publikationsserver der RWTH Aachen University
Untersuchungen zur Rolle von Neurozytokinen in Hirntumoren
Abstract
dc:descriptionCiliary Neurotrophic Factor (CNTF) and Interleukin-6 (IL-6) influence the survival and the differentiation of neuronal and glial cells. CNTF induces reactive transformation of astrocytes in vivo and has been shown to promote proliferation of neuronal tumor cell lines in vitro. Thus, CNTF is a candidate growth and/or differentiation factor for neuronal and glial tumors. Effects of neurocytokines are mediated trough specific receptor components. In this study the expression of CNTF and IL-6 and its specific receptor components in vivo and in vitro were analyzed. In the majority of the examined astrocytomas and glioblastomas prominent CNTF-R alpha mRNA expression was detected. Likewise, two of four glioblastoma cell lines expressed CNTF-R alpha. Quantitative analysis of the performed northern blots revealed no significant elevated CNTF-R alpha levels of the gliomas compared to the controls. Nevertheless, huge amounts of CNTF-R alpha that are expressed by certain tumors support the thesis that CNTF is involved in the complex process of transformation of astrocytomas. In vitro studies with various cell lines showed differential expression patterns of CNTF, CNTF-R alpha, IL-6 and IL-6R alpha. Stimulation of different neuro-ectodermal and muscle cell lines with rCNTF and rIL-6 induced expression of the transcription factor c-fos. Interestingly, in most cell lines a co-expression of CNTF and IL-6 and its receptors was measured. Thus, it appears reasonable to speculate that CNTF and IL-6 influence growth and differentiation in vitro and in vivo via an autocrine loop.
Degree
thesis:*- Grantor dc:publisher
- Publikationsserver der RWTH Aachen University
- Year dc:date
- 2001
Author and committee
dc:creator, dc:contributor.*- Author dc:creator
-
- Züchner, Stephan
- Contributors dc:contributor
-
- Weis, Joachim
Subjects
dc:subject × 2Rights
dc:rights- Statement dc:rights
-
- info:eu-repo/semantics/openAccess
- Language dc:language
- ger