Increased capillary permeability in rat brain induced by factors secreted by cultured C6 glioma cells: role in peritumoral brain edema

1991 ◽  
Vol 10 (1) ◽  
pp. 13-25 ◽  
Author(s):  
Takanori Ohnishil ◽  
Peter B. Sher ◽  
Jerome B. Posner ◽  
William R. Shapiro ◽  
George C. Cotzias
2017 ◽  
Vol 39 (4) ◽  
pp. 258-263 ◽  
Author(s):  
L D Liubich ◽  
L M Kovalevska ◽  
M I Lisyany ◽  
V M Semenova ◽  
T A Malysheva ◽  
...  

The aim of the work was to study the impact of fetal rat brain cell supernatant (FRBCS) on the expression of transforming growth factor β1 (TGF-β1) and p53 in C6 cells of rat glioma in vitro. Materials and Methods: FRBCS was obtained from suspensions of fetal rat brain cells on the 14th (E14) day of gestation. C6 glioma cells were cultured for 48 h in the presence of FRBCS or FRBCS + anti-TGF-β1 monoclonal antibody. Immunocytochemical staining for TGF-β1 and p53 was performed. Results: The proportion of TGF-β1-immunopositive tumor cells in C6 glioma cultures was statistically significantly higher than in the control cell cultures of normal fetal rat brain. FRBCS reduced the proportion of TGF-β1-immunopositive tumor cells and increased the proportion of p53-immunopositive cells in C6 glioma cultures. In cells cultured with FRBCS + anti-TGF-β1 monoclonal antibody, the above effects of FRBCS were abrogated. Conclusion: The obtained results suggest that TGF-β1 seems to be responsible for decrease in TGF-β1 expression and increase in p53 expression in C6 glioma cells treated with FRBCS.


2002 ◽  
Vol 70 (1) ◽  
pp. 24-30 ◽  
Author(s):  
Martha C. Garcia ◽  
Glenn Ward ◽  
Yee-Chung Ma ◽  
Norman Salem ◽  
Hee-Yong Kim

1993 ◽  
Vol 86 (2) ◽  
pp. 117-125 ◽  
Author(s):  
Nobuhisa Nagano ◽  
Hiroshi Sasaki ◽  
Masaru Aoyagi ◽  
Kimiyoshi Hirakawa

2001 ◽  
Vol 94 (4) ◽  
pp. 596-604 ◽  
Author(s):  
Adília Hormigo ◽  
David R. Friedlander ◽  
Perry A. Brittis ◽  
David Zagzag ◽  
Martin Grumet

Object. A variant of C6 glioma cells, C6R-G/H cells express hygromycin phosphotransferase (HPT) and appear to have reduced tumorigenicity in the embryonic brain. The goal of this study was to investigate their reduced capacity to generate tumors in the adult rat brain. Methods. Cell lines were implanted into rat brains and tumorigenesis was evaluated. After 3 weeks, all rats with C6 cells showed signs of neurological disease, whereas rats with C6R-G/H cells did not and were either killed then or allowed to survive until later. Histological studies were performed to analyze tumor size, malignancy, angiogenesis, and cell proliferation. Cells isolated from rat brain tumors were analyzed for mutation to HPT by testing their sensitivity to hygromycin. Conclusions. The results indicate that HPT suppresses tumor formation. Three weeks after implantation, only 44% of animals implanted with C6R-G/H cells developed tumors, whereas all animals that received C6 glioma cells developed high-grade gliomas. The C6R-G/H cells filled a 20-fold smaller maximal cross-sectional area than the C6 cells, and exhibited less malignant characteristics, including reduced angiogenesis, mitosis, and cell proliferation. Similar results were obtained in the brain of nude rats, indicating that the immune system did not play a significant role in suppressing tumor growth. The combination of green fluorescent protein (GFP) and HPT was more effective in suppressing tumorigenesis than either plasmid by itself, indicating that the GFP may protect against inactivation of the HPT. Interestingly, hygromycin resistance was lost in tumor cells that were recovered from a group of animals in which C6R-G/H cells formed tumors, confirming the correlation of HPT with reduced tumorigenicity.


1991 ◽  
Vol 9 (4) ◽  
pp. 427-433 ◽  
Author(s):  
William J. Goldberg ◽  
Edward R. Laws ◽  
Jerald J. Bernstein

1993 ◽  
Vol 35 (1) ◽  
pp. 92-102 ◽  
Author(s):  
C. D. Wilson ◽  
B. Parameswaran ◽  
G. R. Molloy

1988 ◽  
Vol 462 (2) ◽  
pp. 265-274 ◽  
Author(s):  
Huw G. Jenkins ◽  
Jane Martin ◽  
Michael F. Dean

1983 ◽  
Vol 279 (1-2) ◽  
pp. 217-228 ◽  
Author(s):  
O. Kempski ◽  
L. Chaussy ◽  
U. Gross ◽  
M. Zimmer ◽  
A. Baethmann

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