scholarly journals Interleukin-1β and transforming growth factor-β cooperate to induce neurosphere formation and increase tumorigenicity of adherent LN-229 glioma cells

2012 ◽  
Vol 3 (1) ◽  
pp. 5 ◽  
Author(s):  
Lei Wang ◽  
Ziyan Liu ◽  
Sivasai Balivada ◽  
Tej Shrestha ◽  
Stefan Bossmann ◽  
...  
1996 ◽  
Vol 36 (3) ◽  
pp. 145-150 ◽  
Author(s):  
Hirofumi NAGANUMA ◽  
Atsushi SASAKI ◽  
Eiji SATOH ◽  
Mitsuyasu NAGASAKA ◽  
Shin NAKANO ◽  
...  

1994 ◽  
Vol 41 (S2) ◽  
pp. C198-C200 ◽  
Author(s):  
M. H. M. Meijers ◽  
C. M. Aisa ◽  
M. E. J. Billingham ◽  
R. G. G. Russell ◽  
R. A. D. Bunning

1992 ◽  
Vol 76 (5) ◽  
pp. 850-855 ◽  
Author(s):  
Timothy C. Ryken ◽  
Vincent C. Traynelis ◽  
Ramon Lim

✓ The mitogenic and morphological effects of acidic fibroblast growth factor (aFGF) and transforming growth factor-β (TGF-β) were assessed on cultured fetal rat astrocytes and C6 rat glioma cells in the presence and absence of serum. Astrocytes incubated with aFGF exhibited an increase in mitotic activity and characteristic morphological changes involving extensive process formation and rounding of cell bodies. Astrocytes incubated with TGF-β underwent a slight decrease in mitotic activity and remained morphologically unchanged. Cells exposed to a combination of aFGF and TGF-β demonstrated an attenuation of both the mitogenic and morphological changes observed in the presence of aFGF alone. The C6 glioma cells cultured in the presence of aFGF underwent a characteristic morphological change from a rounded piling cell mass to a more spindle-shaped bipolar cell layer, accompanied by an increase in mitotic activity. In contrast to the astrocyte cultures, increased growth and similar morphological effects were produced by TGF-β. The combination of aFGF and TGF-β did not result in attenuation of the mitogenic and morphological changes (as seen in astrocytic cells). These results suggest that, in normal fetal rat astrocytes, TGF-β is capable of attenuating the mitogenic and morphological changes induced by aFGF in vitro. In the transformed C6 glioma cell line, aFGF and TGF-β elicit similar mitogenic and morphological changes, without evidence of an antagonistic interaction as seen in normal astrocytes.


2020 ◽  
Vol 318 (3) ◽  
pp. F754-F762
Author(s):  
Eduardo C. Alexandre ◽  
Nailong Cao ◽  
Shinsuke Mizoguchi ◽  
Tetsuichi Saito ◽  
Masahiro Kurobe ◽  
...  

Prostate inflammation (PI) is a clinical condition associated with infection and/or inflammation of the prostate. It is a common disease frequently associated to lower urinary tract (LUT) symptoms. The urethra is an understudied structure in the LUT and plays a fundamental role in the urinary cycle. Here, we proposed to evaluate the effect of PI on the urethra tissue. Male Sprague-Dawley rats were used, and PI was induced by formalin injection into the ventral lobes of the prostate. The pelvic urethra at the prostatic level was harvested for histological analysis, contraction (electrical field stimulation and phenylephrine), and relaxation (sodium nitroprusside/MK-571) experiments. Various gene targets [cytochrome c oxidase subunit 2, transforming growth factor-β1, interleukin-1β, hypoxia-inducible factor-1α, α1A-adrenoceptor, inositol 1,4,5-trisphosphate receptor type 1, voltage-gated Ca2+ channel subunit-α1D, neuronal nitric oxide synthase, soluble guanylyl cyclase, phosphodiesterase 5A, protein kinase CGMP-dependent 1, and multidrug resistance-associated protein 5 (MRP5; ATP-binding cassette subfamily C member 5)] were quantified, and cGMP levels were measured. No histological changes were detected, and functional assays revealed decreased contraction and increased relaxation of urethras from the PI group. The addition of MK-571 to functional assays increased urethral relaxation. Genes associated with inflammation were upregulated in urethras from the PI group, such as cytochrome oxidase c subunit 2, transforming growth factor-β1, interleukin-1β, and hypoxia-inducible factor-1α. We also found increased expression of L-type Ca2+ channels and the neuronal nitric oxide synthase enzyme and decreased expression of the MRP5 pump. Finally, cGMP production was enhanced in urethral tissue of PI animals. The results indicate that PI is associated with proinflammatory gene expression in the urethra without histologically evident inflammation and that PI produces a dysfunctional urethra and MRP5 pump downregulation, which results in cGMP accumulation inside the cell. These findings would help to better understand LUT dysfunctions associated with PI and the role of MRP pumps in the control of LUT function.


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