Cytochrome P450 (CYP) 2W1 affect steroid secretion in adrenocortical cell line and tumor tissues

2020 ◽  
Author(s):  
Barbara Altieri ◽  
Silviu Sbiera ◽  
Isabel Weigand ◽  
Marco Volante ◽  
Sonja Steinhauer ◽  
...  
2005 ◽  
Vol 113 (S 1) ◽  
Author(s):  
O Zwermann ◽  
A Braun ◽  
E Lalli ◽  
F Beuschlein ◽  
M Reincke

2009 ◽  
Vol 28 (3) ◽  
pp. 370-378 ◽  
Author(s):  
Susanne Rudzok ◽  
Eike Schmücking ◽  
Carolin Graebsch ◽  
Olf Herbarth ◽  
Mario Bauer

2018 ◽  
Vol 12 (2) ◽  
pp. 138-144 ◽  
Author(s):  
Sandra R. Lepri ◽  
Daniele Sartori ◽  
Simone C. Semprebon ◽  
Adrivanio Baranoski ◽  
Giuliana C. Coatti ◽  
...  

2007 ◽  
Vol 172 ◽  
pp. S57-S58
Author(s):  
Erik Ullerås ◽  
Åsa Ohlsson ◽  
Agneta Oskarsson

PLoS ONE ◽  
2014 ◽  
Vol 9 (4) ◽  
pp. e93261 ◽  
Author(s):  
Dora Molina-Ortiz ◽  
Rafael Camacho-Carranza ◽  
José Francisco González-Zamora ◽  
Jaime Shalkow-Kalincovstein ◽  
Rocío Cárdenas-Cardós ◽  
...  

2002 ◽  
Vol 30 (4) ◽  
pp. 400-405 ◽  
Author(s):  
S Takahashi ◽  
T Takahashi ◽  
S Mizobuchi ◽  
M Matsumi ◽  
K Morita ◽  
...  

Cytotoxic free radicals generated during the metabolism of carbon tetrachloride by cytochrome P450 2E1 (CYP2E1) are thought to cause hepatotoxicity. Here, the cytotoxic effects of carbon tetrachloride in a liver cell line expressing CYP2E1 (HLE/2E1) are compared with those in the mother cell line (HLE). The effects of carbon tetrachloride on the gene expression of HSP70, a potential marker of oxidative stress, were also examined. The viability of HLE/2E1 cells after exposure to carbon tetrachloride was significantly decreased compared with that of HLE cells. Northern blot analysis revealed that the HSP70 mRNA level was significantly increased after carbon tetrachloride treatment in both cell lines, while the magnitude of its increase was much greater in HLE/2E1 cells than in HLE cells. These results suggest that the oxidative stress induced by CYP2E1 plays an important role in the increase in cytotoxicity of carbon tetrachloride in CYP2E1-overexpressing cells.


2017 ◽  
Vol 29 (6) ◽  
pp. 1144 ◽  
Author(s):  
R. M. P. Rocha ◽  
L. F. Lima ◽  
I. R. Brito ◽  
G. M. Silva ◽  
H. H. V. Correia ◽  
...  

The aim of the present study was to evaluate the effect of anti-Müllerian hormone (AMH), with and without FSH, on the in vitro development of isolated caprine preantral follicles, as well as follicular steroid production and mRNA levels of AMH, hormone receptors (AMH and FSH), CYP19A1 (cytochrome P450, family 19, subfamily A, polypeptide 1), CYP17 (cytochrome P450, family 17, subfamily A, polypeptide 1), HSD3B (3-beta-hydroxysteroid dehydrogenase) and Myc (myelocytomatosis oncogene). Isolated secondary follicles were cultured in minimum essential medium alpha (α-MEM+) alone or supplemented with 50 ng mL–1 AMH and/or 100 ng mL–1 FSH added sequentially on different days of culture. Follicles were cultured for a total of 18 days, with different media during the first (Days 0–9) and second (Days 10–18) halves of the culture period, resulting in six treatment groups, as follows: α-MEM+/α-MEM+, FSH/FSH, AMH/AMH, AMH+FSH/AMH+FSH, AMH/FSH, and FSH/AMH. Follicle development was evaluated on the basis of follicular growth, oocyte maturation and steroid secretion. There was a decrease in follicular growth rate in the AMH, AMH + FSH and AMH/FSH treatment groups compared with α-MEM+ and FSH treatment groups (P < 0.05). However, the different culture conditions had no effect on rates of meiotic resumption and steroid secretion (P > 0.05). Moreover, follicles cultured in the presence of FSH had lower levels of AMH receptor type II (AMHRII) mRNA compared with non-cultured control (freshly isolated follicles), and the AMH and AMH/FSH treatment groups. In conclusion, AMH reduces the follicular growth rate of isolated goat preantral follicles in vitro without affecting follicular survival.


2004 ◽  
Vol 33 (2) ◽  
pp. 511-522 ◽  
Author(s):  
J Liu ◽  
X-D Li ◽  
A Ora ◽  
P Heikkilä ◽  
A Vaheri ◽  
...  

Adrenocorticotropin is the major regulator of adrenocortical development and function. It acts mainly through the cAMP-dependent protein kinase A (PKA) pathway. Our aim was to study the interaction of tumor necrosis factor-α (TNFα) and the PKA pathway in adrenocortical cell proliferation and apoptosis. The PKA activator Dibutyryl cAMP ((Bu)2cAMP) strongly induced differentiation and inhibited proliferation in the human adrenocortical cell line NCI-H295R (H295R). TNFα induced apoptosis of H295R cells. Interestingly, (Bu)2cAMP treatment clearly enhanced TNFα-induced apoptosis in H295R cells, but not in another human adrenocortical cell line SW-13, the mouse adrenocortical Y-1 cell line or the human HeLa cell line. This synergistic effect was not due to the (Bu)2cAMP-induced glucocorticoid secretion since dexamethasone had no significant effect on the TNFα-induced apoptosis. (Bu)2cAMP treatment rapidly increased the expression of the proto-oncogene c-myc in H295R cells, but not in SW-13, Y-1 or HeLa cells. In transient c-myc transfection assay, c-myc expression associated with decreased expression of the proliferation marker Ki-67 in H295R cells. In conclusion, cAMP-dependent protein kinase activation reduced proliferation and augmented TNFα-induced apoptosis in adrenocortical H295R cells, and these effects were associated with increased c-myc expression.


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