scholarly journals Effects of hypertonic stress on transforming growth factor-β activity in normal rat kidney cells

1998 ◽  
Vol 53 (6) ◽  
pp. 1654-1660 ◽  
Author(s):  
Toshihiro Sugiura ◽  
Atsushi Yamauchi ◽  
Hiroshi Kitamura ◽  
Yasuko Matusoka ◽  
Masaru Horio ◽  
...  
1985 ◽  
Vol 5 (9) ◽  
pp. 2289-2297 ◽  
Author(s):  
E J van Zoelen ◽  
W J van de Ven ◽  
H J Franssen ◽  
T M van Oostwaard ◽  
P T van der Saag ◽  
...  

Mouse neuroblastoma Neuro-2A cells produce transforming growth factors during exponential growth in a defined hormone-free medium, which, on Bio-Gel columns in 1 M HAc, elute at a molecular size of 15 to 20 kilodaltons (kDa). These neuroblastoma-derived transforming growth factors have strong mitogenic activity, but they do not compete with epidermal growth factor for receptor binding (E. J. J. van Zoelen, D. R. Twardzik, T. M. J. van Oostwaard, P. T. van der Saag, S. W. de Laat, and G. J. Todaro, Proc. Natl. Acad. Sci. U.S.A. 81:4085-4089, 1984). In this study approximately 80% of the mitogenic activity was immunoprecipitated by antibodies raised against platelet-derived growth factor (PDGF). Immunoblotting indicated a true molecular size of 32 kDa for this PDGF-like growth factor. Analysis of poly(A)+ RNA from Neuro-2A cells demonstrated the expression of the c-sis oncogene in this cell line, whereas in vitro translation of the RNA yielded a 20-kDa protein recognized by anti-PDGF antibodies. Separation by reverse-phase high-pressure liquid chromatography demonstrated the presence of two distinct mitogenic activities in neuroblastoma-derived transforming growth factor preparations, one of which is antigenically related to PDGF. Both activities had the ability to induce anchorage-independent growth in normal rat kidney cells, both in the presence and in the absence of epidermal growth factor. It is concluded that Neuro-2A cells express c-sis with concomitant production and secretion of a PDGF-like growth factor, which plays a role in the induction of phenotypic transformation on normal rat kidney cells.


1991 ◽  
Vol 11 (3) ◽  
pp. 171-180 ◽  
Author(s):  
Yun-Chi Yeh ◽  
E. Robert Burns ◽  
John Yeh ◽  
Hsing-Wu Yeh

The cooperative cell kinetic actions of ET-1 with TGF-α or EGF in normal rat kidney fibroblasts (NRK-49F) and KNRK cells (Kirsten MSV transformed) were analyzed by [3H]-thymidine incorporation assay and flow cytometry. A marked synergistic effect of TGF-α and ET-1 (or EGF and ET-1) on DNA synthesis and G1 to S transition was observed in NRK cells; 15–20% S for TGF-α and 12% S for ET-1 alone but 45–50% S in combination. There was no detectable effect on cell cycle kinetics by TGF-α (1 ng/ml) or EGF (1 ng/ml) plus ET-1 (1 ng/ml) in KNRK cells treated for 22 hours. Insulin, insulin-like growth factor I (IGF-I), fibroblast growth factor (FGF), platelet derived growth factor (PDGF), and transforming growth factor β (TGF-β) were also tested and found to have no significant synergistic effects on ET-1 actions. Our findings suggest that the combination of TGF-α (EGF) and ET-1 is an important part of an intricate network which coordinates progression of G1 to S phase in normal cells.


2004 ◽  
Vol 286 (3) ◽  
pp. F509-F515 ◽  
Author(s):  
Joshua M. Stern ◽  
Jie Chen ◽  
Randi B. Silver ◽  
Dix P. Poppas ◽  
E. Darracott Vaughan ◽  
...  

Interactions between transforming growth factor-β (TGF-β) and nitric oxide (NO) are important in the pathophysiology of unilateral ureteral obstruction (UUO). Dopamine (DA) is a vasoactive renal mediator active at the D1A receptor (D1AR), which has not been studied in UUO; therefore, we examined the interactions among DA, TGF-β, and NO in UUO. In vivo, UUO was carried out in rats with or without concurrent treatment with 1D11, a monoclonal antibody to TGF-β, for 14 days. In vitro, NRK-52E cells (normal rat kidney tubules) were treated with DA, and NO and TGF-β release were examined. UUO resulted in a 70% decrease in the expression of renal D1AR, confirmed by both Western blot analysis and immunohistochemistry. 1D11 treatment restored expression to 60% of control values. DA treatment decreased NRK-52E release of TGF-β by 80%; conversely, DA significantly increased NO release from NRK-52E cells. These results suggest that DA modulates the release of cytokines, which are involved in the fibrotic and apoptotic sequelae of UUO, and that these effects are independent of DA's known vasoactive properties.


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