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The Scientific World Journal
Volume 2012, Article ID 189290, 10 pages
Research Article

Angiotensins Inhibit Cell Growth in GH3 Lactosomatotroph Pituitary Tumor Cell Culture: A Possible Involvement of the p44/42 and p38 MAPK Pathways

1Department of Endocrinology, The County Hospital of Kutno, 52 Kosciuszki Street, 99-300 Kutno, Poland
2Department of Immunoendocrinology, Chair of Endocrinology, Medical University of Lodz, Dr. Sterling 3 Street, 91-425 Lodz, Poland
3Clinic of Endocrinology, Medical University of Lodz, Dr. Sterling 3 Street, 91-425 Lodz, Poland

Received 18 October 2011; Accepted 22 December 2011

Academic Editor: Dzung H. Dinh

Copyright © 2012 Dorota Ptasinska-Wnuk et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


The local renin-angiotensin system is present in the pituitary. We investigated the effects of angiotensins on GH3 lactosomatotroph cells proliferation in vitro and the involvement of p44/42 and p38 MAPK inhibitors in the growth-regulatory effects of angiotensins. Materials and Methods. Cell viability using the Mosmann method and proliferation by the measurement of BrdU incorporation during DNA synthesis were estimated. Results. Ang II and ang IV decreased the viability and proliferation of GH3 cells. Inhibitor of p44/42 MAPK attenuated the effects of ang II on cell viability and proliferation but did not affect the ang 5-8-dependent actions. Inhibitor of p38 MAPK prevented the decrease in the number of GH3 cells in ang-II- and ang-IV-treated groups. Conclusions. The growth-inhibitory effect of ang II is possibly mediated by the p44/42 MAPK. The p38 MAPK appears to mediate the inhibitory effects of both ang II and ang 5–8 upon cell survival.