This Article Full Text Full Text (PDF) Purchase Article View Shopping Cart Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Request Copyright Permission Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Goh, E. L. K. Articles by Lobie, P. E. Search for Related Content PubMed PubMed Citation Articles by Goh, E. L. K. Articles by Lobie, P. E.

Growth Hormone Promotion of Tubulin Polymerization Stabilizes the Microtubule Network and Protects Against Colchicine-Induced Apoptosis¹

Institute of Molecular and Cell Biology and Defence Medical Research Institute (E.L.K.G., P.E.L.), National University of Singapore, Singapore 117609, Republic of Singapore; and Karolinska Institutet (T.J.P.), Institution för Medicinsk Näringslära, NOVUM, Huddinge 14186, Sweden

Address all correspondence and requests for reprints to: Peter E. Lobie, Institute of Molecular and Cell Biology, An Institute Affiliated to National University of Singapore, 30 Medical Drive, Singapore 117609, Republic of Singapore. E-mail: mcbpel{at}mcbsgs1.imcb.nus.edu.sg

We have investigated the effect of GH on microtubular physiology in Chinese hamster ovary (CHO) cells stably transfected with the complementary DNA for the rat GH receptor (CHO-GHR_1–638). We show here that after 30 min of human GH (hGH) treatment of CHO-GHR_1–638 cells, there was a significant increase in the level of polymerization of all four tubulin isoforms (-, ß-, -, and tyrosinated -tubulin) compared with the serum-deprived state. However, this transient increase in the levels of polymerized tubulin after hGH treatment was particularly pronounced for ß- and tyr -tubulin. For - and -tubulin, the hGH-induced increase in polymerization state lasted to approximately 3 h and then declined by 7 h, whereas for ß- and tyr -tubulin there was a decrease in the polymerization state at 1–2 h after hGH treatment compared with the level at 30 min (but still greater than the serum-deprived state) followed by a second but lesser wave of increased polymerization lasting to 7 h. The changes in the polymerization state of the tubulins were not accompanied by comparative changes in the level of total cellular tubulin. The proline rich box 1 region of the GH receptor was required for hGH to stimulate tubulin polymerization indicative that this event is JAK dependent. Increased tubulin polymerization still occurred in response to hGH in a receptor truncation lacking the carboxyl terminal half of the intracellular domain of the GH receptor indicative that hGH induced changes in intracellular calcium concentration is not required for tubulin polymerization. Prior treatment of CHO-GHR_1–638 cells with hGH retarded colchicine induced microtubule depolymerization and also prevented colchicine induced apoptotic cell death. The integrity of the microtubule network was not required for GH-induced STAT5 mediated transcription as treatment of cells with colchicine, vincristine, or vinblastine did not alter the fold stimulation of the STAT5 mediated transcriptional response to GH. Thus one consequence of cellular treatment with GH is alteration in microtubule physiology.

This article has been cited by other articles:

				G. R. Reddy, M. J. Pushpanathan, R. F. Ransom, L. B. Holzman, F. C. Brosius III, M. Diakonova, P. Mathieson, M. A. Saleem, E. O. List, J. J. Kopchick, et al. Identification of the Glomerular Podocyte as a Target for Growth Hormone Action Endocrinology, May 1, 2007; 148(5): 2045 - 2055. [Abstract] [Full Text] [PDF]

				T. Phung-Koskas, A. Pilon, C. Pous, C. Betzina, M. Sturm, M.-L. Bourguet-Kondracki, G. Durand, and A. Drechou STAT5B-mediated Growth Hormone Signaling Is Organized by Highly Dynamic Microtubules in Hepatic Cells J. Biol. Chem., January 14, 2005; 280(2): 1123 - 1131. [Abstract] [Full Text] [PDF]

				C. Steindler, Z. Li, M. Algarte, A. Alcover, V. Libri, J. Ragimbeau, and S. Pellegrini Jamip1 (Marlin-1) Defines a Family of Proteins Interacting with Janus Kinases and Microtubules J. Biol. Chem., October 8, 2004; 279(41): 43168 - 43177. [Abstract] [Full Text] [PDF]

				K.-C. Leung, G. Johannsson, G. M. Leong, and K. K. Y. Ho Estrogen Regulation of Growth Hormone Action Endocr. Rev., October 1, 2004; 25(5): 693 - 721. [Abstract] [Full Text] [PDF]

				K. K. Kaulsay, T. Zhu, W. F. Bennett, K.-O. Lee, and P. E. Lobie The Effects of Autocrine Human Growth Hormone (hGH) on Human Mammary Carcinoma Cell Behavior Are Mediated via the hGH Receptor Endocrinology, February 1, 2001; 142(2): 767 - 777. [Abstract] [Full Text] [PDF]

				J. Herrington, M. Diakonova, L. Rui, D. R. Gunter, and C. Carter-Su SH2-B Is Required for Growth Hormone-induced Actin Reorganization J. Biol. Chem., April 21, 2000; 275(17): 13126 - 13133. [Abstract] [Full Text] [PDF]

				A. Biason-Lauber, M. Zachmann, and E. J. Schoenle Effect of Leptin on CYP17 Enzymatic Activities in Human Adrenal Cells: New Insight in the Onset of Adrenarche Endocrinology, April 1, 2000; 141(4): 1446 - 1454. [Abstract] [Full Text] [PDF]

				K. K. Kaulsay, H. C. Mertani, K.-O. Lee, and P. E. Lobie Autocrine Human Growth Hormone Enhancement of Human Mammary Carcinoma Cell Spreading Is Jak2 Dependent Endocrinology, April 1, 2000; 141(4): 1571 - 1584. [Abstract] [Full Text] [PDF]

				T. Zhu and P. E. Lobie Janus Kinase 2-dependent Activation of p38 Mitogen-activated Protein Kinase by Growth Hormone. RESULTANT TRANSCRIPTIONAL ACTIVATION OF ATF-2 AND CHOP, CYTOSKELETAL RE-ORGANIZATION AND MITOGENESIS J. Biol. Chem., January 21, 2000; 275(3): 2103 - 2114. [Abstract] [Full Text] [PDF]

				H. C. Mertani, T. Zhu, E. L. K. Goh, K.-O. Lee, G. Morel, and P. E. Lobie Autocrine Human Growth Hormone (hGH) Regulation of Human Mammary Carcinoma Cell Gene Expression. IDENTIFICATION OF CHOP AS A MEDIATOR OF hGH-STIMULATED HUMAN MAMMARY CARCINOMA CELL SURVIVAL J. Biol. Chem., June 8, 2001; 276(24): 21464 - 21475. [Abstract] [Full Text] [PDF]