Am J Physiol Cell Physiol Ad Instruments
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
 QUICK SEARCH:   [advanced]


     


Am J Physiol Cell Physiol 282: C1290-C1297, 2002; doi:10.1152/ajpcell.00351.2001
0363-6143/02 $5.00
This Article
Right arrow Full Text
Right arrow Full Text (PDF)
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Right arrow Citation Map
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in Web of Science
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Web of Science (25)
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Yuan, Q.
Right arrow Articles by Johnson, L. R.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Yuan, Q.
Right arrow Articles by Johnson, L. R.
Vol. 282, Issue 6, C1290-C1297, June 2002

Polyamine depletion prevents camptothecin-induced apoptosis by inhibiting the release of cytochrome c

Qing Yuan, Ramesh M. Ray, and Leonard R. Johnson

Department of Physiology, The University of Tennessee Health Science Center, Memphis, Tennessee 38163

C1297, 2002; 10.1152/ajpcell.00351.2001.We have shown previously that depletion of polyamines delays apoptosis induced by camptothecin in rat intestinal epithelial cells (IEC-6). Mitochondria play an important role in the regulation of apoptosis in mammalian cells because apoptotic signals induce mitochondria to release cytochrome c. The latter interacts with Apaf-1 to activate caspase-9, which in turn activates downstream caspase-3. Bcl-2 family proteins are involved in the regulation of cytochrome c release from mitochondria. In this study, we examined the effects of polyamine depletion on the activation of the caspase cascade, release of cytochrome c from mitochondria, and expression and translocation of Bcl-2 family proteins. We inhibited ornithine decarboxylase, the first rate-limiting enzyme in polyamine synthesis, with alpha -difluoromethylornithine (DFMO) to deplete cells of polyamines. Depletion of polyamines prevented camptothecin-induced release of cytochrome c from mitochondria and decreased the activity of caspase-9 and caspase-3. The mitochondrial membrane potential was not disrupted when cytochrome c was released. Depletion of polyamines decreased translocation of Bax to mitochondria during apoptosis. The expression of antiapoptotic proteins Bcl-xL and Bcl-2 was increased in DFMO-treated cells. Caspase-8 activity and cleavage of Bid were decreased in cells depleted of polyamines. These results suggest that polyamine depletion prevents IEC-6 cells from apoptosis by preventing the translocation of Bax to mitochondria, thus preventing the release of cytochrome c.

polyamines; alpha -difluoromethylornithine; mitochondria; Bcl-2 protein; caspase-9


This article has been cited by other articles:


Home page
Am. J. Physiol. Cell Physiol.Home page
M. A. Arndt, V. Battaglia, E. Parisi, M. J. Lortie, M. Isome, C. Baskerville, D. P. Pizzo, R. Ientile, S. Colombatto, A. Toninello, et al.
The arginine metabolite agmatine protects mitochondrial function and confers resistance to cellular apoptosis
Am J Physiol Cell Physiol, June 1, 2009; 296(6): C1411 - C1419.
[Abstract] [Full Text] [PDF]


Home page
Am. J. Physiol. Gastrointest. Liver Physiol.Home page
W. Deng, M. J. Viar, and L. R. Johnson
Polyamine depletion inhibits irradiation-induced apoptosis in intestinal epithelia
Am J Physiol Gastrointest Liver Physiol, September 1, 2005; 289(3): G599 - G606.
[Abstract] [Full Text] [PDF]


Home page
Cancer Res.Home page
J. P. Carson, N. Zhang, G. M. Frampton, N. P. Gerry, M. E. Lenburg, and M. F. Christman
Pharmacogenomic Identification of Targets for Adjuvant Therapy with the Topoisomerase Poison Camptothecin
Cancer Res., March 15, 2004; 64(6): 2096 - 2104.
[Abstract] [Full Text] [PDF]


Home page
Am. J. Physiol. Gastrointest. Liver Physiol.Home page
S. Bhattacharya, R. M. Ray, and L. R. Johnson
Prevention of TNF-{alpha}-induced apoptosis in polyamine-depleted IEC-6 cells is mediated through the activation of ERK1/2
Am J Physiol Gastrointest Liver Physiol, March 1, 2004; 286(3): G479 - G490.
[Abstract] [Full Text] [PDF]


Home page
Am. J. Physiol. Gastrointest. Liver Physiol.Home page
S. Bhattacharya, R. M. Ray, M. J. Viar, and L. R. Johnson
Polyamines are required for activation of c-Jun NH2-terminal kinase and apoptosis in response to TNF-{alpha} in IEC-6 cells
Am J Physiol Gastrointest Liver Physiol, November 1, 2003; 285(5): G980 - G991.
[Abstract] [Full Text] [PDF]


Home page
Am. J. Physiol. Gastrointest. Liver Physiol.Home page
W. Deng, D.-A. Wang, E. Gosmanova, L. R. Johnson, and G. Tigyi
LPA protects intestinal epithelial cells from apoptosis by inhibiting the mitochondrial pathway
Am J Physiol Gastrointest Liver Physiol, May 1, 2003; 284(5): G821 - G829.
[Abstract] [Full Text] [PDF]




HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
Visit Other APS Journals Online