Am J Physiol Cell Physiol Track the topics, authors and articles important to you
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
QUICK SEARCH:   [advanced]


     

Am J Physiol Cell Physiol 254: C267-C271, 1988;
0363-6143/88 $5.00
This Article
Right arrow Full Text (PDF)
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
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 Google Scholar
Google Scholar
Right arrow Articles by Stanton, R. C.
Right arrow Articles by Seifter, J. L.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Stanton, R. C.
Right arrow Articles by Seifter, J. L.

AJP - Cell Physiology, Vol 254, Issue 2 C267-C271, Copyright © 1988 by American Physiological Society

ARTICLES

Epidermal growth factor rapidly activates the hexose monophosphate shunt in kidney cells

R. C. Stanton and J. L. Seifter
Brigham and Women's Hospital, Boston, Massachusetts 02115.

Epidermal growth factor (EGF) is a potent mitogen that rapidly activates plasma membrane Na+-H+ exchangers, thereby causing intracellular alkalinization. The rise in intracellular pH (pHi) may be an important signal for cell growth. However, recent studies have dissociated Na+-H+ exchange activity and/or alkalinization from cellular proliferation. We have studied the role of EGF in the growth of rat renal proximal tubule (PT) cells in primary culture and monitored the early effects of EGF on pHi in these cells using microfluorimetry and the pHi probe, 2',7'-biscarboxyethyl-5(6)-carboxyfluorescein (BCECF). EGF increased DNA synthesis in growing PT cells and produced transient alkalinization (2-3 min) due to activation of Na+-H+ exchange. In contrast, in the absence of extracellular Na+, EGF administration caused pHi to decrease. This acidification was prevented by 2-deoxy-D-glucose and 6-aminonicotinamide, inhibitors of glucose utilization and the hexose monophosphate shunt (HMP), respectively. EGF was also found to stimulate HMP shunt activity in PT cells using an isotopic method for distinguishing between glucose utilization through the HMP shunt vs. glycolysis. Because EGF caused both cytoplasmic acidifying (HMP activation) and alkalinizing (Na+-H+ exchange activation) processes, we propose that the primary role for the activation of Na+-H+ exchange during growth may be to extrude acid from the cell in order to maintain pHi at levels permissive for cell growth.


This article has been cited by other articles:


Home page
 J. Biol. Chem.Home page
J. M. Bryson, P. E. Coy, K. Gottlob, N. Hay, and R. B. Robey
Increased Hexokinase Activity, of Either Ectopic or Endogenous Origin, Protects Renal Epithelial Cells against Acute Oxidant-induced Cell Death
J. Biol. Chem., March 22, 2002; 277(13): 11392 - 11400.
[Abstract] [Full Text] [PDF]

Home page
 Am. J. Physiol. Cell Physiol.Home page
W.-N. Tian, L. D. Braunstein, K. Apse, J. Pang, M. Rose, X. Tian, and R. C. Stanton
Importance of glucose-6-phosphate dehydrogenase activity in cell death
Am J Physiol Cell Physiol, May 1, 1999; 276(5): C1121 - C1131.
[Abstract] [Full Text] [PDF]

Home page
 J. Biol. Chem.Home page
W.-N. Tian, L. D. Braunstein, J. Pang, K. M. Stuhlmeier, Q.-C. Xi, X. Tian, and R. C. Stanton
Importance of Glucose-6-phosphate Dehydrogenase Activity for Cell Growth
J. Biol. Chem., April 24, 1998; 273(17): 10609 - 10617.
[Abstract] [Full Text] [PDF]

Home page
 J. Biol. Chem.Home page
Z. Zhang, K. Apse, J. Pang, and R. C. Stanton
High Glucose Inhibits Glucose-6-phosphate Dehydrogenase via cAMP in Aortic Endothelial Cells
J. Biol. Chem., December 15, 2000; 275(51): 40042 - 40047.
[Abstract] [Full Text] [PDF]


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