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 275: C1104-C1112, 1998;
0363-6143/98 $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 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 Zhang, Z.
Right arrow Articles by Cohen, D. M.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Zhang, Z.
Right arrow Articles by Cohen, D. M.
Vol. 275, Issue 4, C1104-C1112, October 1998

Hypotonicity activates transcription through ERK-dependent and -independent pathways in renal cells

Zheng Zhang, Xiao-Yan Yang, and David M. Cohen

Divisions of Nephrology and Molecular Medicine, Oregon Health Sciences University and Portland Veterans Affairs Medical Center, Portland, Oregon 97201

Acute hypotonic shock (50% dilution of medium with sterile water, but not with isotonic NaCl) activated the extracellular signal response kinase (ERK) mitogen-activated protein (MAP) kinases in renal medullary cells, as measured by Western analysis with a phospho-ERK-specific antibody and by in vitro kinase assay of epitope-tagged ERKs immunoprecipitated from stable HA-ERK transfectants. Hypotonicity also activated the transcription factor and ERK substrate Elk-1 in a partially PD-98059-sensitive fashion, as assessed by chimeric reporter gene assay. Consistent with these data, hypotonic stress activated transcription of the immediate-early gene transcription factor Egr-1 in a partially PD-98059-sensitive fashion. Hypotonicity-inducible Egr-1 transcription was mediated in part through 5'-flanking regions containing serum response elements and in part through the minimal Egr-1 promoter. Elimination of the Ets motifs adjacent to key regulatory serum response elements in the Egr-1 promoter diminished the effect of hypotonicity but failed to abolish it. Interestingly, hypotonicity also transiently activated p38 and c-Jun NH2-terminal kinase 1, as determined by immunoblotting with anti-phospho-MAP kinase antibodies. Taken together, these data strongly suggest that hypotonicity activates immediate-early gene transcription in renal medullary cells via MAP kinase kinase-dependent and -independent mechanisms.

urea; kidney; signal transduction; p38; stress-activated protein kinase; c-Jun amino-terminal kinase


This article has been cited by other articles:


Home page
 Am. J. Physiol. Cell Physiol.Home page
M.-B. Nielsen, S. T. Christensen, and E. K. Hoffmann
Effects of osmotic stress on the activity of MAPKs and PDGFR-{beta}-mediated signal transduction in NIH-3T3 fibroblasts
Am J Physiol Cell Physiol, April 1, 2008; 294(4): C1046 - C1055.
[Abstract] [Full Text] [PDF]

Home page
 Exp. Biol. Med.Home page
D. Xu, L. Wang, J. E. Olson, and L. Lu
Asymmetrical Response of p38 Kinase Activation to Volume Changes in Primary Rat Astrocytes
Experimental Biology and Medicine, November 1, 2001; 226(10): 927 - 933.
[Abstract] [Full Text] [PDF]

Home page
 Am. J. Respir. Cell Mol. Bio.Home page
N. Jin, N. Hatton, D. R. Swartz, X.-l. Xia, M. A. Harrington, S. H. Larsen, and R. A. Rhoades
Hypoxia Activates Jun-N-Terminal Kinase, Extracellular Signal-Regulated Protein Kinase, and p38 Kinase in Pulmonary Arteries
Am. J. Respir. Cell Mol. Biol., November 1, 2000; 23(5): 593 - 601.
[Abstract] [Full Text]

Home page
 Am. J. Physiol. Renal Physiol.Home page
W. Tian, Z. Zhang, and D. M. Cohen
MAPK signaling and the kidney
Am J Physiol Renal Physiol, October 1, 2000; 279(4): F593 - F604.
[Abstract] [Full Text] [PDF]

Home page
 BloodHome page
L. Liu, J. C. Tsai, and W. C. Aird
Egr-1 gene is induced by the systemic administration of the vascular endothelial growth factor and the epidermal growth factor
Blood, September 1, 2000; 96(5): 1772 - 1781.
[Abstract] [Full Text] [PDF]

Home page
 J. Biol. Chem.Home page
J. D. Hoffert, V. Leitch, P. Agre, and L. S. King
Hypertonic Induction of Aquaporin-5 Expression through an ERK-dependent Pathway
J. Biol. Chem., March 17, 2000; 275(12): 9070 - 9077.
[Abstract] [Full Text] [PDF]

Home page
 Am. J. Physiol. Cell Physiol.Home page
S. Zhuang, S.-I. Hirai, and S. Ohno
Hyperosmolality induces activation of cPKC and nPKC, a requirement for ERK1/2 activation in NIH/3T3 cells
Am J Physiol Cell Physiol, January 1, 2000; 278(1): C102 - C109.
[Abstract] [Full Text] [PDF]

Home page
 Am. J. Physiol. Renal Physiol.Home page
Z. Zhang, X.-Y. Yang, S. P. Soltoff, and D. M. Cohen
PI3K signaling in the murine kidney inner medullary cell response to urea
Am J Physiol Renal Physiol, January 1, 2000; 278(1): F155 - F164.
[Abstract] [Full Text] [PDF]

Home page
 J. Biol. Chem.Home page
T. de Jager, T. Pelzer, S. Muller-Botz, A. Imam, J. Muck, and L. Neyses
Mechanisms of Estrogen Receptor Action in the Myocardium. RAPID GENE ACTIVATION VIA THE ERK1/2 PATHWAY AND SERUM RESPONSE ELEMENTS
J. Biol. Chem., July 20, 2001; 276(30): 27873 - 27880.
[Abstract] [Full Text] [PDF]


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