Journal of the American Society of Nephrology
2007 JASN IMPACT FACTOR 7.111 HOME   AUTHOR INFO   EDITORIAL BOARD   SUBSCRIBE   FEEDBACK   ALERTS   HELP 
    advanced
CURRENT ISSUE ARCHIVES JASN Express ONLINE SUBMISSION


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
Right arrow reprints & permissions
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by HA, T.-S.
Right arrow Articles by KASINATH, B. S.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by HA, T.-S.
Right arrow Articles by KASINATH, B. S.
J Am Soc Nephrol 10:1931-1939, 1999
© 1999 American Society of Nephrology

REGULAR ARTICLES

Regulation of Renal Laminin in Mice with Type II Diabetes

TAE-SUN HA*, JEFFREY L. BARNES*, JENNIFER L. STEWART*, CHEOL W. KO*, JEFFREY H. MINER{ddagger}, DALE R. ABRAHAMSON{dagger}, JOSHUA R. SANES§ and BALAKUNTALAM S. KASINATH*

* Department of Medicine, University of Texas Health Science Center and A. L. Murphy Veterans' Administration Hospital, San Antonio, Texas
{dagger} Department of Cell Biology, University of Alabama, Birmingham, Alabama
{ddagger} Department of Medicine Washington University School of Medicine, St. Louis, Missouri.
§ Department of Anatomy and Neurobiology, Washington University School of Medicine, St. Louis, Missouri.

Correspondence to Dr. B. S. Kasinath, Department of Medicine, University of Texas Health Science Center, 7703 Floyd Curl Drive, San Antonio, TX 78284. Phone: 210-567-4700; Fax: 210-567-4712; E-mail: kasinath{at}uthscsa.edu

Abstract

Abstract. This study examines the regulation of renal laminin in the db/db mouse, a model of type II diabetes characterized by extensive remodeling of extracellular matrix. Immunohistochemistry demonstrated an increase in the contents of laminin chains including ß1 chain in the mesangium and tubular basement membranes at 1,2,3, and 4 mo of diabetes. Immunofluorescence with an antibody against the recently discovered laminin {alpha}5 chain showed that in the normal mouse, the protein had a restricted distribution to the glomerular and tubular basement membranes with scant expression in the mesangium of older mice. In the diabetic mouse, the laminin {alpha}5 chain content of the glomerular and tubular basement membranes was increased, with marked expression in the mesangium. Northern analysis revealed a significant decrease in the renal cortical contents of {alpha}5, ß1, and {gamma}1 chain mRNA in the diabetic mice compared to control, at each of the time points. In situ hybridization showed decreased abundance of {alpha}5 transcripts in the glomeruli of diabetic mice compared to nondiabetic controls. Analysis of mRNA changes by Northern and in situ hybridization studies demonstrated that the reduction in laminin transcripts involved both glomerular and tubular elements. These observations demonstrate that laminin accumulation in the db/db mice with type II diabetes is due to nontranscriptional mechanisms. Because previous investigations in rodents with type I diabetes have shown that the increase in renal laminin content was associated with a corresponding increment in laminin chain transcript levels, it appears that the mechanisms underlying augmentation in renal matrix laminin content may be distinct in the two types of diabetes.




This article has been cited by other articles:


Home page
 J. Biol. Chem.Home page
M. M. Mariappan, M. Shetty, K. Sataranatarajan, G. G. Choudhury, and B. S. Kasinath
Glycogen Synthase Kinase 3{beta} Is a Novel Regulator of High Glucose- and High Insulin-induced Extracellular Matrix Protein Synthesis in Renal Proximal Tubular Epithelial Cells
J. Biol. Chem., November 7, 2008; 283(45): 30566 - 30575.
[Abstract] [Full Text] [PDF]

Home page
 Am. J. Pathol.Home page
K. Sataranatarajan, M. M. Mariappan, M. J. Lee, D. Feliers, G. G. Choudhury, J. L. Barnes, and B. S. Kasinath
Regulation of Elongation Phase of mRNA Translation in Diabetic Nephropathy: Amelioration by Rapamycin
Am. J. Pathol., December 1, 2007; 171(6): 1733 - 1742.
[Abstract] [Full Text] [PDF]

Home page
 DiabetesHome page
M. M. Mariappan, D. Feliers, S. Mummidi, G. G. Choudhury, and B. S. Kasinath
High Glucose, High Insulin, and Their Combination Rapidly Induce Laminin-{beta}1 Synthesis by Regulation of mRNA Translation in Renal Epithelial Cells
Diabetes, February 1, 2007; 56(2): 476 - 485.
[Abstract] [Full Text] [PDF]

Home page
 Am. J. Physiol. Renal Physiol.Home page
M.-J. Lee, D. Feliers, M. M. Mariappan, K. Sataranatarajan, L. Mahimainathan, N. Musi, M. Foretz, B. Viollet, J. M. Weinberg, G. G. Choudhury, et al.
A role for AMP-activated protein kinase in diabetes-induced renal hypertrophy
Am J Physiol Renal Physiol, February 1, 2007; 292(2): F617 - F627.
[Abstract] [Full Text] [PDF]

Home page
 J. Am. Soc. Nephrol.Home page
B. S. Kasinath, M. M. Mariappan, K. Sataranatarajan, M. J. Lee, and D. Feliers
mRNA Translation: Unexplored Territory in Renal Science
J. Am. Soc. Nephrol., December 1, 2006; 17(12): 3281 - 3292.
[Abstract] [Full Text] [PDF]

Home page
 DiabetesHome page
H. Rincon-Choles, T. L. Vasylyeva, P. E. Pergola, B. Bhandari, K. Bhandari, J.-H. Zhang, W. Wang, Y. Gorin, J. L. Barnes, and H. E. Abboud
ZO-1 Expression and Phosphorylation in Diabetic Nephropathy.
Diabetes, April 1, 2006; 55(4): 894 - 900.
[Abstract] [Full Text] [PDF]

Home page
 Am. J. Physiol. Renal Physiol.Home page
D. Feliers, S. Duraisamy, J. L. Barnes, G. Ghosh-Choudhury, and B. S. Kasinath
Translational regulation of vascular endothelial growth factor expression in renal epithelial cells by angiotensin II
Am J Physiol Renal Physiol, March 1, 2005; 288(3): F521 - F529.
[Abstract] [Full Text] [PDF]

Home page
 J. Am. Soc. Nephrol.Home page
M. D. Breyer, E. Bottinger, F. C. Brosius III, T. M. Coffman, R. C. Harris, C. W. Heilig, K. Sharma, and for the AMDCC
Mouse Models of Diabetic Nephropathy
J. Am. Soc. Nephrol., January 1, 2005; 16(1): 27 - 45.
[Abstract] [Full Text] [PDF]

Home page
 DiabetesHome page
V. Thallas-Bonke, C. Lindschau, B. Rizkalla, L. A. Bach, G. Boner, M. Meier, H. Haller, M. E. Cooper, and J. M. Forbes
Attenuation of Extracellular Matrix Accumulation in Diabetic Nephropathy by the Advanced Glycation End Product Cross-Link Breaker ALT-711 via a Protein Kinase C-{alpha}-Dependent Pathway
Diabetes, November 1, 2004; 53(11): 2921 - 2930.
[Abstract] [Full Text] [PDF]

Home page
 HypertensionHome page
M. Ye, J. Wysocki, P. Naaz, M. R. Salabat, M. S. LaPointe, and D. Batlle
Increased ACE 2 and Decreased ACE Protein in Renal Tubules From Diabetic Mice: A Renoprotective Combination?
Hypertension, May 1, 2004; 43(5): 1120 - 1125.
[Abstract] [Full Text] [PDF]

Home page
 Am. J. Physiol. Renal Physiol.Home page
K. Sharma, P. McCue, and S. R. Dunn
Diabetic kidney disease in the db/db mouse
Am J Physiol Renal Physiol, June 1, 2003; 284(6): F1138 - F1144.
[Abstract] [Full Text] [PDF]


HOME CURRENT ISSUE ARCHIVES JASN Express ONLINE SUBMISSION AUTHOR INFO
EDITORIAL BOARD SUBSCRIBE FEEDBACK ALERTS HELP

Copyright © 2008 by the American Society of Nephrology. Online ISSN: 1533-3450 Print ISSN: 1046-6673