AJP - Lung Fuel your research with LabChart
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
QUICK SEARCH:   [advanced]


     

Am J Physiol Lung Cell Mol Physiol 284: L333-L341, 2003. First published October 25, 2002; doi:10.1152/ajplung.00183.2002
1040-0605/03 $5.00
This Article
Right arrow Full Text
Right arrow Full Text (PDF)
Right arrow All Versions of this Article:
284/2/L333    most recent
00183.2002v1
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 ISI 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 ISI Web of Science (16)
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Sood, H. S.
Right arrow Articles by Tyagi, S. C.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Sood, H. S.
Right arrow Articles by Tyagi, S. C.
Vol. 284, Issue 2, L333-L341, February 2003

Peroxisome proliferator ameliorates endothelial dysfunction in a murine model of hyperhomocysteinemia

Harpreet S. Sood, Matthew J. Hunt, and Suresh C. Tyagi

Department of Physiology and Biophysics, University of Mississippi Medical Center, Jackson, Mississippi 39216

To test the hypothesis that endothelial dysfunction in hyperhomocysteinemia was due to increased levels of nitrotyrosine and matrix metalloproteinase (MMP) activity in response to antagonism of peroxisome proliferator-activated receptor-alpha (PPAR-alpha ), cystathionine beta -synthase (CBS) -/+ mice were bred, tail tissue was analyzed for genotype by PCR, and tail vein blood was analyzed for homocysteine (Hcy) by spectrofluorometry. To induce PPAR-alpha , mice were administered 8 µg/ml of ciprofibrate (CF) and grouped: 1) wild type (WT), 2) WT + CF, 3) CBS, 4) CBS + CF (n = 6 in each group). In these four groups of mice, plasma Hcy was 3.0 ± 0.2, 2.5 ± 1.2, 15.2 ± 2.6 (P < 0.05 compared with WT), 11.0 ± 2.9 µmol/l. Mouse urinary protein was 110 ± 11, 86 ± 6, 179 ± 13, 127 ± 9 µg · day-1 · kg-1 by Bio-Rad dye binding assay. Aortic nitrotyrosine was 0.099 ± 0.012, 0.024 ± 0.004, 0.132 ± 0.024 (P < 0.01 compared with WT), 0.05 ± 0.01 (scan unit) by Western analysis. MMP-2 activity was 0.053 ± 0.010, 0.024 ± 0.002, 0.039 ± 0.009, 0.017 ± 0.006 (scan unit) by zymography. MMP-9 was specifically induced in CBS -/+ mice and inhibited by CF treatment. Systolic blood pressure (SPB) was 90 ± 2, 88 ± 16, 104 ± 8 (P < 0.05 compared with WT), 96 ± 3 mmHg. Aortic wall stress [(SPB · radius2/wall thickness)/2(radius + wall thickness)] was 10.2 ± 1.9, 9.7 ± 0.2, 16.6 ± 0.8 (P < 0.05 compared with WT), 13.1 ± 2.1 dyn/cm2. The results suggest that Hcy increased aortic wall stress by increasing nitrotyrosine and MMP-9 activity.

extracellular matrix; matrix metalloproteinase; tissue inhibitor of metalloproteinase; collagen; elastin; cystathionine beta -synthase; nitric oxide; arteriosclerosis; fibrate


This article has been cited by other articles:


Home page
 Am. J. Physiol. Lung Cell. Mol. Physiol.Home page
A. V. Ovechkin, N. Tyagi, U. Sen, D. Lominadze, M. M. Steed, K. S. Moshal, and S. C. Tyagi
3-Deazaadenosine mitigates arterial remodeling and hypertension in hyperhomocysteinemic mice
Am J Physiol Lung Cell Mol Physiol, November 1, 2006; 291(5): L905 - L911.
[Abstract] [Full Text] [PDF]

Home page
 Am. J. Physiol. Renal Physiol.Home page
W. E. Rodriguez, N. Tyagi, I. G. Joshua, J. C. Passmore, J. T. Fleming, J. C. Falcone, and S. C. Tyagi
Pioglitazone mitigates renal glomerular vascular changes in high-fat, high-calorie-induced type 2 diabetes mellitus
Am J Physiol Renal Physiol, September 1, 2006; 291(3): F694 - F701.
[Abstract] [Full Text] [PDF]

Home page
 Circ. Res.Home page
A. M. Devlin and S. R. Lentz
ApoA-I: A Missing Link Between Homocysteine and Lipid Metabolism?
Circ. Res., March 3, 2006; 98(4): 431 - 433.
[Full Text] [PDF]

Home page
 ANGIOLOGYHome page
N. P. Kadoglou, S. S. Daskalopoulou, D. Perrea, and C. D. Liapis
Matrix Metalloproteinases and Diabetic Vascular Complications
Angiology, March 1, 2005; 56(2): 173 - 189.
[Abstract] [PDF]

Home page
 J CARDIOVASC PHARMACOL THERHome page
S. C. Tyagi, W. Rodriguez, A. M. Patel, A. M. Roberts, J. C. Falcone, J. C. Passmore, J. T. Fleming, and I. G. Joshua
Hyperhomocysteinemic Diabetic Cardiomyopathy: Oxidative Stress, Remodeling, and Endothelial-Myocyte Uncoupling
Journal of Cardiovascular Pharmacology and Therapeutics, January 1, 2005; 10(1): 1 - 10.
[Abstract] [PDF]

Home page
 Arterioscler. Thromb. Vasc. Bio.Home page
F. M. Faraci
Hyperhomocysteinemia: A Million Ways to Lose Control
Arterioscler. Thromb. Vasc. Biol., March 1, 2003; 23(3): 371 - 373.
[Full Text] [PDF]


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