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Cited by 75Cardiac Fibrosis and RemodelingCardiovascular Function and Risk FactorsCardiomyopathy and Myosin Studies

Extracellular Matrix Remodeling in the Heart of the Homocysteinemic Obese Rabbit

CARROLL, J, TYAGI, S·2005·American Journal of Hypertension
DOI 10.1016/j.amjhyper.2004.11.035
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Abstract

Despite the strides made toward understanding cardiac abnormalities in obesity-induced hypertension, the composition and concentration of cardiac extracellular matrix (ECM) components resulting from diet-induced obesity are largely unknown. Previous studies from our laboratory have demonstrated differential expression of collagens, growth factors, and homocysteine (Hcy) in pressure overload models of cardiac hypertrophy. The hypothesis of the present study was that left ventricular hypertrophy (LVH) from the combined pressure and volume overload of obesity induced cardiac fibrosis in part by increasing Hcy, increasing transforming growth factor-beta1 (TGF-beta1), and decreasing decorin. Using the rabbit model, we examined the changes in cardiac collagen accumulation, plasma Hcy, left ventricular (LV) TGF-beta1, and LV decorin after 12 weeks of developing obesity. Cardiac fibrosis was analyzed by trichrome stain for collagens. Total collagens types I and III, TGF-beta1, and decorin were analyzed in tissue homogenates by immunoblots and quantitated with a densitometer. After 12 weeks, rabbits eating a high-fat diet had greater body weight (5.38 +/- 0.3 kg v 3.73 +/- 0.6 kg) and greater LV weight (5.08 +/- 0.05 g v 3.86 +/- 0.17 g) compared with lean rabbits. Heart rate was also significantly higher in obese than in lean rabbits (221 +/- 8 v 173 +/- 5 beats/min). Plasma concentrations of circulating Hcy were 16.9 +/- 2.4 micromol/L and 24.3 +/- 1.8 micromol/L in lean and obese rabbits, respectively. Compared with lean rabbits, obese rabbits had increased interstitial and perivascular collagen, a 4-fold increase in the medial/lumen ratio of coronary vessels, a 1.75-fold increase in cardiac collagen I, and a 1.5-fold increase in cardiac collagen III levels. Levels of TGF-beta1 were increased 1.75-fold, whereas decorin levels were significantly reduced in obese compared with lean rabbits. In conclusion, a high-fat diet, even over a period as short as 12 weeks, causes fibrosis in coronary vessels as well as accumulation of collagen in the cardiac interstitium. The accumulation of cardiac collagen was associated with induction of Hcy and TGF-beta1 and with suppression of decorin.

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  • Increased fibrosis in coronary vessels as well as accumulation of collagen in the cardiac interstitium was detected in a high-fat diet-induced rabbit model of obesity.

    “Increased fibrosis in coronary vessels as well as accumulation of collagen in the cardiac interstitium was detected in a high-fat diet-induced rabbit model of obesity (39).”

    From Cardiac remodeling in obesity (2008) · cites this paper as [39]

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Research works printed but not linked: 8

  1. Rolland PH, Friggi A, Barlatier A, Piquet P, Latrille V, Faye MM, Guillou J, Charpiot P, Bodard H, Ghiringhelli O: Hyperhomocys- teinemia-induced vascular damage in the minipigs. Circulation 1995;91:1161-1174.
  2. Tyagi SC: Homocysteine redox-receptor and extracellular matrix regulation in vascular smooth muscle cells. Am J Physiol 1998;274: C396 -C405.
  3. Miller A, Mujumdar V, Shek E, Guillot J, Angelo M, Pakmer L, Tyagi SC: Hyperhomocysteinemia induces multiorgan damage. Heart Vessels 2000;15:135-143.
  4. Carroll JF, Henegar L, Henegar JR: Vascular remodeling in obesity- hypertension (abstract). FASEB J 1999;13:A115.
  5. Loscalzo J: The oxidant stress of hyperhomocysteinemia. J Clin Invest 1996;98:5-6.
  6. Mulvany MJ, Baumbach GL, Aalkjaer C, Heagerty AM: Vascular remodeling. Hypertension 1996;28:505-506.
  7. Pugliese G, Pricci F, Mene P, Romeo G, Nofroni I, Giannini S, Cresci B, Galli G, Rotella CM, Di Mario U, Pugliese F: High gluocose level unmasks a genetic predisposition of enhanced ex- traacellular matrix production in mesangial cells from the milan normotensive strain. J Am Soc Nephrol 1997;8:406 -414.
  8. Boluyt M, Lydia O'Neil, Andrea LM, Oscar B, Brooks W, Conrad CH, Crow TM, Lakatta EG: Alterations in cardiac gene expression during the transition from stable hypertrophy to heart failure. Cir Res 1994;75:23-32.

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Authors
CARROLL, J., & TYAGI, S.
Affiliations
  • University of North Texas Health Science Center (US)
  • University of Louisville (US)
Corresponding author
TYAGI, S
Venue
American Journal of Hypertension
Publisher
Oxford University Press (OUP)
Published
2005-05
Volume
18
Issue
5
Pages
692-698
ISSN
0895-7061 (ISSN-L)
DOI
10.1016/j.amjhyper.2004.11.035
OpenAlex
W2034784349
Cited by
75
References
40
Citations by year
2026: 2 · 2025: 1 · 2023: 5 · 2022: 3 · 2021: 6 · 2020: 4 · 2019: 3 · 2018: 2 · 2017: 2 · 2016: 1 · 2015: 4 · 2014: 4 · 2013: 3 · 2012: 5
FWCI
3.20
Type
journal article
Language
en
Open access
closed
Locations
  • American Journal of Hypertension (publishedVersion)
  • PubMed (publishedVersion)
Funders
  • National Institutes of Health (HL-74185)
  • National Heart, Lung, and Blood Institute (R01HL071010, HL 71010, R01HL074185, HL 74185)
Topics
  • Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Cardiac Fibrosis and Remodeling
  • Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Cardiovascular Function and Risk Factors
  • Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Cardiomyopathy and Myosin Studies
Keywords
extracellular matrix remodeling, myocardial fibrosis, homocysteine, obesity, left ventricular hypertrophy, TGF-β1, decorin, collagen deposition, high-fat diet, pressure and volume overload, rabbit model
MeSH terms
Animals, Collagen, Coronary Vessels, Extracellular Matrix, Female, Homocysteine, Hypertrophy, Multiple Organ Failure, Myocardium, Obesity, Rabbits, Transforming Growth Factor beta, Transforming Growth Factor beta1

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