Connective Tissue Remodeling: Cross-Talk between Endothelins and Matrix Metalloproteinases

Abraham, David; Ponticos, Markella; Nagase, Hideaki

doi:10.2174/157016105774329480

Cited by 43 publications

(27 citation statements)

References 81 publications

(112 reference statements)

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“…Initially investigated for potent vasoactive properties, evidence for ET-1 involvement in extracellular matrix turnover in disease states has been mounting (1,2,21,38,46). Clinical trials using ET A receptor antagonist in congestive heart failure patients reported lower systemic vascular resistance that resulted in higher cardiac index (6,31).…”

Section: Discussionmentioning

confidence: 99%

ET_Aselective receptor antagonism prevents ventricular remodeling in volume-overloaded rats

Murray¹,

McMillan²,

Brower³

et al. 2009

American Journal of Physiology-Heart and Circulatory Physiology

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Murray DB, McMillan R, Brower GL, Janicki JS. ETA selective receptor antagonism prevents ventricular remodeling in volume-overloaded rats. Am J Physiol Heart Circ Physiol 297: H109 -H116, 2009. First published May 8, 2009 doi:10.1152/ajpheart.00968.2008.-The objective of this study was to investigate the ability of selective endothelin receptor subtype A (ET A) endothelin receptor antagonism (ETA) to prevent the acute myocardial remodeling process secondary to volume overload. Left ventricular tissue from sham-operated (Sham) and untreated (Fist), and TBC-3214 (Fist ϩ ETA, 25 mg ⅐ kg Ϫ1 ⅐ day Ϫ1 )-treated fistula animals was analyzed for mast cell density, matrix metalloproteinase (MMP) activity, and extracellular collagen volume fraction (CVF) 1 and 5 days following the initiation of volume overload. Compared with Fist, ETA treatment prevented the increase in left ventricular mast cell density at 1 day and 5 days. Additionally, at 1 day postfistula, a substantial decrease in MMP-2 activity below Sham levels was observed following endothelin receptor antagonism (1.7 Ϯ 0.7 vs. 0.3 Ϯ 0.3 vs. 0.9 Ϯ 0.2 arbitrary activity units, Fist vs. Fist ϩ ETA vs. Sham, P Յ 0.05). This same effect was also seen at 5 days postfistula (1.9 Ϯ 0.3 vs. 0.5 Ϯ 0.1 arbitrary activity units, Fist vs. Fist ϩ ETA, P Յ 0.05). The marked decrease in myocardial CVF seen in Fist hearts (0.7 Ϯ 0.1 vs. 1.6 Ϯ 0.1% myocardial area, Fist vs. Sham, P Յ 0.05) was prevented by ETA (1.7 Ϯ 0.1% Fist ϩ ETA, P Ͻ 0.05 vs. Fist). This preservation of the collagen matrix was also present on day 5 in the TBC-treated group vs. the Fist group (1.0 Ϯ 0.1 vs. 1.4 Ϯ 0.1%, Fist vs. Fist ϩ ETA, P Յ 0.01). Furthermore, an 8-wk preventative treatment with ETA significantly attenuated the increase in left ventricular end systolic and diastolic volumes compared with untreated fistula hearts. In conclusion, the novel findings of this study indicate that the activation of cardiac mast cells and subsequent MMP activation/collagen degradation during the acute stages of volume overload are prevented by blockade of the ET A receptor subtype. Furthermore, by preventing these events, ET-1 antagonism was efficacious in attenuating ventricular dilatation and limiting the development of structural and functional deficits.endothelin-1; mast cell; matrix metalloproteinase; TBC-3214 ENDOTHELIN (ET)-1 is a potent neurohormone produced throughout the cardiovascular system, and the observation that plasma ET-1 is elevated in patients with heart failure is suggestive of a role in the pathophysiology of heart failure (16,19,34,40,47). The cardiovascular effects of ET-1 (a 21-amino-acid peptide) are dictated by binding to one of two G protein-linked receptor subtypes [endothelin receptor subtypes A (ET A ) or B (ET B )] (23). In the heart and vasculature, binding and activation of ET A is known to mediate powerful vasoconstrictor and pressor affects, in addition to chronotropic and ionotropic effects (12,25). The ET B receptor subtype is responsible for systemic clearance of circulating ...

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Section: Discussionmentioning

confidence: 99%

ET_Aselective receptor antagonism prevents ventricular remodeling in volume-overloaded rats

Murray¹,

McMillan²,

Brower³

et al. 2009

American Journal of Physiology-Heart and Circulatory Physiology

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“…Several lines of investigation in other biologic systems have established that ET-1 affects the synthesis of MMPs (18). Koyama and Tanaka (19) have recently shown that ET-1 stimulates the production of MMP-3 in cultured rat astrocytes.…”

Section: Discussionmentioning

confidence: 99%

Prevention of Inflammation-Associated Preterm Birth by Knockdown of the Endothelin-1-Matrix Metalloproteinase-1 Pathway

Wang

Yen

Chen

et al. 2010

Mol Med

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Premature delivery occurs in 12% of all births, accounts for nearly half of neonatal morbidity and is increasing in frequency. Current therapeutic approaches to preterm delivery are ineffective and present serious risks to both the mother and fetus. Although there are multiple factors that contribute to the etiology of preterm birth, the single most common cause is infection. Recently, using cDNA microarray analysis of human placental tissue, we demonstrated that human placental matrix metalloproteinase-1 (MMP-1) is upregulated during labor. In a separate line of investigation, we have shown that blockade of endothelin-1 (ET-1) action through the use of an endothelin-converting enzyme-1 (ECE-1) inhibitor, an established commercially available endothelin receptor antagonist or a novel quinolone-derived endothelin receptor antagonist synthesized by our group also prevents preterm labor and delivery in a mouse model. We have now shown that induction of preterm labor with lipopolysaccharide in our mouse model is associated with increased levels of MMP-1. Furthermore, we showed that silencing the ECE-1/ET-1 pathway by using ECE-1 RNA interference prevents both the onset of preterm labor and upregulation of MMP-1. The data indicate that ET-1 and MMP-1 act in the same molecular pathway in preterm labor.

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“…Pro-MMPs lie dormant within the ECM and are activated by various signals (Murphy et al, 1999;Davidson et al, 2002;Tsuruda et al, 2004;Nagase et al, 2006;Amalinei et al, 2007;Ra and 2008). Misregulation of MMP activity contributes to multiple diseases (metastatic carcinoma, cardiovascular disease, rheumatoid arthritis, osteoarthritis, oral diseases) and is also implicated in preterm labor (Davidson et al, 2002;Abraham et al, 2005;Hofmann et al, 2005;Vadillo-Ortega and Estrada-Gutierrez, 2005;Lemaitre and D'Armiento, 2006;Liu et al, 2006;Mon et al, 2006;Cockle et al, 2007). The dynamic interaction between ECM synthesis/ assembly and degradation via MMPs is an exquisite balancing act that mediates both embryonic development and tissue homeostasis.…”

Section: Extracellular Matrix Proteinsmentioning

confidence: 99%

Dynamic interactions between cells and their extracellular matrix mediate embryonic development

Goody

Henry

2010

Molecular Reproduction Devel

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SUMMARYCells and their surrounding extracellular matrix microenvironment interact throughout all stages of life. Understanding the continuously changing scope of cell-matrix interactions in vivo is crucial to garner insights into both congenital birth defects and disease progression. A current challenge in the field of developmental biology is to adapt in vitro tools and rapidly evolving imaging technology to study cell-matrix interactions in a complex 4-D environment. In this review, we highlight the dynamic modulation of cell-matrix interactions during development. We propose that individual cell-matrix adhesion proteins are best considered as complex proteins that can play multiple, often seemingly contradictory roles, depending upon the context of the microenvironment. In addition, cell-matrix proteins can also exert different short versus long term effects. It is thus important to consider cell behavior in light of the microenvironment because of the constant and dynamic reciprocal interactions occurring between them. Finally, we suggest that analysis of cell-matrix interactions at multiple levels (molecules, cells, tissues) in vivo is critical for an integrated understanding because different information can be acquired from all size scales.Mol.

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Connective Tissue Remodeling: Cross-Talk between Endothelins and Matrix Metalloproteinases

Cited by 43 publications

References 81 publications

ET_Aselective receptor antagonism prevents ventricular remodeling in volume-overloaded rats

ET_Aselective receptor antagonism prevents ventricular remodeling in volume-overloaded rats

Prevention of Inflammation-Associated Preterm Birth by Knockdown of the Endothelin-1-Matrix Metalloproteinase-1 Pathway

Dynamic interactions between cells and their extracellular matrix mediate embryonic development

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Connective Tissue Remodeling: Cross-Talk between Endothelins and Matrix Metalloproteinases

Cited by 43 publications

References 81 publications

ETAselective receptor antagonism prevents ventricular remodeling in volume-overloaded rats

ETAselective receptor antagonism prevents ventricular remodeling in volume-overloaded rats

Prevention of Inflammation-Associated Preterm Birth by Knockdown of the Endothelin-1-Matrix Metalloproteinase-1 Pathway

Dynamic interactions between cells and their extracellular matrix mediate embryonic development

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ET_Aselective receptor antagonism prevents ventricular remodeling in volume-overloaded rats

ET_Aselective receptor antagonism prevents ventricular remodeling in volume-overloaded rats