Changing Patterns of Gene Expression in the Pulmonary Trunk-banded Rat Heart

LekanneDeprez, Ronald H.; Hoff, Maurice J.B. van den; Boer, Piet A. J. de; Maas, Adrie; Chamuleau, R. A. F. M.; Lamers, Wouter H.; Moorman, Antoon F.M.

doi:10.1006/jmcc.1998.0753

Cited by 28 publications

(27 citation statements)

References 3 publications

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“…Previous studies have demonstrated that mRNA levels of Serca2a in the atria are decreased by mechanical stress (33,38), which is consistent with data from many studies investigating the change in Secra2a transcripts in the pressure or volume-overloaded ventricles (10,23,26,42). Also, Bauer et al (7) demonstrated that, in the pig ventricle, in a similar model, mRNA levels of Serca decrease and mRNA levels of atrial natriuretic factor (ANF) increase.…”

Section: Discussionsupporting

confidence: 74%

Pulmonary artery banding alters the expression of Ca²⁺transport proteins in the right atrium in rabbits

Gupta¹,

Varian²,

Bal³

et al. 2009

American Journal of Physiology-Heart and Circulatory Physiology

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Subsequently, the right atrium (RA) has to contract against a higher afterload, but it is unknown to what extent ventricular dysfunction has an effect on the atrial contractility. We hypothesized that right ventricular pressure overload may have an affect on atrial contractility and Ca 2ϩ transport protein expression. Therefore, we induced pressure overload of the right ventricle by PAB for 10 wk in rabbits and examined the changes in the expression of Ca 2ϩ transport proteins in the atrium. We demonstrate that PAB significantly decreased the expression of sarco(endo)plasmic reticulum Ca 2ϩ -ATPase (Serca) 2a while expression of Na ϩ /Ca 2ϩ exchanger-1 was significantly upregulated in the RA but not in the left atria of rabbit hearts, indicating that pressure is the major trigger. A decrease in Serca2a expression was concomitant with a significant decrease in sarcolipin (SLN), possibly indicating a compensatory role of SLN. The decreased expression of SLN was unable to completely restore sarcoplasmic reticulum Ca 2ϩ uptake function of Serca2a. Functional contractile assessments in isolated trabeculae showed no difference between PAB-and sham-operated rabbits at 1 Hz but displayed an enhanced force development at higher frequencies and in the presence of isoproterenol, while twitch timing was unaffected. Our results indicate that right ventricular mechanical overload due to PAB affects the expression of the Ca 2ϩ -handling proteins in the RA in rabbits.calcium ion transport proteins; pressure overload; sarcoplasmic reticulum

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Section: Discussionsupporting

confidence: 74%

Pulmonary artery banding alters the expression of Ca²⁺transport proteins in the right atrium in rabbits

Gupta¹,

Varian²,

Bal³

et al. 2009

American Journal of Physiology-Heart and Circulatory Physiology

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“…Obviously, in an animal model of HF symptoms such as fatigue or breathlessness are difficult to detect and quantify. Thus, very few studies have employed animal models of right-sided HF and often rather loose criteria for HF diagnosis (such as ruffled fur or weight loss combined with cardiac hypertrophy) have been used (LekanneDeprez et al, 1998). Studies of left-sided HF are much better established but still do not address symptoms.…”

Section: Discussionmentioning

confidence: 99%

“…The differences between previous hypertrophy studies and the present HF study were probably due to a much higher degree of constriction of the pulmonary artery in our PTB model (0.9 mm vs. 1.7-1.1 mm in other studies). To the best of our knowledge only one previous study has used PTB to induce overt HF and it lacked information on ARTICLE IN PRESS important parameters such as RV pressures since its focus was not on characterization of the PTB HF model (LekanneDeprez et al, 1998).…”

Section: Present Findings Vs Previous Studiesmentioning

confidence: 99%

“…However, slippage of the band and the obvious difficulties ensuring the same degree of constriction among the banded animals when using a surgical nylon thread led us to believe that banding with titanium clips would be a more reliable method to create PTB HF rats. Indeed, in another PTB study using surgical nylon thread, about 25% of the banded rats showed no hypertrophy (LekanneDeprez et al, 1998) suggesting that this was a less reliable way of banding. As all PTB rats in this study showed pronounced hypertrophy, banding with clips was a very reliable method.…”

Section: Inter-individual Variationsmentioning

confidence: 99%

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Characterization of a rat model of right-sided heart failure induced by pulmonary trunk banding

Schou

Peters

Kim

et al. 2007

Journal of Experimental Animal Science

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Animal models of disease are essential for cardiovascular research. However, animal models of right-sided heart failure are few and remain poorly characterized. The aim with this study was to establish a rat model of right-sided heart failure (HF) using pulmonary trunk banding (PTB) and subsequently to characterize the systemic and cardiac changes in this model, including protein expression of SERCA2 and a-sarcomeric actin. Rats underwent banding or sham operation. To evaluate the development of HF over time three groups were included in this study. They were killed 2-3, 5-7 or 16-17 weeks after operation, respectively. PTB rats showed marked hypertrophy of the right ventricle (RV). Catheterization of the RV showed a three-to four-fold increase in right ventricular systolic and diastolic pressures as well as increased dP/dT max and dP/dT min. Plasma analyses revealed increased liver enzymes in most PTB groups and post mortem examination revealed congestion of the liver as well as formation of ascites and hydrothorax in many PTB rats. Immunoblotting of the RV revealed no changes in SERCA2 or a-sarcomeric actin. In conclusion, PTB was an effective method to induce right-sided HF. The presence of HF was confirmed by severe signs of backward failure in conjunction with markedly elevated RV pressures and reduced RV ejection fraction (EF). r

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“…There have been multiple previous studies of increased RV afterload in many mammalian models, including cats (15,47), dogs (22,45), pigs (4,16), rabbits (5,19,23), and rats (8,11,20,33,36,53). The advantages of a well-characterized murine model, particularly in the ability to alter murine gene expression, are well known.…”

Section: Continuedmentioning

confidence: 99%

Molecular and physiological characterization of RV remodeling in a murine model of pulmonary stenosis

Urashima

Zhao²,

Wagner³

et al. 2008

American Journal of Physiology-Heart and Circulatory Physiology

108

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physiological characterization of RV remodeling in a murine model of pulmonary stenosis. Am J Physiol Heart Circ Physiol 295: H1351-H1368, 2008. First published June 27, 2008 doi:10.1152/ajpheart.91526.2007 dysfunction is a common long-term complication in patients after the repair of congenital heart disease. Previous investigators have examined the cellular and molecular mechanisms of left ventricular (LV) remodeling, but little is known about the stressed RV. Our purpose was to provide a detailed physiological characterization of a model of RV hypertrophy and failure, including RV-LV interaction, and to compare gene alterations between afterloaded RV versus LV. Pulmonary artery constriction was performed in 86 mice. Mice with mild and moderate pulmonary stenosis (PS) developed stable hypertrophy without decompensation. Mice with severe PS developed edema, decreased RV function, and high mortality. Tissue Doppler imaging demonstrated septal dyssynchrony and deleterious RV-LV interaction in the severe PS group. Microarray analysis showed 196 genes with increased expression and 1,114 with decreased expression. Several transcripts were differentially increased in the afterloaded RV but not in the afterloaded LV, including clusterin, neuroblastoma suppression of tumorigenicity 1, Dkk3, Sfrp2, formin binding protein, annexin A7, and lysyl oxidase. We have characterized a murine model of RV hypertrophy and failure, providing a platform for studying the physiological and molecular events of RV remodeling. Although the molecular responses of the RV and LV to afterload stress are mostly concordant, there are several key differences, which may represent targets for RV failure-specific therapy. gene expression; right ventricle; tetralogy of Fallot THE RIGHT VENTRICLE IS UNIQUELY at risk in patients with complex congenital heart disease involving right-sided obstructive lesions (e.g., tetralogy of Fallot, tetralogy/pulmonary atresia) and in patients with systemic right ventricles (1,40,46). Increased stress on the right ventricle in the form of increased hemodynamic loading (pressure and/or volume) may result in abnormalities in cardiac structure, function, metabolism, coronary perfusion, neurohormonal activation, and molecular signaling. These stresses lead to both adaptive and maladaptive structural and molecular remodeling of the right ventricle and deleterious effects on the left ventricle through ventricular-ventricular interaction and may limit long-term survival (3,7,29,42). For many of these patients, detrimental conditions for the right ventricle exist throughout life, even after successful repair or palliation. As surgical techniques for the primary repair of complex forms of congenital heart disease improve, long-term survival and quality of life will depend on our ability to preserve long-term right ventricular (RV) function. Decisions regarding the ideal time for surgical reintervention will need to be based on more quantitative rather than qualitative measures.Developing a better understanding of the molecu...

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Changing Patterns of Gene Expression in the Pulmonary Trunk-banded Rat Heart

Cited by 28 publications

References 3 publications

Pulmonary artery banding alters the expression of Ca²⁺transport proteins in the right atrium in rabbits

Pulmonary artery banding alters the expression of Ca²⁺transport proteins in the right atrium in rabbits

Characterization of a rat model of right-sided heart failure induced by pulmonary trunk banding

Molecular and physiological characterization of RV remodeling in a murine model of pulmonary stenosis

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Changing Patterns of Gene Expression in the Pulmonary Trunk-banded Rat Heart

Cited by 28 publications

References 3 publications

Pulmonary artery banding alters the expression of Ca2+transport proteins in the right atrium in rabbits

Pulmonary artery banding alters the expression of Ca2+transport proteins in the right atrium in rabbits

Characterization of a rat model of right-sided heart failure induced by pulmonary trunk banding

Molecular and physiological characterization of RV remodeling in a murine model of pulmonary stenosis

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Product

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Pulmonary artery banding alters the expression of Ca²⁺transport proteins in the right atrium in rabbits

Pulmonary artery banding alters the expression of Ca²⁺transport proteins in the right atrium in rabbits