Angiotensin Type 2 Receptor Stimulation Ameliorates Left Ventricular Fibrosis and Dysfunction via Regulation of Tissue Inhibitor of Matrix Metalloproteinase 1/Matrix Metalloproteinase 9 Axis and Transforming Growth Factor beta 1 in the Rat Heart

Dilyara Lauer; Svetlana Slavic; Manuela Sommerfeld; Christa Thoene-Reineke; Yuliya Sharkovska; Anders Hallberg; Bjorn Dahlof; Ulrich Kintscher; Thomas Unger; Ulrike Muscha Steckelings; Elena Kaschina

doi:10.1161/HYPERTENSIONAHA.113.02522

Angiotensin Type 2 Receptor Stimulation Ameliorates Left Ventricular Fibrosis and Dysfunction via Regulation of Tissue Inhibitor of Matrix Metalloproteinase 1/Matrix Metalloproteinase 9 Axis and Transforming Growth Factor beta 1 in the Rat Heart

Dilyara Lauer, Svetlana Slavic, Manuela Sommerfeld, Christa Thoene-Reineke, Yuliya Sharkovska, Anders Hallberg, Bjorn Dahlof, Ulrich Kintscher, Thomas Unger, Ulrike Muscha Steckelings, Elena Kaschina^*

^*Corresponding author for this work

Bedrijfsbureau CARIM

Research output: Contribution to journal › Article › Academic › peer-review

Abstract

Left ventricular (LV) remodeling is the main reason for the development of progressive cardiac dysfunction after myocardial infarction (MI). This study investigated whether stimulation of the angiotensin type 2 receptor is able to ameliorate post-MI cardiac remodeling and what the underlying mechanisms may be. MI was induced in Wistar rats by permanent ligation of the left coronary artery. Treatment with the angiotensin type 2 receptor agonist compound 21 (0.03 mg/kg) was started 6 hours post-MI and continued for 6 weeks. Hemodynamic parameters were measured by echocardiography and intracardiac catheter. Effects on proteolysis were studied in heart tissue and primary cardiac fibroblasts. Compound 21 significantly improved systolic and diastolic functions, resulting in improved ejection fraction (71.2?4.7% versus 53.4?7.0%; P

Original language	English
Pages (from-to)	E60-E67
Journal	Hypertension
Volume	63
Issue number	3
DOIs	https://doi.org/10.1161/HYPERTENSIONAHA.113.02522
Publication status	Published - Mar 2014

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Lauer, D., Slavic, S., Sommerfeld, M., Thoene-Reineke, C., Sharkovska, Y., Hallberg, A., Dahlof, B., Kintscher, U., Unger, T., Steckelings, U. M., & Kaschina, E. (2014). Angiotensin Type 2 Receptor Stimulation Ameliorates Left Ventricular Fibrosis and Dysfunction via Regulation of Tissue Inhibitor of Matrix Metalloproteinase 1/Matrix Metalloproteinase 9 Axis and Transforming Growth Factor beta 1 in the Rat Heart. Hypertension, 63(3), E60-E67. https://doi.org/10.1161/HYPERTENSIONAHA.113.02522

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title = "Angiotensin Type 2 Receptor Stimulation Ameliorates Left Ventricular Fibrosis and Dysfunction via Regulation of Tissue Inhibitor of Matrix Metalloproteinase 1/Matrix Metalloproteinase 9 Axis and Transforming Growth Factor beta 1 in the Rat Heart",

abstract = "Left ventricular (LV) remodeling is the main reason for the development of progressive cardiac dysfunction after myocardial infarction (MI). This study investigated whether stimulation of the angiotensin type 2 receptor is able to ameliorate post-MI cardiac remodeling and what the underlying mechanisms may be. MI was induced in Wistar rats by permanent ligation of the left coronary artery. Treatment with the angiotensin type 2 receptor agonist compound 21 (0.03 mg/kg) was started 6 hours post-MI and continued for 6 weeks. Hemodynamic parameters were measured by echocardiography and intracardiac catheter. Effects on proteolysis were studied in heart tissue and primary cardiac fibroblasts. Compound 21 significantly improved systolic and diastolic functions, resulting in improved ejection fraction (71.2?4.7% versus 53.4?7.0%; P",

author = "Dilyara Lauer and Svetlana Slavic and Manuela Sommerfeld and Christa Thoene-Reineke and Yuliya Sharkovska and Anders Hallberg and Bjorn Dahlof and Ulrich Kintscher and Thomas Unger and Steckelings, {Ulrike Muscha} and Elena Kaschina",

year = "2014",

month = mar,

doi = "10.1161/HYPERTENSIONAHA.113.02522",

language = "English",

volume = "63",

pages = "E60--E67",

journal = "Hypertension",

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publisher = "LIPPINCOTT WILLIAMS & WILKINS",

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Lauer, D, Slavic, S, Sommerfeld, M, Thoene-Reineke, C, Sharkovska, Y, Hallberg, A, Dahlof, B, Kintscher, U, Unger, T, Steckelings, UM & Kaschina, E 2014, 'Angiotensin Type 2 Receptor Stimulation Ameliorates Left Ventricular Fibrosis and Dysfunction via Regulation of Tissue Inhibitor of Matrix Metalloproteinase 1/Matrix Metalloproteinase 9 Axis and Transforming Growth Factor beta 1 in the Rat Heart', Hypertension, vol. 63, no. 3, pp. E60-E67. https://doi.org/10.1161/HYPERTENSIONAHA.113.02522

Angiotensin Type 2 Receptor Stimulation Ameliorates Left Ventricular Fibrosis and Dysfunction via Regulation of Tissue Inhibitor of Matrix Metalloproteinase 1/Matrix Metalloproteinase 9 Axis and Transforming Growth Factor beta 1 in the Rat Heart. / Lauer, Dilyara; Slavic, Svetlana; Sommerfeld, Manuela et al.
In: Hypertension, Vol. 63, No. 3, 03.2014, p. E60-E67.

Research output: Contribution to journal › Article › Academic › peer-review

TY - JOUR

T1 - Angiotensin Type 2 Receptor Stimulation Ameliorates Left Ventricular Fibrosis and Dysfunction via Regulation of Tissue Inhibitor of Matrix Metalloproteinase 1/Matrix Metalloproteinase 9 Axis and Transforming Growth Factor beta 1 in the Rat Heart

AU - Lauer, Dilyara

AU - Slavic, Svetlana

AU - Sommerfeld, Manuela

AU - Thoene-Reineke, Christa

AU - Sharkovska, Yuliya

AU - Hallberg, Anders

AU - Dahlof, Bjorn

AU - Kintscher, Ulrich

AU - Unger, Thomas

AU - Steckelings, Ulrike Muscha

AU - Kaschina, Elena

PY - 2014/3

Y1 - 2014/3

N2 - Left ventricular (LV) remodeling is the main reason for the development of progressive cardiac dysfunction after myocardial infarction (MI). This study investigated whether stimulation of the angiotensin type 2 receptor is able to ameliorate post-MI cardiac remodeling and what the underlying mechanisms may be. MI was induced in Wistar rats by permanent ligation of the left coronary artery. Treatment with the angiotensin type 2 receptor agonist compound 21 (0.03 mg/kg) was started 6 hours post-MI and continued for 6 weeks. Hemodynamic parameters were measured by echocardiography and intracardiac catheter. Effects on proteolysis were studied in heart tissue and primary cardiac fibroblasts. Compound 21 significantly improved systolic and diastolic functions, resulting in improved ejection fraction (71.2?4.7% versus 53.4?7.0%; P

AB - Left ventricular (LV) remodeling is the main reason for the development of progressive cardiac dysfunction after myocardial infarction (MI). This study investigated whether stimulation of the angiotensin type 2 receptor is able to ameliorate post-MI cardiac remodeling and what the underlying mechanisms may be. MI was induced in Wistar rats by permanent ligation of the left coronary artery. Treatment with the angiotensin type 2 receptor agonist compound 21 (0.03 mg/kg) was started 6 hours post-MI and continued for 6 weeks. Hemodynamic parameters were measured by echocardiography and intracardiac catheter. Effects on proteolysis were studied in heart tissue and primary cardiac fibroblasts. Compound 21 significantly improved systolic and diastolic functions, resulting in improved ejection fraction (71.2?4.7% versus 53.4?7.0%; P

U2 - 10.1161/HYPERTENSIONAHA.113.02522

DO - 10.1161/HYPERTENSIONAHA.113.02522

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SP - E60-E67

JO - Hypertension

JF - Hypertension

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Lauer D, Slavic S, Sommerfeld M, Thoene-Reineke C, Sharkovska Y, Hallberg A et al. Angiotensin Type 2 Receptor Stimulation Ameliorates Left Ventricular Fibrosis and Dysfunction via Regulation of Tissue Inhibitor of Matrix Metalloproteinase 1/Matrix Metalloproteinase 9 Axis and Transforming Growth Factor beta 1 in the Rat Heart. Hypertension. 2014 Mar;63(3):E60-E67. doi: 10.1161/HYPERTENSIONAHA.113.02522