Improvement of defective sarcoplasmic reticulum Ca2+ transport in diabetic heart of transgenic rats expressing the human kallikrein-1 gene

Carsten Tschöpe; Frank Spillmann; Uwe Rehfeld; Matthias Koch; Dirk Westermann; Christine Altmann; Andreas Dendorfer; Thomas Walther; Michael Bader; Martin Paul; Heinz Peter Schultheiss; Roland Vetter

doi:10.1096/fj.04-1614fje

Improvement of defective sarcoplasmic reticulum Ca²⁺ transport in diabetic heart of transgenic rats expressing the human kallikrein-1 gene

Carsten Tschöpe^*, Frank Spillmann, Uwe Rehfeld, Matthias Koch, Dirk Westermann, Christine Altmann, Andreas Dendorfer, Thomas Walther, Michael Bader, Martin Paul, Heinz Peter Schultheiss, Roland Vetter

^*Corresponding author for this work

Institute of Experimental and Clinical Pharmacology and Toxicology

26 Citations (Scopus)

Abstract

Transgenic cardiac expression of the bradykinin (BK) -forming enzyme human tissue kallikrein 1 (hKLK1) in rats is known to attenuate the development of cardiac fibrosis and left ventricular dysfunction in diabetic cardiomyopathy. To examine whether improved diastolic and systolic performance in diabetic hKLK1-expressing hearts may be due to rescued sarcoplasmic reticulum (SR) Ca2+ handling, we studied left ventricular (LV) function and Ca2+-ATPase(SERCA2a)-catalyzed SR Ca2+ transport after induction of streptozotocin (STZ) -induced diabetes mellitus in transgenic rats (TGR) expressing the hKLK1 gene.

Original language	English
Journal	FASEB Journal
Volume	18
Issue number	15
Pages (from-to)	1967-1969
Number of pages	3
ISSN	0892-6638
DOIs	https://doi.org/10.1096/fj.04-1614fje
Publication status	Published - 01.12.2004

Research Areas and Centers

Academic Focus: Center for Brain, Behavior and Metabolism (CBBM)

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This output contributes to the following UN Sustainable Development Goals (SDGs)

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10.1096/fj.04-1614fje

Cite this

Tschöpe, C., Spillmann, F., Rehfeld, U., Koch, M., Westermann, D., Altmann, C., Dendorfer, A., Walther, T., Bader, M., Paul, M., Schultheiss, H. P., & Vetter, R. (2004). Improvement of defective sarcoplasmic reticulum Ca²⁺ transport in diabetic heart of transgenic rats expressing the human kallikrein-1 gene. FASEB Journal, 18(15), 1967-1969. https://doi.org/10.1096/fj.04-1614fje

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title = "Improvement of defective sarcoplasmic reticulum Ca2+ transport in diabetic heart of transgenic rats expressing the human kallikrein-1 gene",

abstract = "Transgenic cardiac expression of the bradykinin (BK) -forming enzyme human tissue kallikrein 1 (hKLK1) in rats is known to attenuate the development of cardiac fibrosis and left ventricular dysfunction in diabetic cardiomyopathy. To examine whether improved diastolic and systolic performance in diabetic hKLK1-expressing hearts may be due to rescued sarcoplasmic reticulum (SR) Ca2+ handling, we studied left ventricular (LV) function and Ca2+-ATPase(SERCA2a)-catalyzed SR Ca2+ transport after induction of streptozotocin (STZ) -induced diabetes mellitus in transgenic rats (TGR) expressing the hKLK1 gene.",

author = "Carsten Tsch{\"o}pe and Frank Spillmann and Uwe Rehfeld and Matthias Koch and Dirk Westermann and Christine Altmann and Andreas Dendorfer and Thomas Walther and Michael Bader and Martin Paul and Schultheiss, {Heinz Peter} and Roland Vetter",

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Tschöpe, C, Spillmann, F, Rehfeld, U, Koch, M, Westermann, D, Altmann, C, Dendorfer, A, Walther, T, Bader, M, Paul, M, Schultheiss, HP & Vetter, R 2004, 'Improvement of defective sarcoplasmic reticulum Ca²⁺ transport in diabetic heart of transgenic rats expressing the human kallikrein-1 gene', FASEB Journal, vol. 18, no. 15, pp. 1967-1969. https://doi.org/10.1096/fj.04-1614fje

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T1 - Improvement of defective sarcoplasmic reticulum Ca2+ transport in diabetic heart of transgenic rats expressing the human kallikrein-1 gene

AU - Tschöpe, Carsten

AU - Spillmann, Frank

AU - Rehfeld, Uwe

AU - Koch, Matthias

AU - Westermann, Dirk

AU - Altmann, Christine

AU - Dendorfer, Andreas

AU - Walther, Thomas

AU - Bader, Michael

AU - Paul, Martin

AU - Schultheiss, Heinz Peter

AU - Vetter, Roland

PY - 2004/12/1

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N2 - Transgenic cardiac expression of the bradykinin (BK) -forming enzyme human tissue kallikrein 1 (hKLK1) in rats is known to attenuate the development of cardiac fibrosis and left ventricular dysfunction in diabetic cardiomyopathy. To examine whether improved diastolic and systolic performance in diabetic hKLK1-expressing hearts may be due to rescued sarcoplasmic reticulum (SR) Ca2+ handling, we studied left ventricular (LV) function and Ca2+-ATPase(SERCA2a)-catalyzed SR Ca2+ transport after induction of streptozotocin (STZ) -induced diabetes mellitus in transgenic rats (TGR) expressing the hKLK1 gene.

AB - Transgenic cardiac expression of the bradykinin (BK) -forming enzyme human tissue kallikrein 1 (hKLK1) in rats is known to attenuate the development of cardiac fibrosis and left ventricular dysfunction in diabetic cardiomyopathy. To examine whether improved diastolic and systolic performance in diabetic hKLK1-expressing hearts may be due to rescued sarcoplasmic reticulum (SR) Ca2+ handling, we studied left ventricular (LV) function and Ca2+-ATPase(SERCA2a)-catalyzed SR Ca2+ transport after induction of streptozotocin (STZ) -induced diabetes mellitus in transgenic rats (TGR) expressing the hKLK1 gene.

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