The effects of transforming growth factor-beta 1 (TGF-beta 1) on the function and structure of sarcoplasmic reticulum (SR) were studied in cultured neonatal rat cardiac myocytes. The cardiac myocytes at days 2 and 6 of culture exhibited spontaneous contraction; however, the rate of contraction increased and became regular, depending on culture day. Ryanodine and norepinephrine (NE) increased the rate of contraction and frequency of Ca2+ oscillations in myocytes at day 2 of culture. Ryanodine did not affect the spontaneous contraction in nontreated and TGF-beta 1-treated myocytes. On the other hand, NE caused negative and positive chronotropic responses in nontreated and TGF-beta 1-treated cells, respectively. In the absence of extracellular Ca2+, ryanodine and NE did not affect the cytoplasmic Ca2+ concentration ([Ca2+]i) in the nontreated cells, whereas NE increased [Ca2+]i but ryanodine did not in the TGF-beta 1-treated cells. SR structures in TGF-beta 1-treated cells developed more than those in nontreated cells. The results indicate that TGF-beta 1 plays an important role in the upregulation of SR function and structure of cultured neonatal rat cardiac myocytes.
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http://dx.doi.org/10.1152/ajpheart.1997.272.6.H2639 | DOI Listing |
Mol Med
January 2025
The First People's Hospital of Lin'an District, No. 360, Yikang Street, Jinnan Subdistrict, Lin'an District, Hangzhou, Zhejiang, 311300, China.
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View Article and Find Full Text PDFPLoS One
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Precision Laboratory of Vascular Medicine, Shanxi Cardiovascular Hospital Affiliated Shanxi Medical University, Taiyuan, PR China.
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Drug Des Devel Ther
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School of Basic Medicine, Jiamusi University, Jiamusi, Heilongjiang, 154000, People's Republic of China.
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View Article and Find Full Text PDFFunct Integr Genomics
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Department of Cardiology, Guizhou Provincial People`s Hospital, 83 Zhongshan East Road, Guiyang City, 550002, Guizhou Province, China.
Metabolic reprogramming, the shifting from fatty acid oxidation to glucose utilization, improves cardiac function as heart failure (HF) progresses. Leptin plays an essential role in regulating glucose metabolism. However, the crosstalk between leptin and metabolic reprogramming is poorly understood.
View Article and Find Full Text PDFCardiovasc Res
January 2025
Department of Pathophysiology, Shenzhen University Medical School, Shenzhen 518060, China.
Aims: Decrease in repolarizing K+ currents, particularly the fast component of transient outward K+ current (Ito,f), prolongs action potential duration (APD) and predisposes the heart to ventricular arrhythmia during cardiac hypertrophy. Histone deacetylases (HDACs) have been suggested to participate in the development of cardiac hypertrophy, and class I HDAC inhibition has been found to attenuate pathological remodeling. This study investigated the potential therapeutic effects of HDAC2 on ventricular arrhythmia in pressure overload-induced cardiac hypertrophy.
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