The inhibitory effect of trilinolein on norepinephrine-induced β-myosin heavy chain promoter activity, reactive oxygen species generation, and extracellular signal-regulated kinase phosphorylation in neonatal rat cardiomyocytes

2004 ◽  
Vol 11 (1) ◽  
pp. 11-18 ◽  
Author(s):  
Ju-Chi Liu ◽  
Paul Chan ◽  
Jin-Jer Chen ◽  
Horng-Mo Lee ◽  
Wen-Sen Lee ◽  
...  
Keyword(s):  
Promoter Activity ◽  
Reactive Oxygen Species Generation ◽  
Inhibitory Effect ◽  
Neonatal Rat ◽  
Oxygen Species ◽  
Rat Cardiomyocytes ◽  
Extracellular Signal Regulated Kinase ◽  
Neonatal Rat Cardiomyocytes ◽  
Extracellular Signal ◽  
Kinase Phosphorylation

scholarly journals α1-Adrenergic stimulation of FGF-2 promoter in cardiac myocytes and in adult transgenic mouse hearts

1999 ◽  
Vol 276 (3) ◽  
pp. H826-H833 ◽  
Author(s):  
Karen A. Detillieux ◽  
Johanna T. A. Meij ◽  
Elissavet Kardami ◽  
Peter A. Cattini
Keyword(s):  
Transcription Initiation ◽  
Promoter Activity ◽  
Intraperitoneal Administration ◽  
Initiation Site ◽  
Neonatal Rat ◽  
Transcriptional Level ◽  
Adrenergic Stimulation ◽  
Rat Cardiomyocytes ◽  
Neonatal Rat Cardiomyocytes ◽  
Stimulation Of

Fibroblast growth factor (FGF-2), a mitogenic, angiogenic, and cardioprotective agent, is reported to be released from the postnatal heart by a mechanism of transient remodeling of the sarcolemma during contraction. This release can be increased with adrenergic stimulation. RNA blotting was used to assess whether FGF-2 synthesis in neonatal rat cardiomyocytes might also be regulated by adrenergic stimulation. FGF-2 RNA levels were increased after treatment with norepinephrine for 6 h or with the α-adrenergic agonist phenylephrine for 48 h. To assess an effect on transcription, neonatal rat cardiomyocytes were transfected with a hybrid rat FGF-2 promoter/luciferase gene (−1058FGFp. luc) and treated with norepinephrine or phenylephrine for 6 or 48 h, respectively. FGF-2 promoter activity was increased two- to sevenfold in an α1-specific manner. Putative phenylephrine-responsive elements (PEREs) were identified at positions −780 and −761 relative to a major transcription initiation site. However, deletion analysis of −1058FGFp. luc showed that the phenylephrine response was independent of the putative PEREs, cell contraction, and Ca2+ influx. In transgenic mice expressing −1058FGFp. luc, a significant three- to sevenfold stimulation of FGF-2 promoter activity was detected in the hearts of two independent lines 6 h after intraperitoneal administration of phenylephrine (50 mg/kg). This increase was still apparent at 24 h but was not detected at 48 h posttreatment. Analysis of FGF-2 mRNA in normal mouse hearts revealed accumulation of the 6.1-kb transcript at 24 h. Control of local FGF-2 synthesis at the transcriptional level through adrenergic stimulation may be important in the response to injury as well as in the maintenance of a healthy myocardium.

Inhibitory effect of trilinolein on endothelin-1-induced c-fos gene expression in cultured neonatal rat cardiomyocytes

2005 ◽  
Vol 372 (2) ◽  
pp. 160-167 ◽  
Author(s):  
Hung-Yu Yang ◽  
Ju-Chi Liu ◽  
Yen-Ling Chen ◽  
Cheng-Hsien Chen ◽  
Heng Lin ◽  
...  
Keyword(s):  
Gene Expression ◽  
Inhibitory Effect ◽  
Neonatal Rat ◽  
Rat Cardiomyocytes ◽  
Endothelin 1 ◽  
Neonatal Rat Cardiomyocytes

scholarly journals Leptin Induces Hypertrophy via Endothelin-1–Reactive Oxygen Species Pathway in Cultured Neonatal Rat Cardiomyocytes

Circulation ◽  
2004 ◽  
Vol 110 (10) ◽  
pp. 1269-1275 ◽  
Author(s):  
Fang-Ping Xu ◽  
Min-Sheng Chen ◽  
Yan-Zhen Wang ◽  
Quan Yi ◽  
Shu-Bing Lin ◽  
...  
Keyword(s):  
Reactive Oxygen Species ◽  
Reactive Oxygen ◽  
Neonatal Rat ◽  
Oxygen Species ◽  
Rat Cardiomyocytes ◽  
Endothelin 1 ◽  
Neonatal Rat Cardiomyocytes

Abstract 72: Hydrogen Sulfide Prevents Myocardial Hypertrophy in a Klf5-dependent Manner

2015 ◽  
Vol 117 (suppl_1) ◽  
Author(s):  
Guoliang Meng ◽  
Liping Xie ◽  
Yong Ji
Keyword(s):  
Oxidative Stress ◽  
Hydrogen Sulfide ◽  
Promoter Activity ◽  
Myocardial Hypertrophy ◽  
Neonatal Rat ◽  
Cardiomyocyte Hypertrophy ◽  
Dependent Manner ◽  
Ang Ii ◽  
Rat Cardiomyocytes ◽  
Neonatal Rat Cardiomyocytes

Rationale: H 2 S is a gasotransmitter that regulates multiple cardiovascular functions. Krüppel-like transcription factor (KLF) exerts diverse functions in the cardiovascular system. Objectives: The aim of present study was to investigate the effect of hydrogen sulfide (H 2 S) on myocardial hypertrophy. Methods and results: Myocardial samples of 22 patients with left ventricle hypertrophy were collected and underwent histological and molecular biological analysis. Spontaneously hypertensive rats (SHR) and neonatal rat cardiomyocytes were studied for functional and signaling response to GYY4137, a H 2 S-releasing compound. Expression of cystathionine -lyase (CSE), a main enzyme for H 2 S generation in human heart, decreased in human hypertrophic myocardium, while KLF5 expression increased. In SHR treated with GYY4137 for 4 weeks, myocardial hypertrophy was inhibited as evidenced by improvement in cardiac structural parameters, heart mass index, size of cardiac myocytes and expression of atrial natriuretic peptide (ANP). Levels of oxidative stress and phosphorylation of mitogen-activated protein kinases were also decreased after H 2 S treatment. H 2 S diminished expression of the KLF5 in myocardium of SHR and in neonatal rat cardiomyocytes rendered hypertrophy by angiotensin II (Ang II). H 2 S also inhibited ANP promoter activity and ANP expression in Ang II-induced neonatal rat cardiomyocyte hypertrophy, and these effects were suppressed by KLF5 knockdown. KLF5 promoter activity was increased by Ang II stimulation, and this was reversed by H 2 S. H 2 S also decreased activity of specificity protein-1 (SP-1) binding to the KLF5 promoter and attenuated KLF5 nuclear translocation by Ang II stimulation. Conclusion: H 2 S attenuated myocardial hypertrophy, which might be related to inhibiting oxidative stress and decreasing ANP transcription activity in a KLF5-dependent manner.

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