Norepinephrine has growth-promoting effects in cardiac myocytes. The present study in cultured neonatal rat cardiac myocytes tested the hypothesis that norepinephrine also stimulates expression of vascular endothelial growth factor (VEGF), an important angiogenic factor. As assessed by polymerase chain reaction cardiac myocytes and non-myocytes expressed all three isoforms of rat VEGF, with the short isoform (VEGF 121 ) preferentially expressed in non-myocytes. When cardiac myocytes were stimulated with 1 micro M norepinephrine for 24 h in the presence or absence of the specific alpha - and beta -adrenoceptor antagonists prazosin and propranolol, respectively, VEGF mRNA levels and splice variant pattern did not change, whereas atrial natriuretic peptide mRNA levels increased 3 to 4-fold. CoCl(2) increased VEGF mRNA levels in cardiac myocytes five-fold. When cardiac myocytes were cultured with conditioned medium from non-myocytes that had been stimulated with norepinephrine for 24 h VEGF mRNA increased 2-fold. The increase was blocked by antibodies neutralizing TGF beta. These data suggest that norepinephrine stimulates myocardial angiogenesis by a paracrine mechanism that involves cardiac non-myocytes and TGF beta.
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http://dx.doi.org/10.1023/B:AGEN.0000029411.76494.33 | DOI Listing |
Acute myocardial infarction (AMI) causes ischemic damage and cardiac remodeling that ultimately progresses into ischemic cardiomyopathy (ICM). Coronary revascularization reduces morbidity and mortality from an MI, however, reperfusion also induces oxidative stress that drives cardiac myocyte (CM) dysfunction and ICM. Oxidative stress in CMs leads to reactive oxygen species (ROS) production and mitochondrial damage.
View Article and Find Full Text PDFCardiovasc Diabetol
January 2025
Department of Cardiology, The Affiliated Hospital, Key Laboratory of Medical Electrophysiology, Ministry of Education, Institute of Cardiovascular Research, Basic Medicine Research Innovation Center for Cardiometabolic Diseases, Ministry of Education, Southwest Medical University, Luzhou, 646000, Sichuan, China.
Globally, cardiovascular diseases remain among the leading causes of mortality, highlighting the urgent need for innovative research models. Consequently, the development of accurate models that simulate cardiac function holds significant scientific and clinical value for both disease research and therapeutic interventions. Cardiac organoids, which are three-dimensional structures derived from the induced differentiation of stem cells, are particularly promising.
View Article and Find Full Text PDFStem Cell Res
December 2024
Agnes Ginges Centre for Molecular Cardiology at Centenary Institute, The University of Sydney, Sydney, Australia; Faculty of Medicine and Health, The University of Sydney, Sydney, Australia. Electronic address:
Catecholaminergic polymorphic ventricular tachycardia (CPVT) is an inherited cardiac disease characterised by adrenergic-induced arrhythmias. The leading causes of CPVT are pathogenic variants in cardiac ryanodine receptor 2 (RYR2) and rarely, in cardiac calsequestrin-2 (CASQ2) genes, which are major components of Ca handling in cardiac myocytes. This resource builds upon an established induced pluripotent stem cell line generated from a family with autosomal dominant CPVT due to a heterozygous variant in CASQ2 c.
View Article and Find Full Text PDFFASEB J
January 2025
National Key Laboratory of Space Medicine, China Astronaut Research and Training Center, Beijing, China.
Microgravity-induced cardiac remodeling and dysfunction present significant challenges to long-term spaceflight, highlighting the urgent need to elucidate the underlying molecular mechanisms and develop precise countermeasures. Previous studies have outlined the important role of miRNAs in cardiovascular disease progression, with miR-199a-3p playing a crucial role in myocardial injury repair and the maintenance of cardiac function. However, the specific role and expression pattern of miR-199a-3p in microgravity-induced cardiac remodeling remain unclear.
View Article and Find Full Text PDFCell Commun Signal
January 2025
Department of Vascular & Cardiology, Ruijin Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, China.
Purpose: Cardiomyocyte death is a major cytopathologic response in acute myocardial infarction (AMI) and involves complex inflammatory interactions. Although existing reports indicating that mixed lineage kinase domain-like protein (MLKL) is involved in macrophage necroptosis and inflammasome activation, the downstream mechanism of MLKL in necroptosis remain poorly characterized in AMI.
Methods: MLKL knockout mice (MLKL), RIPK3 knockout mice (RIPK3), and macrophage-specific MLKL conditional knockout mice (MLKL) were established.
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