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and decrease future atherothrombotic events ( Giugliano et al . 2013 ). However, the application of PTA to PVD is largely limited due to the high restenosis rate ( Jones et al . 2013 ). Intimal hyperplasia is a major process of restenosis after PTA
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Introduction Hyperglycemia is believed to play a major role in the development of diabetic macrovascular complications, including atherosclerosis and restenosis, which are responsible for the most of disability and mortality observed in
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Proliferation and directed migration of vascular cells are key components in vascular diseases such as atherosclerosis and restenosis following percutaneous transluminal coronary angioplasty. However, the precise cellular and molecular mechanisms involved in the control of vascular cell proliferation or migration at the tissue level remain largely undefined. Molecules contributing to these processes are elaborated by distinct cell types and act in both autocrine and paracrine modes. They include two broad classes, polypeptide growth factors and vasoactive G-protein-coupled receptor (GPCR) agonists. Examples of the former, such as platelet-derived growth factor, bind to and activate cell surface receptor tyrosine kinases, initiating intracellular biochemical signaling pathways associated with cell proliferation or migration. In contrast, recent evidence suggests that vasoactive GPCR agonists (e.g. angiotensin II, endothelin-1, alpha-thrombin) elicit cell growth indirectly by inducing the production of autocrine or paracrine factors in vascular cells. Recent studies have identified activin A as a novel component of conditioned medium obtained from GPCR agonist-stimulated vascular smooth muscle cells (SMCs). Although activin A alone only weakly stimulated rat aortic SMC DNA synthesis, it demonstrated a potent co-mitogenic effect in combination with either epidermal growth factor (EGF) or heparin binding EGF-like growth factor in these cells, increasing DNA synthesis by up to 5- and 4-fold respectively. Furthermore, in a rat carotid-injury model, activin A mRNA was upregulated within 6 h after injury, followed by increases in immunoreactive protein detected in the expanding neointima 7 to 14 days later. Taken together, these results indicate that activin A is a common vascular SMC-derived growth factor induced by vasoactive agonists that may, either alone or in combination with other factors, contribute to fibroproliferative vascular diseases.
Departments of, Human Nutritional Sciences, Physiology, Molecular Physiology Laboratory, University of Manitoba, Winnipeg, Manitoba, Canada R3T 2N2
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Departments of, Human Nutritional Sciences, Physiology, Molecular Physiology Laboratory, University of Manitoba, Winnipeg, Manitoba, Canada R3T 2N2
Departments of, Human Nutritional Sciences, Physiology, Molecular Physiology Laboratory, University of Manitoba, Winnipeg, Manitoba, Canada R3T 2N2
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Departments of, Human Nutritional Sciences, Physiology, Molecular Physiology Laboratory, University of Manitoba, Winnipeg, Manitoba, Canada R3T 2N2
Departments of, Human Nutritional Sciences, Physiology, Molecular Physiology Laboratory, University of Manitoba, Winnipeg, Manitoba, Canada R3T 2N2
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-promoting agents ( Matsuda et al . 2002 ), possibly by sequestering growth factors ( Wang et al . 2005 ). Matsuda et al . (2002) also reported that adiponectin reduced neointimal hyperplasia in response to arterial injury (restenosis), a process that is
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development of vascular diseases such as atherosclerosis, vein-graft atherosclerosis and angioplasty-induced restenosis ( Ip et al . 1990 ). Many studies suggest that estrogen replacement therapy reduces the number of coronary events after coronary
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Instituto de Investigación Biosanitaria GRANADA, Hospitales Universitarios de Granada, Universidad de Granada, Granada, Spain
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Instituto de Investigación Biosanitaria GRANADA, Hospitales Universitarios de Granada, Universidad de Granada, Granada, Spain
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Instituto de Investigación Biosanitaria GRANADA, Hospitales Universitarios de Granada, Universidad de Granada, Granada, Spain
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Departamento de Fisiología, Facultad de Medicina, Granada, Spain
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physiological and pathological states. In this context, endothelial dysfunction can be improved by the administration of L-arginine in many diseases, including hypertension, atherosclerosis, hyperglycemia, restenosis/postcoronary angioplasty and reperfusion
Department of Immunology, School of Medicine, Shandong University, Jinan, Shandong 250012, People’s Republic of China
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Department of Immunology, School of Medicine, Shandong University, Jinan, Shandong 250012, People’s Republic of China
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Department of Immunology, School of Medicine, Shandong University, Jinan, Shandong 250012, People’s Republic of China
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Department of Immunology, School of Medicine, Shandong University, Jinan, Shandong 250012, People’s Republic of China
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Department of Immunology, School of Medicine, Shandong University, Jinan, Shandong 250012, People’s Republic of China
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Department of Immunology, School of Medicine, Shandong University, Jinan, Shandong 250012, People’s Republic of China
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Department of Immunology, School of Medicine, Shandong University, Jinan, Shandong 250012, People’s Republic of China
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increasingly considered a highly active segment of vascular tissue that contributes to a variety of disease pathologies, including atherosclerosis and restenosis ( Shi et al. 1996 , 1997 , Houtkamp et al. 2001 , Sartore et al. 2001 ). However, no data
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and inhibition of coronary smooth muscle cell growth by somatostatin analogues in human coronary smooth muscle cells. A potential treatment for restenosis? Circulation 89 1511 –1517. Hall JE , Brands MW, Zappe DH
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Department of Human Metabolism, Robert Hague Centre for Diabetes and Endocrinology, Medical School, The University of Sheffield, Sheffield S10 2RX, UK
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-inflammatory cytokines, decreasing inflammation-induced apoptosis and promoting proliferation ( Williams et al . 2002 , Nakamura et al . 2006 ). Although some studies have linked abnormal VSMC proliferation to the pathogenesis of both atherosclerosis and re-stenosis
