scholarly journals The Role of Uridine Adenosine Tetraphosphate in the Vascular System

2011 ◽  
Vol 2011 ◽  
pp. 1-7 ◽  
Author(s):  
Takayuki Matsumoto ◽  
Rita C. Tostes ◽  
R. Clinton Webb
Keyword(s):  
Smooth Muscle ◽  
Cardiovascular Diseases ◽  
Endothelial Dysfunction ◽  
Arterial Hypertension ◽  
Smooth Muscle Cells ◽  
Vascular Function ◽  
Purinergic Receptors ◽  
Potential Role ◽  
Vascular System

The endothelium plays a pivotal role in vascular homeostasis, and endothelial dysfunction is a major feature of cardiovascular diseases, such as arterial hypertension, atherosclerosis, and diabetes. Recently, uridine adenosine tetraphosphate (Up4A) has been identified as a novel and potent endothelium-derived contracting factor (EDCF). Up4A structurally contains both purine and pyrimidine moieties, which activate purinergic receptors. There is an accumulating body of evidence to show that Up4A modulates vascular function by actions on endothelial and smooth muscle cells. In this paper, we discuss the effects of Up4A on vascular function and a potential role for Up4A in cardiovascular diseases.

scholarly journals MicroRNA-143/-145 in Cardiovascular Diseases

2015 ◽  
Vol 2015 ◽  
pp. 1-9 ◽  
Author(s):  
Wang Zhao ◽  
Shui-Ping Zhao ◽  
Yu-Hong Zhao
Keyword(s):  
Smooth Muscle ◽  
Cardiovascular Diseases ◽  
Vascular Smooth Muscle Cells ◽  
Essential Role ◽  
Recent Progress ◽  
Potential Role ◽  
Phenotypic Switching ◽  
Diagnostic Biomarkers ◽  
Potential Strategy

MicroRNAs (miRNAs) play an essential role in the onset and development of many cardiovascular diseases. Increasing evidence shows that miRNAs can be used as potential diagnostic biomarkers for cardiovascular diseases, and miRNA-based therapy may be a promising therapy for the treatment of cardiovascular diseases. The microRNA-143/-145 (miR-143/-145) cluster is essential for differentiation of vascular smooth muscle cells (VSMCs) and determines VSMC phenotypic switching. In this review, we summarize the recent progress in knowledge concerning the function of miR-143/-145 in the cardiovascular system and their role in cardiovascular diseases. We discuss the potential role of miR-143/-145 as valuable biomarkers for cardiovascular diseases and explore the potential strategy of targeting miR-143 and miR-145.

Role of PDGF-B and PDGFR-beta in recruitment of vascular smooth muscle cells and pericytes during embryonic blood vessel formation in the mouse

Development ◽  
1999 ◽  
Vol 126 (14) ◽  
pp. 3047-3055 ◽  
Author(s):  
M. Hellstrom ◽  
M. Kal n ◽  
P. Lindahl ◽  
A. Abramsson ◽  
C. Betsholtz
Keyword(s):  
Endothelial Cells ◽  
Smooth Muscle ◽  
Vascular Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Vascular Smooth Muscle Cells ◽  
Vascular System ◽  
Muscle Cells ◽  
Brdu Labeling ◽  
Pdgfr Beta

Development of a vascular system involves the assembly of two principal cell types - endothelial cells and vascular smooth muscle cells/pericytes (vSMC/PC) - into many different types of blood vessels. Most, if not all, vessels begin as endothelial tubes that subsequently acquire a vSMC/PC coating. We have previously shown that PDGF-B is critically involved in the recruitment of pericytes to brain capillaries and to the kidney glomerular capillary tuft. Here, we used desmin and alpha-smooth muscle actin (ASMA) as markers to analyze vSMC/PC development in PDGF-B−/− and PDGFR-beta−/− embryos. Both mutants showed a site-specific reduction of desmin-positive pericytes and ASMA-positive vSMC. We found that endothelial expression of PDGF-B was restricted to immature capillary endothelial cells and to the endothelium of growing arteries. BrdU labeling showed that PDGFR-beta-positive vSMC/PC progenitors normally proliferate at sites of endothelial PDGF-B expression. In PDGF-B−/− embryos, limb arterial vSMC showed a reduced BrdU-labeling index. This suggests a role of PDGF-B in vSMC/PC cell proliferation during vascular growth. Two modes of vSMC recruitment to newly formed vessels have previously been suggested: (1) de novo formation of vSMC by induction of undifferentiated perivascular mesenchymal cells, and (2) co-migration of vSMC from a preexisting pool of vSMC. Our data support both modes of vSMC/PC development and lead to a model in which PDGFR-beta-positive vSMC/PC progenitors initially form around certain vessels by PDGF-B-independent induction. Subsequent angiogenic sprouting and vessel enlargement involves PDGF-B-dependent vSMC/PC progenitor co-migration and proliferation, and/or PDGF-B-independent new induction of vSMC/PC, depending on tissue context.

scholarly journals Crucial role of RAGE in inappropriate increase of smooth muscle cells from patients with pulmonary arterial hypertension

PLoS ONE ◽  
2018 ◽  
Vol 13 (9) ◽  
pp. e0203046 ◽  
Author(s):  
Kazufumi Nakamura ◽  
Masakiyo Sakaguchi ◽  
Hiromi Matsubara ◽  
Satoshi Akagi ◽  
Toshihiro Sarashina ◽  
...  
Keyword(s):  
Smooth Muscle ◽  
Pulmonary Arterial Hypertension ◽  
Arterial Hypertension ◽  
Smooth Muscle Cells ◽  
Crucial Role ◽  
Muscle Cells ◽  
Pulmonary Arterial

scholarly journals Mitochondria depletion abolishes agonist-induced Ca2+ plateau in airway smooth muscle cells: potential role of H2O2

2010 ◽  
Vol 298 (2) ◽  
pp. L178-L188 ◽  
Author(s):  
Taoxiang Chen ◽  
Liping Zhu ◽  
Tao Wang ◽  
Hong Ye ◽  
Kewu Huang ◽  
...  
Keyword(s):  
Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Airway Smooth Muscle ◽  
Potential Role ◽  
Reactive Oxygen Species Generation ◽  
Muscle Cells ◽  
Airway Smooth Muscle Cells ◽  
Cellular Energy ◽  
Dependent Mechanism

The mechanisms by which mitochondria regulate the sustained phase of agonist-induced responses in cytosolic Ca2+ concentration as an independent organelle in whole is not clear. By exposing to ethidium bromide and supplying pyruvate and uridine, we established mitochondrial DNA (mtDNA)-depleted rat airway smooth muscle cells (RASMCs) with maintained cellular energy. Upon an exposure to 2 μM histamine, [Ca2+]i in control RASMCs increased to a peak followed by a plateau above baseline, whereas [Ca2+]i in mtDNA-depleted RASMCs jumped to a peak and then declined to baseline without any plateau. mtDNA depletion apparently attenuated intracellular reactive oxygen species generation induced by histamine. By coexposure to 2 μM histamine and 0.1 μM exogenous H2O2, which did not affect [Ca2+]i by itself, the above difference in [Ca2+]i kinetics in mtDNA-depleted RASMCs was reversed. Intracellular H2O2 decomposition abolishes histamine-induced sustained elevation in [Ca2+]i in RASMCs. Thus, mitochondria regulate agonist-induced sustained [Ca2+]i elevation by a H2O2-dependent mechanism.

scholarly journals The role of microRNA in the diagnosis of cardiovascular diseases in obese patients

2021 ◽  
Vol 23 (4) ◽  
pp. 358-362
Author(s):  
Teona A. Shvangiradze ◽  
◽  
Irina Z. Bondarenko ◽  
Ekaterina A. Troshina ◽  
◽  
...  
Keyword(s):  
Cardiovascular Diseases ◽  
Endothelial Dysfunction ◽  
Potential Role ◽  
Modern Society ◽  
Initial Step ◽  
Obese Patients ◽  
Altered Expression ◽  
Global Problem ◽  
Increased Risk

Obesity remains a global problem in modern society. It is commonly associated with an increased risk of cardiovascular diseases (CVD). The search for specific and sensitive biomarkers of CVD continues. Currently, a lot of studies focused on the potential role of microRNA (miRNA) in CVD development and progression. MiRNAs are involved in various pathological disorders associated with CVD. Endothelial dysfunction is considered as the initial step in the pathogenesis of many CVD, and atherosclerosis in particular. Altered expression of several miRNAs is associated with the development of endothelial dysfunction. Some miRNAs are considered as potential therapeutic targets. Further studies to evaluate the role of miRNAs in the pathogenesis of CVD are needed. It will improve the diagnosis and treatment of CVD in patients with obesity.

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