keyword
MENU ▼
Read by QxMD icon Read
search

Vsmc

keyword
https://www.readbyqxmd.com/read/28445811/liraglutide-a-glp-1-receptor-agonist-inhibits-vascular-smooth-muscle-cell-proliferation-by-enhancing-amp-activated-protein-kinase-and-cell-cycle-regulation-and-delays-atherosclerosis-in-apoe-deficient-mice
#1
Teruo Jojima, Kohsuke Uchida, Kazumi Akimoto, Takanori Tomotsune, Kazunori Yanagi, Toshie Iijima, Kunihiro Suzuki, Kikuo Kasai, Yoshimasa Aso
BACKGROUND AND AIMS: Several studies have demonstrated that both native glucagon-like peptide-1 (GLP-1) and GLP-1 receptor agonists suppress the progression of atherosclerosis in animal models. METHODS: We investigated whether liraglutide, a GLP-1 analogue, could prevent the development of atherosclerosis in apolipoprotein E knockout mice (ApoE(-/-)) on a high-fat diet. We also examined the influence of liraglutide on angiotensin II-induced proliferation of rat vascular smooth muscle cells (VSMCs) via enhancement of AMP-activated protein kinase (AMPK) signaling and regulation of cell cycle progression...
April 7, 2017: Atherosclerosis
https://www.readbyqxmd.com/read/28444175/predictive-value-of-telomere-length-on-outcome-following-acute-myocardial-infarction-evidence-for-contrasting-effects-of-vascular-vs-blood-oxidative-stress
#2
Marios Margaritis, Fabio Sanna, George Lazaros, Ioannis Akoumianakis, Sheena Patel, Alexios S Antonopoulos, Chloe Duke, Laura Herdman, Costas Psarros, Evangelos K Oikonomou, Cheerag Shirodaria, Mario Petrou, Rana Sayeed, George Krasopoulos, Regent Lee, Dimitris Tousoulis, Keith M Channon, Charalambos Antoniades
Aims: Experimental evidence suggests that telomere length (TL) is shortened by oxidative DNA damage, reflecting biological aging. We explore the value of blood (BTL) and vascular TL (VTL) as biomarkers of systemic/vascular oxidative stress in humans and test the clinical predictive value of BTL in acute myocardial infarction (AMI). Methods and results: In a prospective cohort of 290 patients surviving recent AMI, BTL measured on admission was a strong predictor of all-cause [hazard ratio (HR) [95% confidence interval (CI)]: 3...
April 24, 2017: European Heart Journal
https://www.readbyqxmd.com/read/28429763/microrna-26a-targets-mapk6-to-inhibit-smooth-muscle-cell-proliferation-and-vein-graft-neointimal-hyperplasia
#3
Juanjuan Tan, Liguo Yang, Cuicui Liu, Zhiqiang Yan
Neointima formation is the major reason for vein graft failure. However, the underlying mechanism is unclear. The aim of this study was to determine the role of miR-26a in the development of neointimal hyperplasia of autogenous vein grafts. Using autologous jugular vein grafts in the rat carotid artery as a model, we found that miR-26a was significantly downregulated in grafted veins as well as proliferating vascular smooth muscle cells (VSMCs) stimulated with platelet-derived growth factor-BB (PDGF-BB). Overexpression of miR-26a reduced the proliferation and migration of VSMCs...
April 21, 2017: Scientific Reports
https://www.readbyqxmd.com/read/28424290/skin-derived-precursors-from-human-subjects-with-type-2-diabetes-yield-dysfunctional-vascular-smooth-muscle-cells
#4
Sarah Katherina Steinbach, Terrence M Yau, Maral Ouzounian, Husam Abdel-Qadir, Mark Chandy, Thomas Waddell, Mansoor Husain
Objective: Few methods enable molecular and cellular studies of vascular aging or type-2 diabetes (T2D). Here we report a new approach to studying human vascular smooth muscle cell (VSMC) pathophysiology by examining VSMCs differentiated from progenitors found in skin. Approach and Results: Skin-derived precursors (SKPs) were cultured from biopsies (N=164, ~1 cm(2)) taken from the edges of surgical incisions of older adults (N=158; males 72%; mean age 62.7±13 years) undergoing cardiothoracic surgery, and differentiated into VSMCs at high efficiency (>80% yield)...
April 19, 2017: Clinical Science (1979-)
https://www.readbyqxmd.com/read/28418526/empirically-determined-vascular-smooth-muscle-cell-mechano-adaptation-law
#5
Kerianne E Steucke, Zaw Win, Taylor R Stemler, Emily E Walsh, Jennifer L Hall, Patrick W Alford
Cardiovascular disease can alter the mechanical environment of the vascular system, leading to mechano-adaptive growth and remodeling. Predictive models of arterial mechano-adaptation could improve patient treatments and outcomes in cardiovascular disease. Vessel-scale mechano-adaptation includes remodeling of both the cells and extracellular matrix. Here, we aimed to experimentally measure and characterize a phenomenological mechano-adaptation law for vascular smooth muscle cells (VSMCs) within an artery. To do this, we developed a highly controlled and reproducible system for applying a chronic step-change in strain to individual VSMCs with in vivo like architecture, and tracked the temporal cellular stress evolution...
April 13, 2017: Journal of Biomechanical Engineering
https://www.readbyqxmd.com/read/28413470/identification-of-genes-associated-with-the-effect-of-inflammation-on-the-neurotransmission-of-vascular-smooth-muscle-cell
#6
Shujie Gan, Shenlong Qiu, Yiwen Feng, Yanping Zhang, Qin Qian, Zhong Wan, Jingdong Tang
Vascular smooth muscle cell (VSMC) accumulation and hypertrophy are common in vascular disorders, and inflammation has a crucial role in the development of these diseases. To investigate the effect of inflammation on the neurotransmission of VSMC, bioinformatic analysis was performed, following next generation sequencing. Genes of lipopolysaccharide (LPS)-treated A7r5 cells and phosphate-buffered saline (PBS)-treated A7r5 cells were sequenced via next generation sequencing, and each assay was repeated three times...
April 2017: Experimental and Therapeutic Medicine
https://www.readbyqxmd.com/read/28386846/different-effects-of-neuropeptide-y-on-proliferation-of-vascular-smooth-muscle-cells-via-regulation-of-geminin
#7
Zhou-Qin Jiang, You-Li Zhou, Xia Chen, Lin-Yu Li, Shi-Yu Liang, Shu Lin, Mao-Qin Shu
The proliferation-promoting effect of neuropeptide Y (NPY) always functions in low-serum-cultured vascular smooth muscle cells (VSMCs), and the phenotypic switch of VSMCs is regulated by concentrations of serum. Whether the property of the NPY proliferative effect in VSMCs relies on phenotype of VSMCs is unclear. We aimed to explore the role of NPY on proliferation of different VSMC phenotypes in the pathogenesis of atherosclerosis. By stimulating A10 cells with 200 nM NPY in 0.5 or 10% serum, 3H-thymidine and 5-ethynyl-2'-deoxyuridine (EdU) and CCK8 measurements were used to detect VSMC proliferation...
April 6, 2017: Molecular and Cellular Biochemistry
https://www.readbyqxmd.com/read/28386842/vitamin-k2-inhibits-rat-vascular-smooth-muscle-cell-calcification-by-restoring-the-gas6-axl-akt-anti-apoptotic-pathway
#8
Cuiting Qiu, Haijun Zheng, Huiren Tao, Wenjun Yu, Xiaoyu Jiang, Aiqin Li, Hui Jin, Anlin Lv, Huan Li
Vascular calcification is associated with cardiovascular disease as a complication of hypertension, hyperlipidemia, diabetes mellitus, and chronic kidney disease. Vitamin K2 (VK2) delays vascular calcification by an unclear mechanism. Moreover, apoptosis modulates vascular smooth muscle cell (VSMC) calcification. This paper aimed to study VK2-modified VSMC calcification and survival cell signaling mediated by growth arrest-specific gene 6 (Gas6) and its tyrosine kinase receptor Axl. Primary-cultured VSMCs were dose-dependently treated with VK2 in the presence of calcification medium for 8 days, or pre-treated for 1 h with/without the Axl inhibitor R428 (2 μmol/L) or the caspase inhibitor Z-VAD-fmk (20 μmol/L) followed by treatment with VK2 (10 μmol/L) or rmGas6 (200 nmol/L) in calcification medium for 8 days...
April 6, 2017: Molecular and Cellular Biochemistry
https://www.readbyqxmd.com/read/28386356/folic-acid-inhibits-dedifferentiation-of-pdgf-bb-induced-vascular-smooth-muscle-cells-by-suppressing-mtor-p70s6k-signaling
#9
Sunlei Pan, Hui Lin, Hangqi Luo, Feidan Gao, Liping Meng, Changzuan Zhou, Chengjian Jiang, Yan Guo, Zheng Ji, Jufang Chi, Hangyuan Guo
OBJECTIVE: Folic acid (FA) supplementation reduces the risk of atherosclerosis and stroke. Phenotypic change from differentiated to dedifferentiated vascular smooth muscle cells (VSMCs) plays an important role in atherosclerosis development; however, the exact mechanisms remain unknown. This study aimed to assess whether FA through mammalian target of rapamycin (mTOR)/P70S6K signaling inhibits platelet derived growth factor (PDGF-BB) induced VSMC dedifferentiation. METHODS: VSMCs from primary cultures were identified by morphological observation and α-smooth muscle actin (α-SM-actin, α-SMA) immunocytochemistry...
2017: American Journal of Translational Research
https://www.readbyqxmd.com/read/28376489/triiodothyronine-potentiates-vasorelaxation-via-pkg-vasp-signaling-in-vascular-smooth-muscle-cells
#10
Sherin Samuel, Kuo Zhang, Yi-Da Tang, A Martin Gerdes, Maria Alicia Carrillo-Sepulveda
BACKGROUND/AIMS: Vascular relaxation caused by Triiodothyronine (T3) involves direct activation of endothelial cells (EC) and vascular smooth muscle cells (VSMC). Activation of protein kinase G (PKG) has risen as a novel contributor to the vasorelaxation mechanism triggered by numerous stimuli. We hypothesize that T3-induced vasorelaxation involves PKG/vasodilator-stimulated phosphoprotein (VASP) signaling pathway in VSMC. METHODS: Human aortic endothelial cells (HAEC) and VSMC were treated with T3 for short (2 to 60 minutes) and long term (24 hours)...
April 4, 2017: Cellular Physiology and Biochemistry
https://www.readbyqxmd.com/read/28374979/matrix-metalloproteinase-mmp-2-activity-is-associated-with-divergent-regulation-of-calponin-1-in-conductance-and-resistance-arteries-in-hypertension-induced-early-vascular-dysfunction-and-remodelling
#11
Juliana M Parente, Camila A Pereira, Gustavo H Oliveira-Paula, José Eduardo Tanus-Santos, Rita C Tostes, Michele M Castro
Matrix metalloproteinase (MMP)-2 participates in hypertension-induced maladaptive vascular remodelling by degrading extra and intracellular proteins. The consequent extracellular matrix rearrangement and phenotype switch of vascular smooth muscle cells (VSMC) lead to increased cellular migration and proliferation. As calponin-1 degradation by MMP-2 may lead to VSMC proliferation during hypertension, the hypothesis of this study is that increased MMP-2 activity contributes to early hypertension-induced maladaptive remodelling in conductance and resistance arteries via regulation of calponin-1...
April 4, 2017: Basic & Clinical Pharmacology & Toxicology
https://www.readbyqxmd.com/read/28371470/role-of-renal-vascular-potassium-channels-in-physiology-and-pathophysiology
#12
REVIEW
Max Salomonsson, Jens Christian Brasen, Charlotte M Sorensen
The control of renal vascular tone is important for the regulation of salt and water balance, blood pressure and the protection against damaging elevated glomerular pressure. The K(+) conductance is a major factor in the regulation of the membrane potential (Vm ) in vascular smooth muscle (VSMC) and endothelial cells (EC). The vascular tone is controlled by Vm via its effect on the opening probability of voltage operated Ca(2+) channels (VOCC) in VSMC. When K(+) conductance increases Vm becomes more negative and vasodilation follows, while deactivation of K(+) channels leads to depolarization and vasoconstriction...
March 30, 2017: Acta Physiologica
https://www.readbyqxmd.com/read/28363746/a-novel-urotensin-ii-receptor-antagonist-kr-36676-prevents-abca1-repression-via-erk-il-1%C3%AE-pathway
#13
Mi-Young Kim, Sattorov Ilyosbek, Byung Ho Lee, Kyu Yang Yi, Yi-Sook Jung
Urotensin II (U-II), the most potent vasoconstrictor peptide known to date, is expressed at a high level in vascular smooth muscle cells (VSMC) and endothelial cells, whereas its receptor, urotensin (UT) receptor, is abundant in monocytes and macrophages of atherosclerotic lesions. U-II is highly present in the coronary arteries of the atherosclerotic patients compared to normal subjects. Recently, U-II was shown to down-regulate ATP binding cassette transporter-A1 (ABCA1) expression, which is responsible for reverse cholesterol transport in macrophages of atherosclerotic lesions...
May 15, 2017: European Journal of Pharmacology
https://www.readbyqxmd.com/read/28362840/aspirin-triggered-resolvin-d1-attenuates-pdgf-induced-vascular-smooth-muscle-cell-migration-via-the-cyclic-adenosine-monophosphate-protein-kinase-a-camp-pka-pathway
#14
Giorgio Mottola, Anuran Chatterjee, Bian Wu, Mian Chen, Michael S Conte
BACKGROUND AND OBJECTIVES: Resolvin D1 (RvD1) is a specialized pro-resolving lipid mediator that has been previously shown to attenuate vascular smooth muscle cell (VSMC) migration, a key process in the development of intimal hyperplasia. We sought to investigate the role of the cAMP/PKA pathway in mediating the effects of the aspirin-triggered epimer 17R-RvD1 (AT-RvD1) on VSMC migration. METHODS: VSMCs were harvested from human saphenous veins. VSMCs were analyzed for intracellular cAMP levels and PKA activity after exposure to AT-RvD1...
2017: PloS One
https://www.readbyqxmd.com/read/28362832/effects-of-p53-knockout-in-vascular-smooth-muscle-cells-on-atherosclerosis-in-mice
#15
Richard Yang Cao, Robert Eves, Lilly Jia, Colin D Funk, Zongchao Jia, Alan S Mak
In vitro and in vivo evidence has indicated that the tumor suppressor, p53, may play a significant role in the regulation of atherosclerotic plaque formation. In vivo studies using global knockout mice models, however, have generated inconclusive results that do not address the roles of p53 in various cell types involved in atherosclerosis. In this study, we have specifically ablated p53 in vascular smooth muscle cells (VSMC) in the ApoE-/- mouse model to investigate the roles of p53 in VSMC in atherosclerotic plaque formation and stability...
2017: PloS One
https://www.readbyqxmd.com/read/28360226/dual-function-for-mature-vascular-smooth-muscle-cells-during-arteriovenous-fistula-remodeling
#16
Jinjing Zhao, Frances L Jourd'heuil, Min Xue, David Conti, Reynold I Lopez-Soler, Roman Ginnan, Arif Asif, Harold A Singer, David Jourd'heuil, Xiaochun Long
BACKGROUND: The arteriovenous fistula (AVF) is the preferred form of hemodialysis access for patients with chronic kidney disease. However, AVFs are associated with significant problems including high incidence of both early and late failures, usually attributed to inadequate venous arterialization and neointimal hyperplasia, respectively. Understanding the cellular basis of venous remodeling in the setting of AVF could provide targets for improving AVF patency rates. METHODS AND RESULTS: A novel vascular smooth muscle cell (VSMC) lineage tracing reporter mouse, Myh11-Cre/ERT2-mTmG, was used to track mature VSMCs in a clinically relevant AVF mouse model created by a jugular vein branch end to carotid artery side anastomosis...
March 30, 2017: Journal of the American Heart Association
https://www.readbyqxmd.com/read/28352317/activation-of-peroxisome-proliferator-activated-receptor-%C3%AE-inhibits-vascular-calcification-by-upregulating-klotho
#17
Lijuan Cheng, Lei Zhang, Jun Yang, Lirong Hao
Cardiovascular diseases are common in patients with chronic kidney disease. One of the key symptoms is the calcification of the vascular smooth muscle cells (VSMCs), which is induced by dysregulated mineral metabolism with high circulating levels of inorganic phosphate (Pi) and calcium. Klotho, which was originally identified as an aging suppressor gene, has been shown to be associated with vascular calcification. Since Klotho was recently identified as a target for nuclear receptor peroxisome proliferator-activated receptor (PPAR) γ, the present study aimed to determine whether PPARγ regulates VSMC calcification through modulating the expression levels of Klotho...
February 2017: Experimental and Therapeutic Medicine
https://www.readbyqxmd.com/read/28351290/keratose-hydrogels-promote-vascular-smooth-muscle-differentiation-from-c-kit-positive-human-cardiac-stem-cells
#18
Benjamin T Ledford, Jamelle Simmons, Miao Chen, Huimin Fan, Catherine Barron, Zhongmin Liu, Mark Van Dyke, Jia-Qiang He
Stem cell-based therapies have demonstrated great potential for the treatment of cardiac diseases, for example, myocardial infarction; however, low cell viability, low retention/engraftment, and uncontrollable in vivo differentiation after transplantation are still major limitations, which lead to low therapeutic efficiency. Biomaterials provide a promising solution to overcome these issues due to their biocompatibility, biodegradability, low/nonimmunogenicity, and low/noncytotoxicity. The present study aimed to investigate the impacts of keratose (KOS) hydrogel biomaterial on cellular viability, proliferation, and differentiation of c-kit(+) human cardiac stem cells (hCSCs)...
April 24, 2017: Stem Cells and Development
https://www.readbyqxmd.com/read/28342976/translating-the-microrna-signature-of-microvesicles-derived-from-human-coronary-artery-smooth-muscle-cells-in-patients-with-familial-hypercholesterolemia-and-coronary-artery-disease
#19
David de Gonzalo-Calvo, Ana Cenarro, Katia Garlaschelli, Fabio Pellegatta, David Vilades, Laura Nasarre, Sandra Camino-Lopez, Javier Crespo, Francesc Carreras, Rubén Leta, Alberico Luigi Catapano, Giuseppe Danilo Norata, Fernando Civeira, Vicenta Llorente-Cortes
AIMS: To analyze the impact of atherogenic lipoproteins on the miRNA signature of microvesicles derived from human coronary artery smooth muscle cells (CASMC) and to translate these results to familial hypercholesterolemia (FH) and coronary artery disease (CAD) patients. METHODS: Conditioned media was collected after exposure of CASMC to atherogenic lipoproteins. Plasma samples were collected from two independent populations of diagnosed FH patients and matched normocholesterolemic controls (Study population 1, N=50; Study population 2, N=24) and a population of patients with suspected CAD (Study population 3, N=50)...
March 23, 2017: Journal of Molecular and Cellular Cardiology
https://www.readbyqxmd.com/read/28342807/myocardin-inhibited-the-gap-protein-connexin-43-via-promoted-mir-206-to-regulate-vascular-smooth-muscle-cell-phenotypic-switch
#20
Hui Li, Yuan Xiang, Li-Juan Fan, Xiao-Yu Zhang, Jia-Peng Li, Cheng-Xi Yu, Le-Yuan Bao, Dong-Sun Cao, Wei-Bing Xing, Xing-Hua Liao, Tong-Cun Zhang
Myocardin is regarded as a key mediator for the change of smooth muscle phenotype. The gap junction protein connexin 43 (Cx43) has been shown to be involved in vascular smooth muscle cells (VSMCs) proliferation and the development of atherosclerosis. However, the role of myocardin on gap junction of cell communication and the relation between myocardin and Cx43 in VSMC phenotypic switch has not been investigated. The goal of the present study is to investigate the molecular mechanism by which myocardin affects Cx43-regulated VSMC proliferation...
June 15, 2017: Gene
keyword
keyword
42800
1
2
Fetch more papers »
Fetching more papers... Fetching...
Read by QxMD. Sign in or create an account to discover new knowledge that matter to you.
Remove bar
Read by QxMD icon Read
×

Search Tips

Use Boolean operators: AND/OR

diabetic AND foot
diabetes OR diabetic

Exclude a word using the 'minus' sign

Virchow -triad

Use Parentheses

water AND (cup OR glass)

Add an asterisk (*) at end of a word to include word stems

Neuro* will search for Neurology, Neuroscientist, Neurological, and so on

Use quotes to search for an exact phrase

"primary prevention of cancer"
(heart or cardiac or cardio*) AND arrest -"American Heart Association"