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https://www.readbyqxmd.com/read/28100269/a-spleen-tyrosine-kinase-inhibitor-attenuates-the-proliferation-and-migration-of-vascular-smooth-muscle-cells
#1
Hyang-Hee Seo, Sang Woo Kim, Chang Youn Lee, Kyu Hee Lim, Jiyun Lee, Eunhyun Choi, Soyeon Lim, Seahyoung Lee, Ki-Chul Hwang
BACKGROUND: Pathologic vascular smooth muscle cell (VSMC) proliferation and migration after vascular injury promotes the development of occlusive vascular disease. Therefore, an effective chemical agent to suppress aberrant proliferation and migration of VSMCs can be a potential therapeutic modality for occlusive vascular disease such as atherosclerosis and restenosis. To find an anti-proliferative chemical agent for VSMCs, we screened an in-house small molecule library, and the selected small molecule was further validated for its anti-proliferative effect on VSMCs using multiple approaches, such as cell proliferation assays, wound healing assays, transwell migration assays, and ex vivo aortic ring assay...
January 18, 2017: Biological Research
https://www.readbyqxmd.com/read/28088345/phenotypic-characterization-of-perivascular-myoid-cell-neoplasms-using-myosin-1b-a-newly-identified-human-pericyte-marker
#2
Shiori Meguro, Taisuke Akamatsu, Sayomi Matsushima, Isao Kosugi, Hideya Kawasaki, Yosifumi Arai, Satoshi Baba, Takashi Tsuchida, Youji Shido, Takafumi Suda, Toshihide Iwashita
Our aim was to identify pericyte-specific markers for the analysis of formalin-fixed paraffin-embedded (FFPE) human tissue samples, and to characterize perivascular myoid cell neoplasms phenotypically. Previously identified pericyte markers failed to distinguish pericytes from other cellular types, such as vascular smooth muscle cells (vSMCs) and fibroblasts, in immunohistochemical (IHC) analysis. However, we compared gene expression profiles between pericytes, vSMCs, and fibroblasts, and performed human skin vasculature IHC analysis, which led to the identification of myosin 1B (MYO1B) as a novel pericyte marker...
January 11, 2017: Human Pathology
https://www.readbyqxmd.com/read/28079127/functional-nanoarchitectures-for-enhanced-drug-eluting-stents
#3
Yomna E Saleh, Mohamed A Gepreel, Nageh K Allam
Different strategies have been investigated to allow for optimum duration and conditions for endothelium healing through the enhancement of coronary stents. In this study, a nanoarchitectured system is proposed as a surface modification for drug eluting stents. Highly oriented nanotubes were vertically grown on the surface of a new Ni-free biocompatible Ti-based alloy, as a potential material for self-expandable stents. The fabricated nanotubes were self-grown from the potential stent substrate, which are also proposed to enhance endothelial proliferation while acting as drug reservoir to hinder Vascular Smooth Muscle Cells (VSMC) proliferation...
January 12, 2017: Scientific Reports
https://www.readbyqxmd.com/read/28076932/aortic-dissection-is-associated-with-reduced-polycystin-1-expression-an-abnormality-that-leads-to-increased-erk-phosphorylation-in-vascular-smooth-muscle-cells
#4
J Feng, S Ge, L Zhang, H Che, C Liang
The vascular smooth muscle cell (VSMC) phenotypic switch is a key pathophysiological change in various cardiovascular diseases, such as aortic dissection (AD), with a high morbidity. Polycystin-1 (PC1) is significantly downregulated in the VSMCs of AD patients. PC1 is an integral membrane glycoprotein and kinase that regulates different biological processes, including cell proliferation, apoptosis, and cell polarity. However, the role of PC1 in intracellular signaling pathways remains poorly understood. In this study, PC1 downregulation in VSMCs promoted the expression of SM22α, ACTA2 and calponin 1 (CNN1) proteins...
December 16, 2016: European Journal of Histochemistry: EJH
https://www.readbyqxmd.com/read/28075455/tnf%C3%A2-%C3%AE-regulates-apoptosis-of-human-vascular-smooth-muscle-cells-through-gap-junctions
#5
Mei Tang, Jun Fang
Inflammatory cytokines are released by immune cells and are able to induce vascular smooth muscle cells (VSMCs) to undergo apoptosis, causing atherosclerotic plaque rupture. Changes in the expression levels of connexins (Cxs) have been demonstrated in VSMCs to be involved in the pathogenesis of atherosclerotic progression. The present study examined the effect of tumor necrosis factor‑α (TNF‑α) on Cx43 expression levels and apoptosis in human VSMCs. Overexpression of Cx43 plasmids notably stimulated VSMC proliferation...
January 5, 2017: Molecular Medicine Reports
https://www.readbyqxmd.com/read/28072480/free-fatty-acids-induce-autophagy-and-lox-1-upregulation-in-cultured-aortic-vascular-smooth-muscle-cells
#6
Cheng-I Cheng, Yueh-Hong Lee, Po-Han Chen, Yu-Chun Lin, Ming-Huei Chou, Ying-Hsien Kao
Elevation of free fatty acids (FFAs) is known to affect microvascular function and contribute to obesity-associated insulin resistance, hypertension, and microangiopathy. Proliferative and synthetic vascular smooth muscle cells (VSMCs) increase intimal thickness and destabilize atheromatous plaques. This study aimed to investigate whether saturated palmitic acid (PA) and monounsaturated oleic acid (OA) modulate autophagy activity, cell proliferation, and vascular tissue remodeling in an aortic VSMC cell line...
November 5, 2016: Journal of Cellular Biochemistry
https://www.readbyqxmd.com/read/28066139/regulation-of-vascular-smooth-muscle-phenotype-by-cross-regulation-of-kr%C3%A3-ppel-like-factors
#7
Jung Min Ha, Sung Ji Yun, Seo Yeon Jin, Hye Sun Lee, Sun Ja Kim, Hwa Kyoung Shin, Sun Sik Bae
Regulation of vascular smooth muscle cell (VSMC) phenotype plays an essential role in many cardiovascular diseases. In the present study, we provide evidence that krüppel-like factor 8 (KLF8) is essential for tumor necrosis factor α (TNFα)-induced phenotypic conversion of VSMC obtained from thoracic aorta from 4-week-old SD rats. Stimulation of the contractile phenotype of VSMCs with TNFα significantly reduced the VSMC marker gene expression and KLF8. The gene expression of KLF8 was blocked by TNFα stimulation in an ERK-dependent manner...
January 2017: Korean Journal of Physiology & Pharmacology
https://www.readbyqxmd.com/read/28063931/long-noncoding-rna-h19-derived-mir-675-aggravates-restenosis-by-targeting-pten
#8
Junyuan Lv, Lei Wang, Jin Zhang, Ruoran Lin, Lun Wang, Weifeng Sun, Huize Wu, Shijie Xin
Restenosis is mainly attributed to excessive proliferation of vascular smooth muscle cells (VSMCs). Noncoding RNAs have been identified as key regulators of diverse pathological processes. We reported that the long noncoding RNA H19 (LncRNA H19) and LncRNA H19-derived microRNA (miR-675) are overexpressed in neointima of balloon-injured artery. Thus, the present study aims to evaluate the role of LncRNA H19 on VSMCs proliferation. To determine the changes of LncRNA H19 and miR-675 expression in the injured arterial wall, the standard rat carotid artery balloon injury model was used...
January 4, 2017: Biochemical and Biophysical Research Communications
https://www.readbyqxmd.com/read/28063668/activation-of-cd137-signaling-accelerates-vascular-calcification-in-vivo-and-vitro
#9
Yao Chen, Abdul Basit Bangash, Juan Song, Wei Zhong, Cuiping Wang, Chen Shao, Zhongqun Wang, Jinchuan Yan
OBJECTIVES: Vascular calcification is a characteristic feature of atherosclerosis and is considered as an independent predictor of cardiovascular risk. CD137 signaling has previously shown to be involved in atherosclerosis. However, the possible role of CD137 signaling in regulation of vascular calcification has not been reported. In the present study, we investigated the effect of CD137 signaling on vascular calcification in ApoE(-/-) mice and in vascular smooth muscle cells (VSMCs) of mice...
December 30, 2016: International Journal of Cardiology
https://www.readbyqxmd.com/read/28038380/the-p2y2-nucleotide-receptor-is-an-inhibitor-of-vascular-calcification
#10
Shaomin Qian, Jenna N Regan, Maxwell T Shelton, April Hoggatt, Khalid S Mohammad, Paul B Herring, Cheikh I Seye
BACKGROUND AND AIMS: Mutations in the 5'-nucleotidase ecto (NT5E) gene that encodes CD73, a nucleotidase that converts AMP to adenosine, are linked to arterial calcification. However, the role of purinergic receptor signaling in the pathology of intimal calcification is not well understood. In this study, we examined whether extracellular nucleotides acting via P2Y2 receptor (P2Y2R) modulate arterial intimal calcification, a condition highly correlated with cardiovascular morbidity. METHODS: Apolipoprotein E, P2Y2R double knockout mice (ApoE(-/-)P2Y2R(-/-)) were used to determine the effect of P2Y2R deficiency on vascular calcification in vivo...
December 15, 2016: Atherosclerosis
https://www.readbyqxmd.com/read/28012647/cd98-regulates-vascular-smooth-muscle-cell-proliferation-in-atherosclerosis
#11
Yvonne Baumer, Sara McCurdy, Martin Alcala, Nehal Mehta, Bog-Hieu Lee, Mark H Ginsberg, William A Boisvert
BACKGROUND AND AIMS: Vascular smooth muscle cells (VSMC) migrate and proliferate to form a stabilizing fibrous cap that encapsulates atherosclerotic plaques. CD98 is a transmembrane protein made of two subunits, CD98 heavy chain (CD98hc) and one of six light chains, and is known to be involved in cell proliferation and survival. Because the influence of CD98hc on atherosclerosis development is unknown, our aim was to determine if CD98hc expressed on VSMC plays a role in shaping the morphology of atherosclerotic plaques by regulating VSMC function...
November 16, 2016: Atherosclerosis
https://www.readbyqxmd.com/read/28010122/lysyl-oxidase-induces-vascular-oxidative-stress-and-contributes-to-arterial-stiffness-and-abnormal-elastin-structure-in-hypertension-role-of-p38mapk
#12
Sonia Martínez-Revelles, Ana Belen Garcia-Redondo, Mª Soledad Avendaño, Saray Varona, Teresa Palao, Mar Orriols, Fernanda R Roque, Ana Fortuño, Rhian M Touyz, Jose Martínez-Gonzalez, Mercedes Salaices, Cristina Rodríguez, Ana María Briones
AIMS: Vascular stiffness, structural elastin abnormalities and increased oxidative stress are hallmarks of hypertension. Lysyl oxidase (LOX) is an elastin cross-linking enzyme that produces H<sub>2</sub>O<sub>2</sub> as by-product. We addressed the interplay between LOX, oxidative stress, vessel stiffness and elastin. RESULTS: Angiotensin II (Ang II)-infused hypertensive mice and spontaneously hypertensive rats (SHR) showed increased vascular LOX expression and stiffness and abnormal elastin structure...
December 23, 2016: Antioxidants & Redox Signaling
https://www.readbyqxmd.com/read/28009720/roscovitine-protects-from-arterial-injury-by-regulating-the-expressions-of-c-jun-and-p27-and-inhibiting-vsmc-proliferation
#13
Yu Liu, Yun-Feng Li, Hong Chang, Jing-Shan Zhao, Jian-Ming Hou, Kun Yu, Jia-Huan Sun, Hong Wang, Ai-Ying Li
PURPOSE: Roscovitine (Rosc) is a selective inhibitor of cyclin-dependent kinases (CDKs) and a promising therapy for various cancers. However, limited information is available on the biological significance of Rosc in vascular smooth muscle cells (VSMCs), the cell type critical for the development of proliferative vascular diseases. In this study, we address the effects of Rosc in regulating VSMC proliferation, both in vitro and in vivo, exploring the underlying molecular mechanisms. METHODS: The proliferations and cell-cycle distributions of in vitro cultured VSMCs, as well as several other cancer cell lines, were examined by cell-counting assay and flow cytometry, respectively...
December 17, 2016: Journal of Cardiovascular Pharmacology
https://www.readbyqxmd.com/read/28008617/n-cadherin-a-novel-and-rapidly-remodelling-site-involved-in-vasoregulation-of-small-cerebral-arteries
#14
Zhe Sun, Min Li, Zhaohui Li, Michael A Hill, Gerald A Meininger
N-cadherin is the major cell-cell adhesion molecule in vascular smooth muscle cells (VSMC). We tested the hypothesis that N-cadherin is part of a novel mechano-sensory mechanism in VSMC and plays an active role in both the arteriolar myogenic response and during changes in vascular tone induced by vasomotor agonists. Intact and pressurized rat superior cerebellar arteries (SCA) were labelled for confocal immunofluorescence imaging. N-cadherin formed punctate adherens junctions (AJ) along the borders between VSMC...
December 23, 2016: Journal of Physiology
https://www.readbyqxmd.com/read/28007970/dual-effects-of-fructose-on-chrebp-and-foxo1-3%C3%AE-are-responsible-for-aldob-upregulation-and-vascular-remodeling
#15
Wei Cao, Tuanjie Chang, Xiao-Qiang Li, Rui Wang, Lingyun Wu
Increased production of methylglyoxal (MG) in vascular tissues is one of the causative factors for vascular remodeling in different subtypes of metabolic syndrome, including hypertension and insulin resistance. Fructose-induced upregulation of aldolase B (AldoB) contributes to increased vascular MG production but the underlying mechanisms have been unclear. Serum levels of MG and fructose were determined in diabetic patients with hypertension. MG level had significant positive correlations with blood pressure and fructose level respectively...
December 22, 2016: Clinical Science (1979-)
https://www.readbyqxmd.com/read/28005306/non-enzymatic-glycation-interferes-with-fibronectin-integrin-interactions-in-vascular-smooth-muscle-cells
#16
Srijita Dhar, Zhe Sun, Gerald A Meininger, Michael A Hill
OBJECTIVE: We aimed to investigate whether advanced non-enzymatic glycation of the extracellular matrix (ECM) protein, fibronectin, impacts its normal integrin-mediated interaction with arteriolar vascular smooth muscle cells (VSMC). METHODS: Atomic force microscopy (AFM) was performed on cultured VSMC from rat cremaster arterioles to study native and glycated fibronectin (FN and gFN) interactions with cellular integrins. AFM probes were functionalized with FN or gFN or with native or glycated albumin (gAlb) as controls...
December 22, 2016: Microcirculation: the Official Journal of the Microcirculatory Society, Inc
https://www.readbyqxmd.com/read/28004124/attenuation-of-neointimal-formation-with-netrin-1-and-netrin-1-preconditioned-endothelial-progenitor-cells
#17
Norika Mengchia Liu, Kin Lung Siu, Ji Youn Youn, Hua Cai
: Restenosis after angioplasty is a serious clinical problem that can result in re-occlusion of the coronary artery. Although current drug-eluting stents have proved to be more effective in reducing restenosis, they have drawbacks of inhibiting reendothelialization to promote thrombosis. New treatment options are in urgent need. We have shown that netrin-1, an axon-guiding protein, promotes angiogenesis and cardioprotection via production of nitric oxide (NO). The present study examined whether and how netrin-1 attenuates neointimal formation in a femoral wire injury model...
December 21, 2016: Journal of Molecular Medicine: Official Organ of the "Gesellschaft Deutscher Naturforscher und Ärzte"
https://www.readbyqxmd.com/read/28004064/-secondary-hyperuricemia-in-chronic-renal-failure-promotes-vascular-calcification-in-rats
#18
Zhe Song, Yang Zhao, Xian Wang, Ming-Jiang Xu
The present study was aimed to explore the effects of hyperuricemia on vascular calcification in chronic renal failure (CRF) and the mechanisms. Adenine diet-induced CRF rat model was used. Twenty-three male 8-week-old Wistar rats were randomly divided into control group (Ctr, n = 5), CRF group (n = 8) and CRF plus allopurinol group (CRF + ALL, n = 10), and the rats were given standard diet plus standard drinking water, adenine diet plus standard drinking water and adenine diet plus allopurinol drinking for 6 weeks, respectively...
December 25, 2016: Sheng Li Xue Bao: [Acta Physiologica Sinica]
https://www.readbyqxmd.com/read/28003360/downregulation-of-insulin-receptor-substrate-1-during-hyperglycemia-induces-vascular-smooth-muscle-cell-dedifferentiation
#19
Gang Xi, Christine Wai, Morris F White, David R Clemmons
Diabetes is a major risk factor for the development of atherosclerosis but the mechanism by which hyperglycemia accelerates lesion development is not well defined. Insulin and insulin like growth factor-I (IGF-I)1 signal through the scaffold protein insulin receptor substrate-1(IRS-1). In diabetes IRS-1 is down regulated and cells become resistant to insulin. Under these conditions the IGF-I receptor signals through an alternate scaffold protein, SHPS-1, resulting in pathophysiologic stimulation of vascular smooth muscle cell (VSMC) migration and proliferation...
December 21, 2016: Journal of Biological Chemistry
https://www.readbyqxmd.com/read/28003268/inhibition-of-srf-myocardin-reduces-aortic-stiffness-by-targeting-vascular-smooth-muscle-cell-stiffening-in-hypertension
#20
Ning Zhou, Jia-Jye Lee, Shaunrick Stoll, Ben Ma, Robert Wiener, Charles Wang, Kevin D Costa, Hongyu Qiu
AIMS: Increased aortic stiffness is a fundamental manifestation of hypertension. However, the molecular mechanisms involved remain largely unknown. We tested the hypothesis that abnormal intrinsic vascular smooth muscle cell (VSMC) mechanical properties in large arteries, but not in distal arteries, contribute to the pathogenesis of aortic stiffening in hypertension, mediated by the serum response factor (SRF)/myocardin signalling pathway. METHODS AND RESULTS: Four month old male spontaneously hypertensive rats (SHR) and normotensive Wistar-Kyoto (WKY) rats were studied...
October 23, 2016: Cardiovascular Research
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