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https://www.readbyqxmd.com/read/29785051/hyaluronan-negatively-regulates-vascular-calcification-involving-bmp2-signaling
#1
Yonglun Kong, Qingchun Liang, Yanting Chen, Pingzhen Yang, Xiaoyu Liu, Yining Li, Siyuan Feng, Ji Wu, Wantao Liu, Jingyi Tang, Huimin Yu, Jing-Song Ou, Lihe Lu, Jianyun Yan
Vascular calcification is a highly regulated biological process similar to bone formation involving osteogenic differentiation of vascular smooth muscle cells (VSMCs). Hyaluronan (HA), a major structural component of the extracellular matrix in cartilage, has been shown to inhibit osteoblast differentiation. However, whether HA affects osteogenic differentiation and calcification of VSMCs remains unclear. In the present study, we used in vitro and ex vivo models of vascular calcification to investigate the role of HA in vascular calcification...
May 21, 2018: Laboratory Investigation; a Journal of Technical Methods and Pathology
https://www.readbyqxmd.com/read/29780355/therapeutic-interference-with-vascular-calcification-lessons-from-klotho-hypomorphic-mice-and-beyond
#2
REVIEW
Florian Lang, Christina Leibrock, Lisann Pelzl, Meinrad Gawaz, Burkert Pieske, Ioana Alesutan, Jakob Voelkl
Medial vascular calcification, a major pathophysiological process associated with cardiovascular disease and mortality, involves osteo-/chondrogenic transdifferentiation of vascular smooth muscle cells (VSMCs). In chronic kidney disease (CKD), osteo-/chondrogenic transdifferentiation of VSMCs and, thus, vascular calcification is mainly driven by hyperphosphatemia, resulting from impaired elimination of phosphate by the diseased kidneys. Hyperphosphatemia with subsequent vascular calcification is a hallmark of klotho-hypomorphic mice, which are characterized by rapid development of multiple age-related disorders and early death...
2018: Frontiers in Endocrinology
https://www.readbyqxmd.com/read/29777903/sox9-is-increased-in-arterial-plaque-and-stenosis-associated-with-synthetic-phenotype-of-vascular-smooth-muscle-cells-and-causes-alterations-in-extracellular-matrix-and-calcification
#3
Antje Augstein, Johannes Mierke, David M Poitz, Ruth H Strasser
Vascular smooth muscle cells (VSMC) exhibit a dual role in progression and maintenance of arteriosclerosis. They are fundamental for plaque stability but also can drive plaque progression. During pathogenic vascular remodeling, VSMC transdifferentiate into a phenotype with enhanced proliferation and migration. Moreover, they exert an increased capacity to generate extracellular matrix proteins. A special lineage of transdifferentiated VSMC expresses Sox9, a multi-functional transcription factor. The aim of the study was to examine the role of Sox9 in phenotypic alterations leading to arteriosclerosis...
May 16, 2018: Biochimica et Biophysica Acta
https://www.readbyqxmd.com/read/29775416/downregulation-of-the-%C3%AE-1-and-%C3%AE-1-subunit-of-sgc-in-arterial-smooth-muscle-cells-of-opscc-is-hpv-independent
#4
Y Korkmaz, H C Roggendorf, O G Siefer, J Seehawer, T Imhof, M Plomann, W Bloch, A Friebe, C U Huebbers
The nitric oxide (NO)-sensitive soluble guanylyl cyclase (sGC) is a heterodimeric enzyme with an α and β subunit. NO binds to heme of the β1 -subunit of sGC, activates the enzyme in the reduced heme iron state in vascular smooth muscle cells (VSMCs), and generates cGMP-inducing vasodilatation and suppression of VSMC proliferation. In the complex tumor milieu with higher levels of reactive oxygen species (ROS), sGC heme iron may become oxidized and insensitive to NO. To change sGC from an NO-insensitive to NO-sensitive state or NO-independent manner, protein expression of sGC in VSMC is required...
May 1, 2018: Journal of Dental Research
https://www.readbyqxmd.com/read/29775408/lack-of-tone-in-mouse-small-mesenteric-arteries-leads-to-outward-remodeling-which-can-be-prevented-by-prolonged-agonist-induced-vasoconstriction
#5
Anika Klein, Philomeena Daphne Joseph, Vibeke Grøsfjeld Christensen, Lars Jørn Jensen, Jens Christian Brings Jacobsen
Inward remodeling of resistance vessels is an independent risk factor for cardiovascular events. Thus far, the remodeling process remains incompletely elucidated, but the activation level of the vascular smooth muscle cell (VSMC) appears to play a central role. Accordingly, previous data suggest that an antagonistic and, supposedly beneficial, response - outward remodeling - may follow prolonged vasodilatation. This study aims to determine if 1) outward remodeling follows 3 days of vessel culture without tone, 2) a similar response can be elicited in a much shorter 4-hour time frame and finally 3) a 4-hour response can be prevented or reversed by the presence of vasoconstrictors in the medium...
May 18, 2018: American Journal of Physiology. Heart and Circulatory Physiology
https://www.readbyqxmd.com/read/29765446/inhibitory-effect-of-pdgf-bb-and-serum-stimulated-responses-in-vascular-smooth-muscle-cell-proliferation-by-hinokitiol-via-up-regulation-of-p21-and-p53
#6
Jiun-Yi Li, Chun-Ping Liu, Wei-Cheng Shiao, Thanasekaran Jayakumar, Yi-Shin Li, Nen-Chung Chang, Shih-Yi Huang, Cheng-Ying Hsieh
Introduction: Vascular smooth muscle cell (VSMC) proliferation plays a major role in the progression of vascular diseases. In the present study, we established the efficacy and the mechanisms of action of hinokitiol, a tropolone derivative found in Chamaecyparis taiwanensis , Cupressaceae, in relation to platelet-derived growth factor-BB (PDGF-BB) and serum-dependent VSMC proliferation. Material and methods: Primary cultured rat VSMCs were pre-treated with hinokitiol and then stimulated by PDGF-BB (10 ng/ml) or serum (10% fetal bovine serum)...
April 2018: Archives of Medical Science: AMS
https://www.readbyqxmd.com/read/29765072/notoginsenoside-r1-inhibits-vascular-smooth-muscle-cell-proliferation-migration-and-neointimal-hyperplasia-through-pi3k-akt-signaling
#7
Haihong Fang, Shilin Yang, Yingying Luo, Cheng Zhang, Yi Rao, Renjing Liu, Yulin Feng, Jun Yu
Restenosis caused by neointimal hyperplasia significantly decreases long-term efficacy of percutaneous transluminal angioplasty (PTA), stenting, and by-pass surgery for managing coronary and peripheral arterial diseases. A major cause of pathological neointima formation is abnormal vascular smooth muscle cell (VSMC) proliferation and migration. Notoginsenoside R1 (NGR1) is a novel saponin that is derived from Panax notoginseng and has reported cardioprotective, neuroprotective and anti-inflammatory effects...
May 15, 2018: Scientific Reports
https://www.readbyqxmd.com/read/29758198/the-lncrna-tug1-mir-145-5p-fgf10-regulates-proliferation-and-migration-in-vsmcs-of-hypertension
#8
Lin Shi, Caijun Tian, Lingzhi Sun, Feifei Cao, Zhaoyang Meng
Vascular remodeling is a characteristic pathological feature of hypertension, it can cause of increasing vascular resistance and decrease of compliance. Vascular smooth muscle cell (VSMCs) dysfunction is the important foundation of vascular remodeling. Increasing evidences have revealed that lncRNA is an important regulatory factor of VSMC function. In this paper, we explored the function of lncRNA TUG1 in vascular remodeling of hypertension. Here, we found that lncRNA TUG1 was highly expressed in aorta of spontaneously hypertensive rats (SHR) rats and promoted the proliferation and migration of VSMCs (SHR-VSMCs)...
May 11, 2018: Biochemical and Biophysical Research Communications
https://www.readbyqxmd.com/read/29756630/a-biomimetic-microfluidic-model-to-study-signalling-between-endothelial-and-vascular-smooth-muscle-cells-under-hemodynamic-conditions
#9
Nicole C A van Engeland, Andreas M A O Pollet, Jaap M J den Toonder, Carlijn V C Bouten, Oscar M J A Stassen, Cecilia M Sahlgren
Cell signalling and mechanics influence vascular pathophysiology and there is an increasing demand for in vitro model systems that enable examination of signalling between vascular cells under hemodynamic conditions. Current 3D vessel wall constructs do not recapitulate the mechanical conditions of the native tissue nor do they allow examination of cell-cell interactions under relevant hemodynamic conditions. Here, we describe a 3D microfluidic chip model of arterial endothelial and smooth muscle cells where cellular organization, composition and interactions, as well as the mechanical environment of the arterial wall are mimicked...
May 14, 2018: Lab on a Chip
https://www.readbyqxmd.com/read/29752344/mir-4463-inhibits-the-migration-of-human-aortic-smooth-muscle-cells-by-amot
#10
Xueqin Wang, Chao Du, Xuemei He, Xian Deng, Yanzheng He, Xiangyu Zhou
Aberrant vascular smooth muscle cell (VSMC) migration has been implicated in a variety of vascular disorders, while the signal pathways governing this process remain unclear. Here, we investigated whether microRNAs (miRNAs), which are strong posttranscriptional regulators of gene expression, could alter VSMC migration. We detected the expression of miR-4463 in the plasma of patients with atherosclerosis and in human aortic smooth muscle cells (HASMCs) under hypoxia-ischemia condition, and investigated the migration effect and its downstream pathways...
May 11, 2018: Bioscience Reports
https://www.readbyqxmd.com/read/29750899/bmp-2-enhances-the-migration-and-proliferation-of-hypoxia-induced-vsmcs-via-actin-cytoskeleton-cd44-and-matrix-metalloproteinase-linkage
#11
Min Yang, Zhiqin Fan, Fei Wang, Zhi-Hua Tian, Bo Ma, Bing Dong, Zhongwu Li, Ming Zhang, Wei Zhao
The persistent proliferation of hypoxia-induced vascular smooth muscle cells (VSMCs) in the arterial wall underlie the development of atherosclerosis. However, the mechanism that regulates the behavior of VSMCs, which involve in actin aggregation, and impedes their migration is still elusive. Here, we report that bone morphogenetic protein 2 (BMP-2) leads to enrichment of CD44 and F-actin stress fiber and secretion of matrix metalloproteinases-2 (MMP-2) during hypoxia in vitro and following artificial hypoxia-induced atherosclerosis exacerbation in vivo...
May 8, 2018: Experimental Cell Research
https://www.readbyqxmd.com/read/29750813/autophagy-mediates-tumor-necrosis-factor-%C3%AE-induced-phenotype-switching-in-vascular-smooth-muscle-a7r5-cell-line
#12
Marina García-Miguel, Jaime A Riquelme, Ignacio Norambuena-Soto, Pablo E Morales, Fernanda Sanhueza-Olivares, Constanza Nuñez-Soto, David Mondaca-Ruff, Nicole Cancino-Arenas, Alejandra San Martín, Mario Chiong
Vascular smooth muscle cells (VSMC) dedifferentiation from a contractile to a synthetic phenotype contributes to atherosclerosis. Atherosclerotic tissue has a chronic inflammatory component with high levels of tumor necrosis factor-α (TNF-α). VSMC of atheromatous plaques have increased autophagy, a mechanism responsible for protein and intracellular organelle degradation. The aim of this study was to evaluate whether TNF-α induces phenotype switching of VSMCs and whether this effect depends on autophagy...
2018: PloS One
https://www.readbyqxmd.com/read/29749489/effects-of-osteoprotegerin-tnfrsf11b-in-two-models-of-abdominal-aortic-aneurysms
#13
Emina Vorkapic, Anne Kunath, Dick Wågsäter
Osteoprotegerin (OPG), additionally termed tumor necrosis factor receptor superfamily member 11B, is produced by vascular smooth muscle cells (VSMCs) and endothelial cells in the vasculature, and its release may be modulated by pro‑inflammatory cytokines, including interleukin‑1β and tumor necrosis factor‑α. The present study investigated the effects of treatment with low‑dose human recombinant OPG on abdominal aortic aneurysm (AAA) development in mice. Mice were treated with 1 µg human recombinant OPG four times (or vehicle) for 2 weeks prior to inducing AAA...
April 27, 2018: Molecular Medicine Reports
https://www.readbyqxmd.com/read/29741760/involvement-of-cgrp-rcp-in-the-caveolin-1-erk1-2-signal-pathway-in-the-static-pressure-induced-proliferation-of-vascular-smooth-muscle-cells
#14
Feng Guo, Li Yang, Jingfei Luo, Haiyan Quan, Zhen Wang, Hongyan Peng, Chenliang Hong, Jie Li, Zhisheng Jiang, Liang Zhang, Xuping Qin
Previous study suggested that the receptor component protein (RCP), one of the components of calcitonin gene-related peptide (CGRP) receptor, plays a multiple role in the cellular signal transduction. The study was designed to investigate whether or not the RCP involved in the regulation of caveolin-1/extracellular signal-regulated kinases-1 and -2 (ERK1/2) signal pathway in the vascular smooth muscle cells (VSMCs) proliferation induced by static pressure. Mouse-derived VSMCs line A10 (A10 VSMCs) was served as project in this experiment...
May 9, 2018: Journal of Cellular Physiology
https://www.readbyqxmd.com/read/29738818/microrna-132-targeting-pten-contributes-to-cilostazol-promoted-vascular-smooth-muscle-cell-differentiation
#15
Wei-Jan Chen, Ying-Hwa Chen, Yu-Juei Hsu, Kwang-Huei Lin, Yung-Hsin Yeh
BACKGROUND AND AIMS: Cilostazol, beyond its antiplatelet effect, is also capable of promoting vascular smooth muscle cell (VSMC) differentiation. The aim of this study was to explore the potential role of PTEN, known to associate with VSMC differentiation, and its related microRNA (miRNA) in cilostazol-dependent effects. METHODS AND RESULTS: Microarray analysis in balloon-injured rat carotid arteries comparing with and without balloon injury revealed that miR-132 was differentially expressed...
April 26, 2018: Atherosclerosis
https://www.readbyqxmd.com/read/29732374/chinese-herbal-medicine-as-a-potential-treatment-of-abdominal-aortic-aneurysm
#16
Sai Wang Seto, Dennis Chang, Hosen Kiat, Ning Wang, Alan Bensoussan
Abdominal aortic aneurysm (AAA) is an irreversible condition where the abdominal aorta is dilated leading to potentially fatal consequence of aortic rupture. Multiple mechanisms are involved in the development and progression of AAA, including chronic inflammation, oxidative stress, vascular smooth muscle (VSMC) apoptosis, immune cell infiltration and extracellular matrix (ECM) degradation. Currently surgical therapies, including minimally invasive endovascular aneurysm repair (EVAR), are the only viable interventions for AAAs...
2018: Frontiers in Cardiovascular Medicine
https://www.readbyqxmd.com/read/29731721/endothelial-aip1-regulates-vascular-remodeling-by-suppressing-nadph-oxidase-2
#17
Jiqin Zhang, Chaofei Chen, Li Li, Huanjiao J Zhou, Fenghe Li, Haifeng Zhang, Luyang Yu, Yuxin Chen, Wang Min
Objective: AIP1 expression is downregulated in human atherosclerotic plaques and global deletion of AIP1 in mice exacerbates atherosclerosis in ApoE-KO mouse models. However, the direct role of AIP1 in endothelium, vascular remodeling and associated vascular diseases has not been determined. Approach and Results: We used endothelial cell (EC)-specific AIP1-deficient (AIP1-ECKO) mice to define the role of AIP1 in vascular remodeling and intima-media thickening in a mouse carotid artery ligation model characterized by both neointimal hyperplasia and inward vessel remodeling...
2018: Frontiers in Physiology
https://www.readbyqxmd.com/read/29723537/ring-finger-protein-10-prevents-neointimal-hyperplasia-by-promoting-apoptosis-in-vitro-and-in-vivo
#18
Guiquan Yu, Jing Chen, Siyu Li, Peng Pu, Wei Huang, Yongpeng Zhao, Xin Peng, Ruiyu Wang, Han Lei
AIMS: Vascular restenosis and neointimal hyperplasia are enhanced in metabolic syndrome (MetS). Vascular smooth muscle cell (VSMC) proliferation is a key step during restenosis and is suppressed by RING finger protein 10 (RNF10). However, the effect of RNF10 on neointimal hyperplasia is unknown. In the present study, we explored whether RNF10 over-expression prevents neointimal hyperplasia in a MetS rat model and in cultured VSMCs exposed to high glucose. MAIN METHODS: An adenovirus encoding RNF10 (Ad-RNF10) or control green fluorescent protein (Ad-GFP) was delivered to balloon-injured carotid arteries in MetS rats and cultured rat VSMCs exposed to high glucose...
April 30, 2018: Life Sciences
https://www.readbyqxmd.com/read/29721770/selenoprotein-s-inhibits-inflammation-induced-vascular-smooth-muscle-cell-calcification
#19
Yali Ye, Weixia Bian, Fen Fu, Jian Hu, Hongmei Liu
Vascular calcification is a prominent feature of many diseases including atherosclerotic cardiovascular disease (CVD), leading to high morbidity and mortality rates. A significant association of selenoprotein S (SelS) gene polymorphism with atherosclerotic CVD has been reported in epidemiologic studies, but the underlying mechanism is far from clear. To investigate the role of SelS in inflammation-induced vascular calcification, osteoblastic differentiation and calcification of vascular smooth muscle cells (VSMCs) induced by lipopolysaccharide (LPS) or tumor necrosis factor (TNF)-α were compared between the cells with and without SelS knockdown...
May 2, 2018: Journal of Biological Inorganic Chemistry: JBIC
https://www.readbyqxmd.com/read/29717623/aortic-sca-1-sup-sup-progenitor-cells-arise-from-the-somitic-mesoderm-lineage-in-mouse
#20
Sarah K Steinbach, Tao Wang, Martha H Carruthers, Angela Li, Rickvinder Besla, Adam P Johnston, Clinton S Robbins, Mansoor Husain
Sca-1<sup>+</sup> progenitor cells in the adult mouse aorta are known to generate vascular smooth muscle cells (VSMC), but their embryological origins and temporal abundance are not known. Using tamoxifen-inducible <i>Myf5-Cre</i><sup>ER</sup> mice, we demonstrate that Sca-1<sup>+</sup> adult aortic cells arise from the somitic mesoderm beginning at E8.5 and continue throughout somitogenesis. <i>Myf5</i> lineage-derived Sca-1<sup>+</sup> cells greatly expand in situ starting at 4 weeks of age and become a major source of aortic Sca-1<sup>+</sup> cells by 6 weeks of age...
May 2, 2018: Stem Cells and Development
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