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vascular smooth muscle cell senescence

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https://www.readbyqxmd.com/read/29643057/defective-base-excision-repair-of-oxidative-dna-damage-in-vascular-smooth-muscle-cells-promotes-atherosclerosis
#1
Aarti Shah, Kelly Gray, Nichola Figg, Alison Finigan, Lakshi Starks, Martin Bennett
Background -Atherosclerotic plaques demonstrate extensive accumulation of oxidative DNA damage, predominantly as 8-oxoguanine (8oxoG) lesions. 8oxoG is repaired by base excision repair (BER) enzymes; however, the mechanisms regulating 8oxoG accumulation in vascular smooth muscle cells (VSMCs) and its effects on their function and in atherosclerosis are unknown. Methods -We studied levels of 8oxoG and its regulatory enzymes in human atherosclerosis, the mechanisms regulating 8oxoG repair and the BER enzyme 8oxoG DNA glycosylase I (OGG1) in VSMCs in vitro, and the effects of reducing 8oxoG in VSMCs in atherosclerosis in ApoE-/- mice...
April 11, 2018: Circulation
https://www.readbyqxmd.com/read/29556500/vascular-senescence-in-cardiovascular-and-metabolic-diseases
#2
Goro Katsuumi, Ippei Shimizu, Yohko Yoshida, Tohru Minamino
In mammals, aging is associated with accumulation of senescent cells. Stresses such as telomere shortening and reactive oxygen species induce "cellular senescence", which is characterized by growth arrest and alteration of the gene expression profile. Chronological aging is associated with development of age-related diseases, including heart failure, diabetes, and atherosclerotic disease, and studies have shown that accumulation of senescent cells has a causative role in the pathology of these age-related disorders...
2018: Frontiers in Cardiovascular Medicine
https://www.readbyqxmd.com/read/29528383/neuregulin-1-attenuates-stress-induced-vascular-senescence
#3
Hadis Shakeri, Andreas B Gevaert, Dorien M Schrijvers, Guido R Y De Meyer, Gilles W De Keulenaer, Pieter-Jan D F Guns, Katrien Lemmens, Vincent F Segers
Aims: Cardiovascular ageing is a key determinant of life expectancy. Cellular senescence, a state of irreversible cell cycle arrest, is an important contributor to ageing due to the accumulation of damaged cells. Targeting cellular senescence could prevent age-related cardiovascular diseases. In this study, we investigated the effects of neuregulin-1 (NRG-1), an epidermal growth factor with cardioprotective and anti-atherosclerotic effects, on cellular senescence. Methods & results: Senescence was induced in cultured rat aortic endothelial cells (ECs) and aortic smooth muscle cells (SMCs) by 2 hours exposure to 30 µM hydrogen peroxide (H2O2)...
March 8, 2018: Cardiovascular Research
https://www.readbyqxmd.com/read/29486395/targeted-gene-expression-analyses-and-immunohistology-suggest-a-pro-proliferative-state-in-tricuspid-aortic-valve-and-senescence-and-viral-infections-in-bicuspid-aortic-valve-associated-thoracic-aortic-aneurysms
#4
Stefan Blunder, Barbara Messner, Bernhard Scharinger, Christian Doppler, Iris Zeller, Andreas Zierer, Günther Laufer, David Bernhard
BACKGROUND AND AIMS: Despite the potential life-threatening consequences of thoracic aortic aneurysms (TAAs), the pathogenesis of these diseases is still poorly understood. While some aspects of TAA formation have been elucidated, the role of vascular smooth muscle cells (SMCs) in both bicuspid aortic valve (BAV)-associated and degenerative tricuspid aortic valve (TAV)-associated TAAs has not yet been fully unravelled. Thus, this work was aimed at uncovering processes in SMC biology that may contribute to TAA formation...
February 5, 2018: Atherosclerosis
https://www.readbyqxmd.com/read/29472548/arginase-ii-activates-mtorc1-through-myosin-1b-in-vascular-cell-senescence-and-apoptosis
#5
Yi Yu, Yuyan Xiong, Jean-Pierre Montani, Zhihong Yang, Xiu-Fen Ming
Type-II L-arginine:ureahydrolase, arginase-II (Arg-II), is shown to activate mechanistic target of rapamycin complex 1 (mTORC1) pathway and contributes to cell senescence and apoptosis. In an attempt to elucidate the underlying mechanism, we identified myosin-1b (Myo1b) as a mediator. Overexpression of Arg-II induces re-distribution of lysosome and mTOR but not of tuberous sclerosis complex (TSC) from perinuclear area to cell periphery, dissociation of TSC from lysosome and activation of mTORC1-ribosomal protein S6 kinase 1 (S6K1) pathway...
February 22, 2018: Cell Death & Disease
https://www.readbyqxmd.com/read/29407880/the-protective-effect-of-resveratrol-on-vascular-aging-by-modulation-of-the-renin-angiotensin-system
#6
Eun Nim Kim, Min Young Kim, Ji Hee Lim, Yaeni Kim, Seok Joon Shin, Cheol Whee Park, Yong-Soo Kim, Yoon Sik Chang, Hye Eun Yoon, Bum Soon Choi
BACKGROUND AND AIMS: This study evaluated the effects of resveratrol on arterial aging and the renin-angiotensin system (RAS) in mice and vascular smooth muscle cells (VSMCs). METHODS: Aging mice were divided into control and resveratrol groups. Histological changes, inflammation, oxidative stress, RAS components, and the expression of AMP-activated protein kinase (AMPK), silent information regulator T1 (SIRT1), peroxisome proliferator-activated receptor-γ co-activator 1α (PGC-1α), and anti-oxidative enzymes was measured in thoracic aortas of 24-month-old mice...
February 2, 2018: Atherosclerosis
https://www.readbyqxmd.com/read/29390191/inducible-knockdown-of-endothelial-protein-tyrosine-phosphatase-1b-promotes-neointima-formation-in-obese-mice-by-enhancing-endothelial-senescence
#7
Marianne Jäger, Astrid Hubert, Rajinikanth Gogiraju, Magdalena L Bochenek, Thomas Münzel, Katrin Schäfer
AIMS: Protein tyrosine phosphatase-1B (PTP1B) is a negative regulator of receptor tyrosine kinase signaling. In this study, we determined the importance of PTP1B expressed in endothelial cells for the vascular response to arterial injury in obesity. RESULTS: Morphometric analysis of vascular lesions generated by 10% ferric chloride (FeCl3) revealed that tamoxifen-inducible endothelial PTP1B deletion (Tie2.ERT2-Cre × PTP1Bfl/fl; End.PTP1B knockout, KO) significantly increased neointima formation, and reduced numbers of (endothelial lectin-positive) luminal cells in End...
February 1, 2018: Antioxidants & Redox Signaling
https://www.readbyqxmd.com/read/29385432/dynamic-and-diverse-changes-in-the-functional-properties-of-vascular-smooth-muscle-cells-in-pulmonary-hypertension
#8
Kurt R Stenmark, Maria G Frid, Brian B Graham, Rubin M Tuder
Pulmonary hypertension (PH) is the end result of interaction between pulmonary vascular tone and a complex series of cellular and molecular events termed "vascular remodeling". The remodeling process, which can involve the entirety of pulmonary arterial vasculature, almost universally involves medial thickening, driven by increased numbers and hypertrophy of its principal cellular constituent, smooth muscle cells (SMCs). It is noted, however that SMCs comprise heterogeneous populations of cells, which can exhibit markedly different proliferative, inflammatory, and extracellular matrix production changes during remodeling...
January 27, 2018: Cardiovascular Research
https://www.readbyqxmd.com/read/29360955/vascular-smooth-muscle-cell-death-autophagy-and-senescence-in-atherosclerosis
#9
Mandy O J Grootaert, Manon Moulis, Lynn Roth, Wim Martinet, Cécile Vindis, Martin R Bennett, Guido R Y De Meyer
In the present review, we describe the causes and consequences of loss of vascular smooth muscle cells (VSMCs) or their function in advanced atherosclerotic plaques and discuss possible mechanisms such as cell death or senescence, and induction of autophagy to promote cell survival. We also highlight the potential use of pharmacological modulators of these processes to limit plaque progression and/or improve plaque stability. VSMCs play a pivotal role in atherogenesis. Loss of VSMCs via initiation of cell death leads to fibrous cap thinning and promotes necrotic core formation and calcification...
March 15, 2018: Cardiovascular Research
https://www.readbyqxmd.com/read/29300828/non-coding-rnas-key-regulators-of-smooth-muscle-cell-fate-in-vascular-disease
#10
Nicholas J Leeper, Lars Maegdefessel
The vascular smooth muscle cell (SMC) is one of the most plastic cells in the body. Understanding how non-coding RNAs (ncRNAs) regulate SMC cell-fate decision making in the vasculature has significantly enhanced our understanding of disease development, and opened up exciting new avenues for potential therapeutic applications. Recent studies on SMC physiology have in addition challenged our traditional view on their role and contribution to vascular disease, mainly in the setting of atherosclerosis as well as aneurysm disease, and restenosis after angioplasties...
March 15, 2018: Cardiovascular Research
https://www.readbyqxmd.com/read/29286156/metformin-induced-activation-of-ampk-inhibits-the-proliferation-and-migration-of-human-aortic-smooth-muscle-cells-through-upregulation-of-p53-and-ifi16
#11
Biao Hao, Yan Xiao, Fang Song, Xiangshu Long, Jing Huang, Maobo Tian, Shiyan Deng, Qiang Wu
The proliferation and migration of vascular smooth muscle cells are significant in the development and progression of atherosclerosis and plaque rupture. Metformin is a widely used antidiabetic drug, which has been reported to inhibit cell growth and migration. The antiproliferative and antimigratory effects of metformin have been attributed to 5' adenosine monophosphate-activated protein kinase (AMPK) activation. The purpose of the present study was to investigate the effects of metformin on primary human aortic muscle cells (HASMCs) in vitro and to clarify the underlying mechanism...
March 2018: International Journal of Molecular Medicine
https://www.readbyqxmd.com/read/29274344/calcium-phosphate-particles-stimulate-interleukin-1%C3%AE-release-from-human-vascular-smooth-muscle-cells-a-role-for-spleen-tyrosine-kinase-and-exosome-release
#12
Yana Dautova, Alexander N Kapustin, Kevin Pappert, Matthias Epple, Hanneke Okkenhaug, Simon J Cook, Catherine M Shanahan, Martin D Bootman, Diane Proudfoot
AIMS: Calcium phosphate (CaP) particle deposits are found in several inflammatory diseases including atherosclerosis and osteoarthritis. CaP, and other forms of crystals and particles, can promote inflammasome formation in macrophages leading to caspase-1 activation and secretion of mature interleukin-1β (IL-1β). Given the close association of small CaP particles with vascular smooth muscle cells (VSMCs) in atherosclerotic fibrous caps, we aimed to determine if CaP particles affected pro-inflammatory signalling in human VSMCs...
February 2018: Journal of Molecular and Cellular Cardiology
https://www.readbyqxmd.com/read/29232676/progressive-development-of-aberrant-smooth-muscle-cell-phenotype-in-abdominal-aortic-aneurysm-disease
#13
Kirsten Riches, Emily Clark, Rebecca J Helliwell, Timothy G Angelini, Karen E Hemmings, Marc A Bailey, Katherine I Bridge, D Julian A Scott, Karen E Porter
Abdominal aortic aneurysm (AAA) is a silent, progressive disease with a high mortality and an increasing prevalence with aging. Smooth muscle cell (SMC) dysfunction contributes to gradual dilatation and eventual rupture of the aorta. Here we studied phenotypic characteristics in SMC cultured from end-stage human AAA (≥5 cm) and cells cultured from a porcine carotid artery (PCA) model of early and end-stage aneurysm. Human AAA-SMC presented a secretory phenotype and expressed elevated levels of the differentiation marker miR-145 (2...
2018: Journal of Vascular Research
https://www.readbyqxmd.com/read/29215061/local-production-of-activated-factor-x-in-atherosclerotic-plaque-induced-vascular-smooth-muscle-cell-senescence
#14
Fumihiro Sanada, Jun Muratsu, Rei Otsu, Hideo Shimizu, Nobutaka Koibuchi, Kazutaka Uchida, Yoshiaki Taniyama, Shinichi Yoshimura, Hiromi Rakugi, Ryuichi Morishita
Our previous study demonstrated that coagulation factor Xa (FXa) induced endothelial cell senescence, resulting in inflammation and impaired angiogenesis. This mechanism is dictated through protease-activated receptors, PARs, insulin-like growth factor-binding protein 5 (IGFBP-5), and p53. Activation of PARs contributes to the pathophysiology of several chronic inflammatory diseases, including atherosclerosis. Thus, we speculated that similar mechanism might participate in the progression of atherosclerotic plaques...
December 7, 2017: Scientific Reports
https://www.readbyqxmd.com/read/29107826/inhibition-of-vascular-smooth-muscle-cells-premature-senescence-with-rutin-attenuates-and-stabilizes-diabetic-atherosclerosis
#15
Yihui Li, Ranran Qin, Hongdan Yan, Feng Wang, Shanying Huang, Yun Zhang, Ming Zhong, Wei Zhang, Zhihao Wang
Atherosclerosis is an age-associated disease; however, diabetic atherosclerosis has higher severity beyond age range for accumulative premature senescent cells in diabetes. Recent findings suggest that rutin, a flavonoid, has potential benefits for diabetic individuals. This study was designed to evaluate the effects of rutin on premature senescence and atherosclerosis. Apolipoprotein E knockout mice exhibiting insulin resistance after 6 weeks of high-fat diet were administered with a low dose of streptozotocin (STZ) to induce diabetes...
January 2018: Journal of Nutritional Biochemistry
https://www.readbyqxmd.com/read/28986099/downregulation-of-pin1-in-human-atherosclerosis-and-its-association-with-vascular-smooth-muscle-cell-senescence
#16
Lei Lv, Meng Ye, Rundan Duan, Kai Yuan, Jiaquan Chen, Wei Liang, Zhaoxiong Zhou, Lan Zhang
OBJECTIVE: Pin1 is prevalently overexpressed in human cancers and implicated to regulate cell growth and apoptosis. Thus far, however, no role for Pin1 has been described in modulating vascular smooth muscle cell (VSMC) senescence. METHODS: Immunohistochemistry and Western blotting were used to assess Pin1 protein level in human normal and atherosclerotic tissues. β-galactosidase staining, cumulative population doubling level, telomerase activity, and relative telomere length measurement were used to confirm VSMC senescence...
October 3, 2017: Journal of Vascular Surgery
https://www.readbyqxmd.com/read/28944849/celastrol-alleviates-angiotensin-ii%C3%A2-mediated-vascular-smooth-muscle-cell-senescence-via-induction-of-autophagy
#17
Xian-Jie Xu, Wei-Bo Zhao, Shi-Bin Feng, Cheng Sun, Qiang Chen, Bing Ni, Hou-Yuan Hu
Reactive oxygen species (ROS) production has been implicated in the promotion of cellular senescence. Celastrol, a quinone methide triterpenoid isolated from the Celastraceae family, exerts antioxidant effects and enhances autophagy in various cell types. Since autophagy serves an important role in regulating ROS, it was hypothesized that the antioxidant effect of celastrol is via enhanced autophagy, thus inhibiting cell senescence. Therefore, the present study used a Senescence β‑Galactosidase Staining kit, western blot analysis and cell cycle analysis to investigate whether celastrol alleviates angiotensin (Ang) II‑induced cellular senescence by upregulating autophagy in vascular smooth muscle cells (VSMCs)...
November 2017: Molecular Medicine Reports
https://www.readbyqxmd.com/read/28932625/vascular-aging-implications-for-cardiovascular-disease-and-therapy
#18
Yohannes T Ghebre, Eduard Yakubov, Wing Tak Wong, Prasanna Krishnamurthy, Nazish Sayed, Andrew G Sikora, Mark D Bonnen
The incidence and prevalence of cardiovascular disease is highest among the elderly, in part, due to deleterious effects of advancing age on the heart and blood vessels. Aging, a known cardiovascular risk factor, is progressively associated with structural and functional changes to the vasculature including hemodynamic disturbance due to increased oxidative stress, premature cellular senescence and impairments in synthesis and/or secretion of endothelium-derived vasoactive molecules. These molecular and physiological changes lead to vessel wall stiffening and thickening, as well as other vascular complications that culminate to loss of vascular tone regulation and endothelial function...
December 2016: Translational Medicine: Current Research
https://www.readbyqxmd.com/read/28798142/accumulation-of-smooth-muscle-22%C3%AE-protein-accelerates-senescence-of-vascular-smooth-muscle-cells-via-stabilization-of-p53-in-vitro-and-in-vivo
#19
Sui-Bing Miao, Xiao-Li Xie, Ya-Juan Yin, Li-Li Zhao, Fan Zhang, Ya-Nan Shu, Rong Chen, Peng Chen, Li-Hua Dong, Yan-Ling Lin, Pin Lv, Dan-Dan Zhang, Xi Nie, Zhen-Ying Xue, Mei Han
OBJECTIVE: Smooth muscle (SM) 22α, an actin-binding protein, displays an upregulated expression as a marker during cellular senescence. However, the causal relationship between SM22α and senescence is poorly understood. This study aimed to investigate the role of SM22α in angiotensin II (Ang II)-induced senescence of vascular smooth muscle cells (VSMCs). APPROACH AND RESULTS: We prepared a model of VSMC senescence induced by Ang II and found that the expression of SM22α in VSMCs was increased in response to chronic Ang II treatment...
October 2017: Arteriosclerosis, Thrombosis, and Vascular Biology
https://www.readbyqxmd.com/read/28797827/interaction-between-mtor-pathway-inhibition-and-autophagy-induction-attenuates-adriamycin-induced-vascular-smooth-muscle-cell-senescence-through-decreased-expressions-of-p53-p21-p16
#20
Jin Young Sung, Kyung Young Lee, Jae-Ryong Kim, Hyoung Chul Choi
Cellular senescence is related to aging and extremely stable proliferative arrest with active metabolism. Senescent cells can activate mammalian target of rapamycin (mTOR) pathway, which plays a crucial role in the regulation of cell metabolism, cellular growth, and autophagy in senescence-associated cardiovascular diseases. Therefore, we examined whether mTOR pathway could induce cellular senescence by inhibition of autophagy in vascular smooth muscle cells (VSMCs). We found that adriamycin-induced VSMC senescence is accompanied by increased activity of mTOR, a major controller of cell growth and a negative regulator of autophagy...
August 7, 2017: Experimental Gerontology
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