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1.
Medisan ; 25(3)2021. graf, ilus
Article in Spanish | LILACS, CUMED | ID: biblio-1287304

ABSTRACT

Introducción: La carótida externa es una arteria muscular que irriga todos los componentes del sistema masticatorio, por lo que la regulación de la dinámica contráctil de su músculo liso vascular es imprescindible para garantizar el tono y el flujo sanguíneo tisular y modular la respuesta inflamatoria. Objetivo: Describir la dinámica contráctil espontánea del musculo liso vascular de la arteria carótida externa. Métodos: Se realizó una investigación experimental en el Instituto de Fisiología Oscar Langerdorff de la Facultad de Medicina, en la Universidad de Rostock, Alemania, de octubre a diciembre del 2018, en la cual se utilizaron 60 anillos de arterias carótidas externas obtenidas de 10 ratas Wistar adultas de ambos sexos. A dichos anillos se les practicó un corte helicoidal y fueron colocados en un baño de órganos, para registrarles, luego, la tensión espontánea desarrollada por el músculo liso vascular contra una carga de 1 gramo, durante diferentes intervalos de tiempo. Resultados: Los registros de la actividad contracción-relajación espontánea del músculo liso vascular de la arteria carótida externa fluctuaron dentro de un rango estrecho de cifras de tensión, con valores máximos de 8,48 ± 0,03 y mínimos de 8,33 ± 0,03, y una diferencia de 0,08 mN/g de músculo. Los valores promedios de tensión en cada intervalo de tiempo fueron muy cercanos, con desviaciones estándar que evidenciaron muy poca dispersión de los datos respecto a la media. La tensión promedio general registrada fue de 8,40 ± 0,032 mN/g. Conclusiones: La dinámica contráctil espontánea desarrollada por el músculo liso vascular de la arteria carótida externa mostró una progresión irregular en el tiempo, con valores promedios de tensión que oscilaron entre 5-10 mN/g de músculo.


Introduction: The external carotid is a muscle artery irrigating all components of the masticatory system, so that the regulation of the contractile dynamics of its vascular smooth muscle is important. Objective: To describe the spontaneous contractile dynamics of the vascular smooth muscle of the external carotid artery. Methods: An experimental investigation was carried out in the Oscar Langerdorff Physiology Institute from the Medicine Faculty at Rostock University, Germany, from October to December 2018, in which 60 rings of the external carotid artery obtained from 10 adult Wistar rats from both sexes. An helical cut was made to each ring and they were placed in an organ bath, to be registered, then, the spontaneous strain developed by the vascular smooth muscle against a charge of 1 g, during different time intervals was registered. Results: The records from the spontaneous contraction-relaxation of the vascular smooth muscle in the external carotid artery fluctuated within a narrow range of strain figures, with maximum values of 8.48 ± 0.03 and minimum of 8.33 ± 0.03, and a difference of 0.08 mN/g of muscle. Average strain values in each time interval were very closed, with standard deviations which evidenced a very small data dispersion regarding the mean. The average general registered strain was 8.40 ± 0.032 mN/g. Conclusions: The spontaneous contractile dynamics developed by the vascular smooth muscle of the external carotid artery showed an irregular progression in time, with average strain values fluctuating between 5-10 mN/g of muscle.


Subject(s)
Carotid Artery, External , Rats, Wistar , Research , Muscle, Smooth, Vascular
2.
Rev inf cient ; 100(5): 1-11, 2021. ilus
Article in Spanish | LILACS | ID: biblio-1348797

ABSTRACT

Introducción: El p-clorofenol alcanforado es un derivado clorofenólico de uso común como medicación intraconducto en Endodoncia. Son escasos los reportes científicos sobre sus efectos en la musculatura lisa vascular arterial y la regulación del flujo sanguíneo local. Objetivo: Determinar el efecto del p-clorofenol alcanforado sobre la dinámica contráctil del músculo liso vascular arterial en el tiempo. Método: Se realizó una investigación experimental preclínica utilizando 14 anillos de aorta obtenidos de ratas Wistar. Los anillos se colocaron en baño de órganos y se preactivaron con noradrenalina, registrándose luego la tensión desarrollada por el músculo liso vascular tras la adición de p-clorofenol alcanforado durante diferentes intervalos de tiempo. Resultados: El 51,4 % de la musculatura lisa vascular se relajó por la acción del p-clorofenol alcanforado. El mayor descenso del tono vascular se produjo entre el tercer y quinto minuto de añadido el medicamento. Las pruebas de Wilcoxon de los rangos con signos evidenciaron diferencias significativas entre la tensión base inicial y la registrada en los diferentes intervalos de tiempo estudiados. Conclusiones: el p-clorofenol alcanforado, induce in vitro, relajación del músculo liso arterial a través de un acoplamiento excitación-contracción de tipo farmacomecánico, la cual se incrementa en función del tiempo.


Introduction: Camphorated p-chlorophenol is a chlorophenolic derivative commonly used as an intra-oral medication in endodontics. Scientific reports on its effects in arterial vascular smooth muscle and local blood flow regulation are scarce. Objective: To determine the effect of camphorated p-chlorophenol on the contractile dynamics of arterial vascular smooth muscle. Method: An experimental and preclinical research was conducted with the use of 14 aortic rings of Wistar rats. The rings were placed in an organ bath and preactivated with noradrenaline, and the tension developed by the vascular smooth muscle at different time intervals was recorded after induction of camphorated p-chlorophenol. Results: Most of the vascular smooth muscle (51.4%) relaxed with the use of camphorated p-chlorophenol. The greatest decrease in vascular tone occurred between the third and fifth minute after use the drug. Wilcoxon rank tests showed significant differences between tension observed at baseline and those recorded at the different time intervals studied. Conclusions: Camphorated p-chlorophenol, induces in vitro, relax the arterial smooth muscle through a pharmacomechanical excitation-contraction link, which increases according to the time.


Introdução: O cânfora-clorofenol é um derivado clorofenólico comumente utilizado como medicamento intracanal em Endodontia. Relatórios científicos sobre seus efeitos no músculo liso vascular arterial e na regulação do fluxo sanguíneo local são escassos. Objetivo: Determinar o efeito da cânfora-clorofenol na dinâmica contrátil do músculo liso vascular arterial ao longo do tempo. Método: Foi realizada investigação experimental pré-clínica com 14 anéis aórticos obtidos de ratos Wistar. Os anéis foram colocados em banho de órgãos e pré-ativados com norepinefrina, em seguida, a tensão desenvolvida pela musculatura lisa vascular foi registrada após a adição de cânfora-clorofenol em diferentes intervalos de tempo. Resultados: 51,4% dos músculos lisos vasculares estavam relaxados pela ação do cânfora-clorofenol. A maior diminuição do tônus vascular ocorreu entre o terceiro e o quinto minuto após a adição do medicamento. Os testes de Wilcoxon das faixas com sinais mostraram diferenças significativas entre a tensão base inicial e a registrada nos diferentes intervalos de tempo estudados. Conclusões: O cânfora-clorofenol induz, in vitro, relaxamento da musculatura lisa arterial por meio de um acoplamento excitação-contração do tipo farmacomecânico, que aumenta em função do tempo.


Subject(s)
Animals , Rats , Chlorophenols/administration & dosage , Muscle, Smooth, Vascular/drug effects , Muscle Tonus/drug effects , Epidemiology, Experimental , Rats, Wistar , Germany
3.
Acta Physiologica Sinica ; (6): 160-174, 2021.
Article in Chinese | WPRIM | ID: wpr-878245

ABSTRACT

Vascular smooth muscle cell (vSMC) is the predominant cell type in the blood vessel wall and is constantly subjected to a complex extracellular microenvironment. Mechanical forces that are conveyed by changes in stiffness/elasticity, geometry and topology of the extracellular matrix have been indicated by experimental studies to affect the phenotype and function of vSMCs. vSMCs perceive the mechanical stimuli from matrix via specialized mechanosensors, translate these stimuli into biochemical signals controlling gene expression and activation, with the consequent modulation in controlling various aspects of SMC behaviors. Changes in vSMC behaviors may further cause disruption of vascular homeostasis and then lead to vascular remodeling. A better understanding of how SMC senses and transduces mechanical forces and how the extracellular mechano-microenvironments regulate SMC phenotype and function may contribute to the development of new therapeutics for vascular diseases.


Subject(s)
Biophysics , Cells, Cultured , Extracellular Matrix , Humans , Muscle, Smooth, Vascular , Myocytes, Smooth Muscle , Phenotype , Vascular Remodeling
4.
Acta Physiologica Sinica ; (6): 82-88, 2021.
Article in Chinese | WPRIM | ID: wpr-878238

ABSTRACT

The research on the molecular mechanism of vascular injury has been a hot topic in recent years since the mechanism can be targeted for the treatment of vascular injury diseases. A large number of studies have found that vascular injury, repair and pathological remodeling are closely related to phenotype switching, abnormal proliferation and migration, and apoptosis of vascular smooth muscle cells (VSMCs). Smooth muscle 22α (SM22α) is a shape change and transformation sensitive F-actin-binding protein. SM22α decorates the contractile filament bundles within cultured VSMCs exhibiting differentiated phenotypes. In addition, SM22α is involved in regulation of cell signaling pathways related to vascular homeostasis and vascular remodeling. Here, we reviewed the recent research progress of SM22α in vascular homeostasis and remodeling.


Subject(s)
Cell Proliferation , Cells, Cultured , Homeostasis , Humans , Muscle Proteins , Muscle, Smooth, Vascular , Myocytes, Smooth Muscle , Phenotype , Vascular Remodeling
5.
Arq. bras. cardiol ; 115(4): 630-636, out. 2020. graf
Article in Portuguese | LILACS, SES-SP | ID: biblio-1131353

ABSTRACT

Resumo Fundamento: A taxa de falha de enxerto de veia safena um ano após a cirurgia de revascularização do miocárdio varia de 10% a 25%. O objetivo deste estudo foi de investigar se a atorvastatina pode reduzir o acúmulo de células musculares lisas vasculares para inibir a hiperplasia intimal por meio da inibição da via p38 MAPK. Métodos: Quarenta e cinco ratos Sprague-Dawley foram randomizados em três grupos. Trinta ratos foram submetidos à cirurgia de enxerto de veia e randomizados para tratamento com veículo ou atorvastatina; quinze ratos foram submetidos à cirurgia sham. Detectamos a hiperplasia intimal por meio de coloração com hematoxilina-eosina e a expressão de proteínas relacionadas por meio de análise imuno-histoquímica e Western blot. Foram realizadas as comparações por análise de variância de fator único e pelo teste da diferença mínima significativa de Fisher, com p < 0,05 considerado significativo. Resultados: A íntima analisada pela coloração com hematoxilina-eosina era dramaticamente mais espessa no grupo controle que no grupo atorvastatina e no grupo sham (p < 0,01). Os resultados da coloração imuno-histoquímica de α-SMA demonstraram que a porcentagem de células positivas para α-SMA no grupo controle era mais alta que no grupo atorvastatina (p < 0,01). Nós também avaliamos α-SMA, PCNA, p38 MAPK e fosforilação de p38 MAPK após o tratamento com estatina por meio de análise de Western blot e os resultados indicaram que a atorvastatina não levou à redução de p38 MAPK (p < 0,05); no entanto, resultou na inibição da fosforilação de p38 MAPK (p < 0,01) e reduziu significativamente os níveis de α-SMA e PCNA, em comparação com o grupo controle (p < 0,01). Conclusão: Nós demonstramos que a atorvastatina pode inibir o acúmulo de células musculares lisas vasculares por meio da inibição da via p38 MAPK e é capaz de inibir a hiperplasia intimal em modelos de enxerto de veia em ratos.


Abstract Background: The rate of saphenous vein graft failure one year after coronary artery bypass grafting ranges from 10% to 25%. The aim of this study was to explore whether atorvastatin can reduce accumulation of vascular smooth muscle cells to inhibit intimal hyperplasia via p38 MAPK pathway inhibition. Methods: Forty-five Sprague-Dawley rats were randomized to three groups. Thirty rats received a vein graft operation, and they were randomized to be treated with vehicle or atorvastatin; fifteen rats received a sham operation. We detected intimal hyperplasia by hematoxylin-eosin staining and related protein expression by immunohistochemical and Western blot analysis. Comparisons were analyzed by single-factor analysis of variance and Fisher's least significant difference test, with p < 0.05 considered significant. Results: The intima analyzed by hematoxylin-eosin staining was dramatically thicker in the control group than in the atorvastatin group and sham group (p < 0.01). The outcomes of immunohistochemical staining of α-SMA demonstrated that the percentage of α-SMA-positive cells in the control group was higher than in the atorvastatin group (p < 0.01). We also evaluated α-SMA, PCNA, p38 MAPK, and phosphorylation of p38 MAPK after statin treatment by Western blot analysis, and the results indicated that atorvastatin did not lead to p38 MAPK reduction (p < 0.05); it did, however, result in inhibition of p38 MAPK phosphorylation (p < 0.01), and it significantly reduced α-SMA and PCNA levels, in comparison with the control group (p < 0.01). Conclusion: We have demonstrated that atorvastatin can inhibit accumulation of vascular smooth muscle cells by inhibiting the p38 MAPK pathway, and it is capable of inhibiting intimal hyperplasia in a rat vein graft model.


Subject(s)
Animals , Rats , Transplants , p38 Mitogen-Activated Protein Kinases , Veins , Rats, Sprague-Dawley , Atorvastatin/therapeutic use , Atorvastatin/pharmacology , Hyperplasia/prevention & control , Hyperplasia/drug therapy , Muscle, Smooth, Vascular
7.
Article in English | WPRIM | ID: wpr-786077

ABSTRACT

Vascular smooth muscle cells (VSMCs) play a pivotal role in the stability and tonic regulation of vascular homeostasis. VSMCs can switch back and forth between highly proliferative (synthetic) and fully differentiated (contractile) phenotypes in response to changes in the vessel environment. Abnormal phenotypic switching of VSMCs is a distinctive characteristic of vascular disorders, including atherosclerosis, pulmonary hypertension, stroke, and peripheral artery disease; however, how the control of VSMC phenotypic switching is dysregulated under pathological conditions remains obscure. Canonical transient receptor potential (TRPC) channels have attracted attention as a key regulator of pathological phenotype switching in VSMCs. Several TRPC subfamily member proteins—especially TRPC1 and TRPC6—are upregulated in pathological VSMCs, and pharmacological inhibition of TRPC channel activity has been reported to improve hypertensive vascular remodeling in rodents. This review summarizes the current understanding of the role of TRPC channels in cardiovascular plasticity, including our recent finding that TRPC6 participates in aberrant VSMC phenotype switching under ischemic conditions, and discusses the therapeutic potential of TRPC channels.


Subject(s)
Atherosclerosis , Cell Plasticity , Homeostasis , Hypertension, Pulmonary , Muscle, Smooth, Vascular , Peripheral Arterial Disease , Phenotype , Plastics , Rodentia , Stroke , Transient Receptor Potential Channels , Vascular Remodeling
8.
Article in English | WPRIM | ID: wpr-787137

ABSTRACT

Aging is one of the risk factors for the development of cardiovascular diseases. During the progression of cellular senescence, cells enter a state of irreversible growth arrest and display resistance to apoptosis. As a flavonoid, quercetin induces apoptosis in various cells. Accordingly, we investigated the relationship between quercetin-induced apoptosis and the inhibition of cellular senescence, and determined the mechanism of oxidative stress-induced vascular smooth muscle cell (VSMC) senescence. In cultured VSMCs, hydrogen peroxide (H₂O₂) dose-dependently induced senescence, which was associated with increased numbers of senescence-associated β-galactosidase-positive cells, decreased expression of SMP30, and activation of p53-p21 and p16 pathways. Along with senescence, expression of the anti-apoptotic protein Bcl-2 was observed to increase and the levels of proteins related to the apoptosis pathway were observed to decrease. Quercetin induced apoptosis through the activation of AMP-activated protein kinase. This action led to the alleviation of oxidative stress-induced VSMC senescence. Furthermore, the inhibition of AMPK activation with compound C and siRNA inhibited apoptosis and aggravated VSMC senescence by reversing p53-p21 and p16 pathways. These results suggest that senescent VSMCs are resistant to apoptosis and quercetin-induced apoptosis attenuated the oxidative stress-induced senescence through activation of AMPK. Therefore, induction of apoptosis by polyphenols such as quercetin may be worthy of attention for its anti-aging effects.


Subject(s)
Aging , AMP-Activated Protein Kinases , Apoptosis , Cardiovascular Diseases , Cellular Senescence , Hydrogen Peroxide , Muscle, Smooth, Vascular , Polyphenols , Quercetin , Risk Factors , RNA, Small Interfering
9.
Article in English | WPRIM | ID: wpr-787133

ABSTRACT

In vascular smooth muscle, K⁺ channels, such as voltage-gated K⁺ channels (Kv), inward-rectifier K⁺ channels (Kir), and big-conductance Ca²⁺-activated K⁺ channels (BK(Ca)), establish a hyperpolarized membrane potential and counterbalance the depolarizing vasoactive stimuli. Additionally, Kir mediates endothelium-dependent hyperpolarization and the active hyperemia response in various vessels, including the coronary artery. Pulmonary arterial hypertension (PAH) induces right ventricular hypertrophy (RVH), thereby elevating the risk of ischemia and right heart failure. Here, using the whole-cell patch-clamp technique, we compared Kv and Kir current densities (I(Kv) and I(Kir)) in the left (LCSMCs), right (RCSMCs), and septal branches of coronary smooth muscle cells (SCSMCs) from control and monocrotaline (MCT)-induced PAH rats exhibiting RVH. In control rats, (1) I(Kv) was larger in RCSMCs than that in SCSMCs and LCSMCs, (2) I(Kv) inactivation occurred at more negative voltages in SCSMCs than those in RCSMCs and LCSMCs, (3) I(Kir) was smaller in SCSMCs than that in RCSMCs and LCSMCs, and (4) I(BKCa) did not differ between branches. Moreover, in PAH rats, I(Kir) and I(Kv) decreased in SCSMCs, but not in RCSMCs or LCSMCs, and I(BKCa) did not change in any of the branches. These results demonstrated that SCSMC-specific decreases in I(Kv) and I(Kir) occur in an MCT-induced PAH model, thereby offering insights into the potential pathophysiological implications of coronary blood flow regulation in right heart disease. Furthermore, the relatively smaller I(Kir) in SCSMCs suggested a less effective vasodilatory response in the septal region to the moderate increase in extracellular K⁺ concentration under increased activity of the myocardium.


Subject(s)
Animals , Coronary Vessels , Heart Diseases , Heart Failure , Hyperemia , Hypertension , Hypertrophy, Right Ventricular , Ischemia , Membrane Potentials , Monocrotaline , Muscle, Smooth , Muscle, Smooth, Vascular , Myocardium , Myocytes, Smooth Muscle , Patch-Clamp Techniques , Potassium Channels , Rats , Septum of Brain
10.
Braz. j. med. biol. res ; 53(3): e8853, 2020. tab, graf
Article in English | LILACS | ID: biblio-1089343

ABSTRACT

Anaphylactic shock can be defined as an acute syndrome, and it is the most severe clinical manifestation of allergic diseases. Anaphylactoid reactions are similar to anaphylactic events but differ in the pathophysiological mechanism. Nitric oxide (NO) inhibitors during anaphylaxis suggest that NO might decrease the signs and symptoms of anaphylaxis but exacerbate associated vasodilation. Therefore, blocking the effects of NO on vascular smooth muscle by inhibiting the guanylate cyclase (GC) would be a reasonable strategy. This study aimed to investigate the effects of NO/cGMP pathway inhibitors methylene blue (MB), Nω-nitro-L-arginine methyl ester hydrochloride (L-NAME), and indigo carmine (IC) in shock induced by compound 48/80 (C48/80) in rats. The effect was assessed by invasive blood pressure measurement. Shock was initiated by C48/80 intravenous bolus injection 5 min before (prophylactic) or after (treatment) the administration of the inhibitors MB (3 mg/kg), L-NAME (1 mg/kg), and IC (3 mg/kg). Of the groups that received drugs as prophylaxis for shock, only the IC group did not present the final systolic blood pressure (SBP) better than the C48/80 group. Regarding shock treatment with the drugs tested, all groups had the final SBP similar to the C48/80group. Altogether, our results suggested that inhibition of GC and NO synthase in NO production pathway was not sufficient to revert hypotension or significantly improve survival.


Subject(s)
Animals , Male , Rats , Cyclic GMP/antagonists & inhibitors , Enzyme Inhibitors/administration & dosage , Anaphylaxis/drug therapy , Muscle, Smooth, Vascular/drug effects , Nitric Oxide/antagonists & inhibitors , Rats, Wistar , NG-Nitroarginine Methyl Ester/administration & dosage , Disease Models, Animal , Indigo Carmine/administration & dosage , Methylene Blue/administration & dosage
11.
Biol. Res ; 53: 44, 2020. graf
Article in English | LILACS | ID: biblio-1131888

ABSTRACT

BACKGROUND: Atherosclerosis (AS) is the main pathological basis of coronary heart disease, cerebral infarction and peripheral vascular disease, which seriously endanger people's life and health. In recent years, long non-coding RNA (lncRNA) has been found to be involved in gene expression regulation, but the research on AS is still in the initial stage. In this study, we mainly studied the role of HCG11 in patients with AS. Quantitative Real-time Polymerase Chain Reaction (QRT-PCR) was used to detect the expression of HCG11 and miR-144 in the serum of AS patients and healthy volunteers. Oxidation Low Lipoprotein (Ox-LDL), interleukin-6 (IL-6) and tumor necrosis factor α (TNF α) radiation were used to establish human vascular smooth muscle cells (VSMCs) in vitro model. Cell proliferation was determined by Cell Counting Kit-8 (CCK-8) assay. The apoptosis rate was determined by flow cytometry (FACS) and terminal deoxynucleotidyl transferase-mediated dUTP-biotin nick end labeling assay (TUNEL) staining. The expression levels of Forkhead box protein F1 (FOXF1), B cell lymphoma-2 (Bcl-2) and BCL2-Associated X (Bax) were detected by qRT-PCR. Luciferase gene reporter and RNA pull down experiments confirmed the relationship between HCG11 and miR-144, miR-144 and FOXF1. RESULTS: This study showed that HCG11 was significantly upregulated in patients with AS, while miR-144 was down-regulated in patients with AS. Ox-LDL and IL-6 in VSMCs induced up-regulation of HCG11 and down-regulation of miR-144. Overexpression of HCG11 promoted the proliferation and inhibited apoptosis of VSMCs. Luciferase gene reporter gene assay showed that HCG11 could bind to miR-144, and miR-144 could bind to FOXF1. Overexpression of miR-144 reversed the effect of HCG11 on VSMCs. CONCLUSIONS: LncRNA HCG11 regulates proliferation and apoptosis of vascular smooth muscle cell through targeting miR-144-3p/FOXF1 axis.


Subject(s)
Humans , Myocytes, Smooth Muscle/cytology , MicroRNAs/genetics , Atherosclerosis/genetics , Forkhead Transcription Factors/genetics , RNA, Long Noncoding/genetics , Apoptosis/genetics , Cell Proliferation/genetics , Muscle, Smooth, Vascular/cytology
12.
Article in Chinese | WPRIM | ID: wpr-828100

ABSTRACT

OBJECTIVE@#To explore the effects of olmesartan on age-associated migration and invasion capacities and microRNA (miRAN) axis in human aortic vascular smooth muscle cells (HA-VSMCs).@*METHODS@#Cultured HA-VSMCs were divided into control group, bleomycin-mediated senescence (BLM) group and bleomycin + olmesartan treatment group. Wound-healing assay and Boyden chambers invasion assay were used to assess the changes in migration and invasion of the cells, gelatin zymography was used to analyze matrix metalloproteinase-2 (MMP-2) activation in the cells. The differentially expressed miRNAs were identified by miRNA microarray assay and validated by quantitative real-time PCR. MiR-3133 inhibitor was used to examine the effects of molecular manipulation of olmesartan on age-associated migration and invasion and MMP-2 activation in the cells.@*RESULTS@#Compared with those of the control group, the percentage of the repopulated cells and the number of cells crossing the basement membrane increased significantly in BLM group [(78.43±12.76)% (42.47±7.22)%, < 0.05; 33.33±5.51 13.00±4.36, < 0.05]. A significant increase of MMP-2 activation was found in BLM group as compared with the control group (1.66 ± 0.27 0.87 ± 0.13, < 0.05). Olmesartan significantly inhibited BLM-induced enhancement of cell migration and invasion and MMP-2 secretion in the cells. MiR-3133 was significantly downregulated in BLM group and upregulated in olmesartan group. Transfection with miR-3133 inhibitor significantly reversed the effects of olmesartan on age-associated migration and invasion of the cells [(85.87±7.39)% (49.77±3.05)%; 34.67±2.31 20.00±4.58, < 0.05] and MMP-2 activation in the cells (1.76±0.19 0.94±0.10, < 0.05).@*CONCLUSIONS@#Olmesartan inhibits the migration and invasion of ageassociated HA-VSMCs probably by upregulating of the miR-3133 axis.


Subject(s)
Cell Movement , Cell Proliferation , Cells, Cultured , Humans , Imidazoles , Matrix Metalloproteinase 2 , MicroRNAs , Genetics , Muscle, Smooth, Vascular , Myocytes, Smooth Muscle , Tetrazoles
13.
Article in Chinese | WPRIM | ID: wpr-878683

ABSTRACT

Kidney is one of the important organs of the body.With both excretory and endocrine functions,it plays a vital role in regulating the normal physiological state.As a precursor of the nitric oxide(NO)synthesis


Subject(s)
Animals , Arginine/physiology , Kidney/physiology , Muscle, Smooth, Vascular , Nitric Oxide/physiology , Rats , Receptors, Adrenergic, alpha-1/physiology , Renal Insufficiency/physiopathology , Signal Transduction , Vasoconstriction
14.
Rev. bras. cir. cardiovasc ; 34(3): 290-296, Jun. 2019. tab, graf
Article in English | LILACS | ID: biblio-1013469

ABSTRACT

Abstract Objective: In this study, we aimed to examine the effects of amitriptyline, fluoxetine, tranylcypromine and venlafaxine on saphenous vein grafts in coronary artery bypass graft surgeries. Methods: 59 patients (40 males and 19 females; mean age 65.1 years, distribution: 45-84 years) who had coronary artery bypass graft surgery between February 2014 and May 2016 were included in the study. After the saphenous vein grafts with intact and denuded endothelium were precontracted with 3×10-6M phenylephrine, amitriptyline, fluoxetine and tranylcypromine were cumulatively added to isolated organ baths in the range of 10-11-3x10-5M, while venlafaxine was added in the range of 10-9-3×10-5M. Then, the antidepressant-induced relaxation responses were recorded isometrically. Results: While the relaxation response of amitriptyline at -6.42 (Log M) was 74.6%, the response at -6.32 (Log M) was 75.5%. While the relaxation response at -6.46 (Log M) of fluoxetine was 68.02%, the response at -6.02 (Log M) was 72.12%. While the relaxation response of tranylcypromine at -7.53 (Log M) was 61.13%, the response at -7.23 (Log M) was 65.53%. While the relaxation response of venlafaxine at -6.21 (Log M) was 29.98%, the response at -5.90 (Log M) was 32.96%. Conclusion: The maximum relaxation at minimum and maximum therapeutic concentrations was obtained with amitriptyline, fluoxetine and tranylcypromine, and the minimum relaxation was obtained with venlafaxine. The relaxation responses were independent of the endothelium.


Subject(s)
Humans , Male , Female , Middle Aged , Aged , Aged, 80 and over , Saphenous Vein/drug effects , Saphenous Vein/transplantation , Tranylcypromine/pharmacology , Fluoxetine/pharmacology , Amitriptyline/pharmacology , Antidepressive Agents/pharmacology , Reference Values , Vasodilation/drug effects , Endothelium, Vascular/drug effects , Coronary Artery Bypass/methods , Analysis of Variance , Transplants/drug effects , Venlafaxine Hydrochloride/pharmacology , Muscle, Smooth, Vascular/drug effects
16.
Chinese Journal of Biotechnology ; (12): 290-297, 2019.
Article in Chinese | WPRIM | ID: wpr-771377

ABSTRACT

To investigate the effect of 27nt-miRNA on the differentiation of mesenchymal stem cells into vascular smooth muscle cells. The highly expression plasmids of 27nt-miRNA and anti-27nt-miRNA, and negative control plasmids were constructed, packaged with lentivirus and transfected into human umbilical cord mesenchymal stem cells (hUCMSCs). Collagen IV was added to induce hUCMSCs differentiation into blood vessel smooth muscle cells (VSMCs). The cell viability was measured by MTT assay. The expression of SMA, SM22α at mRNA and protein levels was determined by RT-PCR, immunocytochemical staining and Western blotting. Compared with the negative control group, the viability of the 27nt-miRNA overexpression group was decreased by 20.48% (P<0.05), and the expression of SMA mRNA and SM22α mRNA and protein was significantly increased (P<0.05); the viability of Anti-27nt-miRNA group was increased 18.07% (P<0.05), and the expression of SMA mRNA and SM22α mRNA and protein was decreased (P<0.05). In summary, 27nt-miRNA promotes mesenchymal stem cells differentiation into vascular smooth muscle cells and inhibits cells viability.


Subject(s)
Cell Differentiation , Cells, Cultured , Humans , Mesenchymal Stem Cells , MicroRNAs , Muscle, Smooth, Vascular , Myocytes, Smooth Muscle
17.
Article in English | WPRIM | ID: wpr-760618

ABSTRACT

BACKGROUND/OBJECTIVES: Vascular inflammation is an important feature in the atherosclerotic process. Recent studies report that leaves and branches of Carpinus turczaninowii (C. turczaninowii) have antioxidant capacity and exert anti-inflammatory effects. However, no study has reported the regulatory effect of C. turczaninowii extract on the arterial inflammatory response. This study therefore investigated modulation of the arterial inflammatory response after exposure to C. turczaninowii extract, using human aortic vascular smooth muscle cells (HAoSMCs). MATERIALS/METHODS: Scavenging activity of free radicals, total phenolic content (TPC), cell viability, mRNA expressions, and secreted levels of cytokines were measured in LPS-stimulated (10 ng/mL) HAoSMCs treated with the C. turczaninowii extract. RESULTS: C. turczaninowii extract contains high amounts of TPC (225.6 ± 21.0 mg of gallic acid equivalents/g of the extract), as well as exerts time-and dose-dependent increases in strongly scavenged free radicals (average 14.8 ± 1.97 µg/mL IC50 at 40 min). Cell viabilities after exposure to the extracts (1 and 10 µg/mL) were similar to the viability of non-treated cells. Cytokine mRNA expressions were significantly suppressed by the extracts (1 and 10 µg/mL) at 6 hours (h) after exposure. Interleukin-6 secretion was dose-dependently suppressed 2 h after incubation with the extract, at 1–10 µg/mL in non-stimulated cells, and at 5 and 10 µg/mL in LPS-stimulated cells. Similar patterns were also observed at 24 h after incubation with the extract (at 1–10 µg/mL in non-stimulated cells, and at 10 µg/mL in the LPS-stimulated cells). Soluble intracellular vascular adhesion molecules (sICAM-1) secreted from non-stimulated cells and LPS-stimulated cells were similarly suppressed in a dose-dependent manner after 24 h exposure to the extracts, but not after 2 h. In addition, sICAM-1 concentration after 24 h treatment was positively related to IL-6 levels after 2 h and 24 h exposure (r = 0.418, P = 0.003, and r = 0.524, P < 0.001, respectively). CONCLUSIONS: This study demonstrates that C. turczaninowii modulates the arterial inflammatory response, and indicates the potential to be applied as a therapeutic use for atherosclerosis.


Subject(s)
Antioxidants , Arteries , Atherosclerosis , Betulaceae , Cell Survival , Cytokines , Free Radicals , Gallic Acid , Humans , Inflammation , Inhibitory Concentration 50 , Interleukin-6 , Muscle, Smooth, Vascular , Phenol , RNA, Messenger
18.
Korean Journal of Medicine ; : 159-169, 2019.
Article in Korean | WPRIM | ID: wpr-759926

ABSTRACT

Cardiovascular morbidity and mortality are very common in patients with chronic kidney disease, which may result in part from vascular calcification. Vascular calcification requires osteoblastic trans-differentiation of vascular smooth muscle cells through an active and highly regulated process that is morphologically and functionally similar to bone formation in a number of ways. Multiple studies have been published on this topic, but the precise mechanism of vascular calcification remains unclear. This review presents recent insights into the mechanism of vascular calcification, as well as therapies that modulate mineral metabolism.


Subject(s)
Humans , Metabolism , Miners , Mortality , Muscle, Smooth, Vascular , Osteoblasts , Osteogenesis , Renal Insufficiency, Chronic , Vascular Calcification
19.
Korean Circulation Journal ; : 615-626, 2019.
Article in English | WPRIM | ID: wpr-759447

ABSTRACT

BACKGROUND AND OBJECTIVES: Angiotensin II (Ang II) has been suggested to accelerate vascular senescence, however the molecular mechanism(s) remain unknown. METHODS: We cultured human coronary artery smooth muscle cells (hCSMCs) and treated Ang II and/or fimasartan. Or we transfected adenoviral vectors expressing CYR61 (Ad-CYR61) or antisense CYR61 (Ad-As-CYR61). Cellular senescence was evaluated senescence-associated β-galactosidase (SA-β-gal) assay. The molecular mechanisms were investigated real-time PCR and western blots. RESULTS: SA-β-gal-positive cells significantly increased in Ang II-treated hCSMCs (5.77±1.43-fold compared with the control). The effect of Ang II was significantly attenuated by pretreatment with the Ang II type 1 receptor blocker, fimasartan (2.00±0.92-fold). The expression of both p53 and p16 senescence regulators was significantly increased by Ang II (p53: 1.39±0.17, p16: 1.19±0.10-fold vs. the control), and inhibited by fimasartan. Cysteine-rich angiogenic protein 61 (CYR61) was rapidly induced by Ang II. Compared with the control, Ad-CYR61-transfected hCSMCs showed significantly increased SA-β-gal-positive cells (3.47±0.65-fold). Upon transfecting Ad-AS-CYR61, Ang II-induced senescence (3.74±0.23-fold) was significantly decreased (1.77±0.60-fold). p53 expression by Ang II was significantly attenuated by Ad-AS-CYR61, whereas p16 expression was not regulated. Ang II activated ERK1/2 and p38 MAPK, which was significantly blocked by fimasartan. ERK and p38 inhibition both regulated Ang II-induced CYR61 expression. However, p53 expression was only regulated by ERK1/2, whereas p16 expression was only attenuated by p38 MAPK. CONCLUSIONS: Ang II induced vascular senescence by the ERK/p38 MAPK–CYR61 pathway and ARB, fimasartan, protected against Ang II-induced vascular senescence.


Subject(s)
Aging , Angiotensin II Type 1 Receptor Blockers , Angiotensin II , Angiotensins , Blotting, Western , Cellular Senescence , Coronary Vessels , Humans , Muscle, Smooth, Vascular , Myocytes, Smooth Muscle , p38 Mitogen-Activated Protein Kinases , Real-Time Polymerase Chain Reaction , Receptor, Angiotensin, Type 1
20.
Article in Korean | WPRIM | ID: wpr-764032

ABSTRACT

Periodontal diseases have been associated with the development of cardiovascular diseases. Accumulating evidences have indicated that Porphyromonas gingivalis, a major periodontopathic pathogen, plays a critical role in the pathogenesis of atherosclerosis. In the present study, we demonstrated that P. gingivalis lipopolysaccharide (LPS) increases the mRNA and protein expression of matrix metalloproteinase-9 (MMP-9) in rat vascular smooth muscle cells. We showed that the MMP-9 expression induced by P. gingivalis LPS is mediated by the activation of signal transducer and activator of transcription 3 (STAT3) in vascular smooth muscle cells. Furthermore, the inhibition of STAT3 activity reduced P. gingivalis LPS-induced migration of vascular smooth muscle cells. Overall, our findings indicate that P. gingivalis LPS stimulates the migration of vascular smooth muscle cells via STAT3-mediated MMP-9 expression.


Subject(s)
Animals , Atherosclerosis , Cardiovascular Diseases , Cell Movement , Matrix Metalloproteinase 9 , Muscle, Smooth, Vascular , Periodontal Diseases , Porphyromonas gingivalis , Porphyromonas , Rats , RNA, Messenger , STAT3 Transcription Factor , Transducers
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