Change in vascular smooth muscle response to 5-HT due to short- or long-term endothelial denudation of the bovine digital vein

Intimal formation of animal carotid arteries induced by balloon endothelial denudation has been considered to be an "accelerated atherosclerosis" model and used in primary screening methods to evaluate natural drugs and chemical candidates. The aim of the present study was to examine whether intimal formation is prevented by Bezoar Bovis (dried cattle gallbladder stones: Niuhuang in Chinese and Go-o in Japanese), which has been used to prevent heart palpitation in patients with hypertension. The intimal-to-medial area ratio in rat carotid arteries 7 days after balloon endothelial denudation was significantly reduced by oral administration of Bezoar Bovis. Bezoar Bovis also suppressed vascular smooth muscle cells (VSMCs) proliferation, which is thought to play important roles in the intimal formation after endothelial damage and also atherosclerosis resulting from long-term inappropriate lifestyle. The present findings suggest that Bezoar Bovis may be useful for preventing atherosclerosis and for protection against restenosis after percutaneous coronary intervention, for which effective reduction method is not currently available.

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Stromal cells from human long-term marrow cultures are mesenchymal cells that differentiate following a vascular smooth muscle differentiation pathway

Blood ◽

10.1182/blood.v82.1.66.bloodjournal82166 ◽

1993 ◽

Vol 82 (1) ◽

pp. 66-76 ◽

Cited By ~ 261

Author(s):

MC Galmiche ◽

VE Koteliansky ◽

J Briere ◽

P Herve ◽

P Charbord

Keyword(s):

Smooth Muscle ◽

Vascular Smooth Muscle ◽

Smooth Muscle Cells ◽

Stromal Cells ◽

Muscle Cells ◽

Mesenchymal Cells ◽

Myoid Cells ◽

Marrow Cultures

In human long-term marrow cultures connective tissue-forming stromal cells are an essential cellular component of the adherent layer where granulomonocytic progenitors are generated from week 2 onward. We have previously found that most stromal cells in confluent cultures were stained by monoclonal antibodies directed against smooth muscle- specific actin isoforms. The present study was carried out to evaluate the time course of alpha-SM-positive stromal cells and to search for other cytoskeletal proteins specific for smooth muscle cells. It was found that the expression of alpha-SM in stromal cells was time dependent. Most of the adherent spindle-shaped, vimentin-positive stromal cells observed during the first 2 weeks of culture were alpha- SM negative. On the contrary, from week 3 to week 7, most interdigitated stromal cells contained stress fibers whose backbone was made of alpha-SM-positive microfilaments. In addition, in confluent cultures, other proteins specific for smooth muscle were detected: metavinculin, h-caldesmon, smooth muscle myosin heavy chains, and calponin. This study confirms the similarity between stromal cells and smooth muscle cells. Moreover, our results reveal that cells in vivo with the phenotype closest to that of stromal cells are immature fetal smooth muscle cells and subendothelial intimal smooth muscle cells; a cell subset with limited development following birth but extensively recruited in atherosclerotic lesions. Stromal cells very probably derive from mesenchymal cells that differentiate along this distinctive vascular smooth muscle cell pathway. In humans, this differentiation seems crucial for the maintenance of granulomonopoiesis. These in vitro studies were completed by examination of trephine bone marrow biopsies from adults without hematologic abnormalities. These studies revealed the presence of alpha-SM-positive cells at diverse locations: vascular smooth muscle cells in the media of arteries and arterioles, pericytes lining capillaries, myoid cells lining sinuses at the abluminal side of endothelial cells or found within the hematopoietic logettes, and endosteal cells lining bone trabeculae. More or less mature cells of the granulocytic series were in intimate contact with the thin cytoplasmic extensions of myoid cells. Myoid cells may be the in vivo counterpart of stromal cells with the above-described vascular smooth muscle phenotype.

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NF-κB pathway mediates vascular smooth muscle response to nicotine

The International Journal of Biochemistry & Cell Biology ◽

10.1016/j.biocel.2012.10.016 ◽

2013 ◽

Vol 45 (2) ◽

pp. 375-383 ◽

Cited By ~ 7

Author(s):

Zhaoxia Wang ◽

Weidong Wu ◽

Maoping Tang ◽

Ying Zhou ◽

Lianyun Wang ◽

...

Keyword(s):

Smooth Muscle ◽

Vascular Smooth Muscle ◽

Muscle Response

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Abstract 641: Expression Of GLUT4 In Vascular Smooth Muscle Affects Endothelial Function In Hypertension.

Hypertension ◽

10.1161/hyp.62.suppl_1.a641 ◽

2013 ◽

Vol 62 (suppl_1) ◽

Author(s):

Kevin B Atkins ◽

Jharna Saha ◽

Frank C Brosius

Keyword(s):

Smooth Muscle ◽

Vascular Smooth Muscle ◽

Kinase Inhibitor ◽

Rho Kinase ◽

Interesting Phenomenon ◽

Glut4 Expression ◽

Endothelial Denudation ◽

Rho Kinase Inhibitor ◽

Total Body ◽

Rats And Mice

Expression of GLUT4 is decreased in arterial smooth muscle of hypertensive rats and mice, and total body overexpression of GLUT4 in mice prevents enhanced arterial reactivity. To demonstrate that the effect on vascular response to GLUT4 overexpression is vascular rather than systemic in origin we utilized smooth muscle-specific GLUT4 transgenic mice (SMG4). GLUT4 expression in aortae of SMG4 compared to WT mice was increased 2-3 fold. Adult wild-type (WT) and SMG4 mice were made hypertensive or not through implantation of angiotensin II (AngII; 1.4mg/kg/d for 2 wks) or vehicle containing osmotic mini-pumps. Both WT and SMG4 mice AngII-treated mice exhibited significantly increased systolic blood pressure. In AngII-treated WT mice (WT-AngII) aortic GLUT4 expression was significantly decreased, whereas GLUT4 expression in aortae of AngII-treated SMG4 mice (SMG4-AngII) was maintained. The phosphorylation of ERM and MYPT1(Thr850) were significantly increased in aortae of WT-AngII compared to WT-Sham and SMG4-AngII mice. Responsiveness to the contractile agonists, phenylephrine, 5-HT, and PGF 2 was significantly increased in endothelium-intact aortic rings from WT-AngII mice, but remained normal in aortae of SMG4-AngII mice. Following pretreatment with Rho-kinase inhibitor Y-27632, relative inhibition of contractility to 5-HT was equal in aortae from WT-AngII and SMG4-AngII-treated mice. With endothelial denudation, contractility to 5-HT was equally enhanced in aortae of WT-AngII and SMG4-AngII-treated mice. Interestingly, whereas acetylcholine stimulated relaxation was significantly decreased in aortic rings of WT-AngII mice, relaxation in rings from SMG4-AngII mice was not significantly different from WT or SMG4. These results demonstrate an interesting phenomenon whereby decreased expression of GLUT4 in vascular smooth muscle leads to an endothelial dysfunction that not only impairs relaxation, but also enhances contractility.

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Metformin decreases hyaluronan synthesis by vascular smooth muscle cells

Journal of Investigative Medicine ◽

10.1136/jim-2019-001156 ◽

2019 ◽

Vol 68 (2) ◽

pp. 383-391 ◽

Cited By ~ 3

Author(s):

Annele Sainio ◽

Piia Takabe ◽

Sanna Oikari ◽

Henriikka Salomäki-Myftari ◽

Markku Koulu ◽

...

Keyword(s):

Smooth Muscle ◽

Vascular Smooth Muscle ◽

Smooth Muscle Cells ◽

Vascular Smooth Muscle Cells ◽

Muscle Cells ◽

Response To Treatment ◽

Long Term Effects

Metformin is the first-line drug in the treatment of type 2 diabetes worldwide based on its effectiveness and cardiovascular safety. Currently metformin is increasingly used during pregnancy in women with gestational diabetes mellitus, even if the long-term effects of metformin on offspring are not exactly known. We have previously shown that high glucose concentration increases hyaluronan (HA) production of cultured human vascular smooth muscle cells (VSMC) via stimulating the expression of hyaluronan synthase 2 (HAS2). This offers a potential mechanism whereby hyperglycemia leads to vascular macroangiopathy. In this study, we examined whether gestational metformin use affects HA content in the aortic wall of mouse offspring in vivo. We also examined the effect of metformin on HA synthesis by cultured human VSMCs in vitro. We found that gestational metformin use significantly decreased HA content in the intima-media of mouse offspring aortas. In accordance with this, the synthesis of HA by VSMCs was also significantly decreased in response to treatment with metformin. This decrease in HA synthesis was shown to be due to the reduction of both the expression of HAS2 and the amount of HAS substrates, particularly UDP-N-acetylglucosamine. As shown here, gestational metformin use is capable to program reduced HA content in the vascular wall of the offspring strongly supporting the idea, that metformin possesses long-term vasculoprotective effects.

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Endothelin-a receptors mediate vascular smooth-muscle response to moderate acidosis in the canine tibial nutrient artery

Journal of Orthopaedic Research® ◽

10.1002/jor.1100140520 ◽

1996 ◽

Vol 14 (5) ◽

pp. 818-822 ◽

Cited By ~ 2

Author(s):

Bruno C. Coessens ◽

Virginia M. Miller ◽

Michael B. Wood

Keyword(s):

Smooth Muscle ◽

Vascular Smooth Muscle ◽

Muscle Response ◽

Nutrient Artery ◽

Endothelin A

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Vascular smooth muscle response to ouabain. Relation of tissue Na+ to the contractile response.

Circulation Research ◽

10.1161/01.res.73.6.1113 ◽

1993 ◽

Vol 73 (6) ◽

pp. 1113-1120 ◽

Cited By ~ 10

Author(s):

L Stewart ◽

C Hamilton ◽

J Ingwall ◽

S Naomi ◽

S Graves ◽

...

Keyword(s):

Smooth Muscle ◽

Vascular Smooth Muscle ◽

Contractile Response ◽

Muscle Response

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Biomechanical strain induces elastin and collagen production in human pluripotent stem cell-derived vascular smooth muscle cells

AJP Cell Physiology ◽

10.1152/ajpcell.00366.2014 ◽

2015 ◽

Vol 309 (4) ◽

pp. C271-C281 ◽

Cited By ~ 42

Author(s):

Maureen Wanjare ◽

Nayan Agarwal ◽

Sharon Gerecht

Keyword(s):

Gene Expression ◽

Smooth Muscle ◽

Vascular Smooth Muscle ◽

Tensile Strain ◽

Collagen Type ◽

Uniaxial Strain ◽

Collagen Type Iii ◽

Elastin Gene ◽

Biomechanical Strain

Blood vessels are subjected to numerous biomechanical forces that work harmoniously but, when unbalanced because of vascular smooth muscle cell (vSMC) dysfunction, can trigger a wide range of ailments such as cerebrovascular, peripheral artery, and coronary artery diseases. Human pluripotent stem cells (hPSCs) serve as useful therapeutic tools that may help provide insight on the effect that such biomechanical stimuli have on vSMC function and differentiation. In this study, we aimed to examine the effect of biomechanical strain on vSMCs derived from hPSCs. The effects of two types of tensile strain on hPSC-vSMC derivatives at different stages of differentiation were examined. The derivatives included smooth muscle-like cells (SMLCs), mature SMLCs, and contractile vSMCs. All vSMC derivatives aligned perpendicularly to the direction of cyclic uniaxial strain. Serum deprivation and short-term uniaxial strain had a synergistic effect in enhancing collagen type I, fibronectin, and elastin gene expression. Furthermore, long-term uniaxial strain deterred collagen type III gene expression, whereas long-term circumferential strain upregulated both collagen type III and elastin gene expression. Finally, long-term uniaxial strain downregulated extracellular matrix (ECM) expression in more mature vSMC derivatives while upregulating elastin in less mature vSMC derivatives. Overall, our findings suggest that in vitro application of both cyclic uniaxial and circumferential tensile strain on hPSC-vSMC derivatives induces cell alignment and affects ECM gene expression. Therefore, mechanical stimulation of hPSC-vSMC derivatives using tensile strain may be important in modulating the phenotype and thus the function of vSMCs in tissue-engineered vessels.

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