VSMCs cells

Chen and Huang examined the possible mechanisms underlying curcumin s antiproliferative and apoptotic effects using the rat VSMC cell line A7r5. Curcumin (1 to lOOpAT) inhibited serumstimulated pHJthymidine incorporation of both A7r5 cells and... 

Another example was done by Opitz et al. They utilized P4HB scaffolds to produce viable ovine blood vessels, and then implanted the blood vessels in the systemic circulation of sheep. Enzymatically derived vascular smooth muscle cells (vSMC) were seeded on the scaffolds both under pulsatile flow and static conditions. Mechanical properties of bioreactor-cultured blood vessels which were obtained from tissue engineering approached those of native aorta. 

MCP-1) VSMCs, and T cells and primates associated atherosclerotic plaques. 

Apo E, apolipoprotein E CAD, coronary artery disease FKN, fractalkine MHC, major histocompatibility complex MCP-1, monocyte chemoattractant protein 1 MMPs, matrix metalloproteinases NK, natural killer oxLDL, oxidized LDL RANTES, regulated on activation, normal T cell expressed and secreted VSMCs, vascular smooth muscle cells. 

Cultured rat vascular smooth muscle cells (VSMCs), grown and prepared for respirometry as described in Doeller et al., 2005 [41], were injected into the respirometer chamber to a concentration of between 105 and 106 cells ml 1. Cell viability remained at >90% throughout experiments. Near 4pM 02, H2S production was stimulated by the addition of L-cysteine and PLP (Fig. 8.8). The initial H2S production rate was approximately 20% of the rat aorta homogenate rate. H2S production rate decreased after the initial rise in H2S concentration, perhaps the result of product feedback inhibition. The addition of the CGL inhibitor BCA showed an effect similar to aorta homogenate. 

FIGURE 8.8 H2S production in vascular tissues. IPS production by aorta homogenate (upper panel), cultured rat vascular smooth muscle cells (VSMCs middle panel), and intact rat aorta occurs after the addition of substrate L-cysteine (L-cys) and cofactor pyridoxal L-phosphate (PLP) for the enzyme CGL located in vascular tissue. H2S production is inhibited after the CGL. 3 cyano-L-alanine (BCA) is added. Ferric Lucina pectinata hemoglobin I (metHb) is added to confirm H2S production. The quantity of metHb-sulfide produced, determined spectrophotometrically, matched the levels of H2S detected by the PHSS (after [41]). 

U74006F, 21-[4-(2,6-di-l-pyrrolidinyl-4-pyrimidinyl)-l-piperazinyl]-16a-methylpregna-l,4,9(ll)-tiene-3,20-dione monomethane sulfonate U74500A, 21-[4-(3,6-bis(diethylamino)-2-pyridinyl)-l-piperazinyl]-16a-methylpregna-1,4,9(1 l)-triene-3,20-dione hydrochloride VSMC, vascular smooth muscle cell VVC, v. vulnificus cytolysin... 

Holland et al. [125] have shown that the potent vascular smooth muscle cell mitogen and phospholipase A2 activator thrombin stimulated superoxide production in human endothelial cells, which was inhibited by the NADPH oxidase inhibitors. Similarly, thrombin enhanced the production of oxygen species and the expression of )Alphos and Rac2 subunits of NADPH oxidase in VSMCs [126,127]. Greene et al. [128] demonstrated that the activator of NO synthase neuropeptide bradykinin is also able to stimulate NADPH oxidase in VSMCs. Similar to XO, NADPH oxidase enhanced superoxide production in pulmonary artery smooth muscle cells upon exposure to hypoxia [129]. 

Lynn et al. [71] demonstrated the damaging effect of arsenite on DNA. It has been shown that arsenite at low concentrations increased DNA oxidative damage in vascular smooth muscle cells (VSMCs) that can be a cause of arsenite-induced atherosclerosis. Bruskov et al. [72] found that heat induced the formation of 8-oxoguanine in DNA solution at pH 6.8, which was supposedly mediated by oxygen radicals. 

The vascular wall is a target for sexual hormones. In the particular case of estrogens, specific receptors have been found in both endothelium and vascular smooth muscle cells (VSMC) (Venkov et al. 1996 Karas et al. 1994). The trophic effects of estrogens on the endothelium have been advocated as crucial against initiation and promotion of atherosclerosis. Thus, cellular and animal models,... 

Since the first report by lino and co-workers in 1994 (lino Tsukioka 1994), asynchronous wave-like [Ca2+]j oscillations have emerged as an universal mode of Ca2+ signalling in in situ VSMCs (Table 1). Confocal microscopy of intracellular Ca2+-sensitive dyes in intact blood vessels, reveals recurrent intracellular Ca2+ waves travelling through the longitudinal axis of the ribbonshaped VSMCs. These waves, which are usually but not always initiated by agonists, do not propagate between cells. 

FIG. 1. Phenylephrine (PE)-mediated asynchronous wave-like [Ca2+] oscillations and contraction in the rabbit inferior vena cava. (A) [Ca2+] oscillations recorded in neighbouring smooth muscle cells within the intact vessel are not synchronized between cells as they each display different frequency of oscillations. (B) Individual Ca2+ spike in PE-mediated [Ca2+]j oscillations are wave-like as different regions (1, 2 and 3) in the same ribbon-shaped VSMC experience sequential rise of [Ca2+] in time. (C) The [PE]-dependence in force generation is compared to the [PE]-dependence in the percentage recruitment of cells, the amplitude of the [Ca2+]j oscillations, the frequency of the [Ca2+]j oscillations and the apparent velocity of the recurring Ca2+ waves. (Experimental traces reproduced, with permission from Lee et al 2001.)... 

In these cultured VSMCs, about 56% of the SR released Ca2+ only in response to CPA (and, presumably, InsP3), and about 22% only in response to Caf only about 15% of the SR responded to both CPA and Caf. Moreover, the same stores could be refilled and re-emptied during a 30-60 min period (the longest times tested). These results indicate that the SR Ca2+ stores are organized into (at least) two classes of small compartments that are relatively stable. It is noteworthy that similar results have been reported in other cell types, including neurons and astrocytes (Golovina... 

Being a gas, NO is freely diffusible and penetrates cell membranes easily. NO is produced by and acts within the endothelium and platelets but is also a paracrine hormone targeting vascular smooth muscle cells (VSMC) and white blood cells. 

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