Vascular smooth muscle cells VSMC

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. 

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]). 

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,... 

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. 

In an effort to investigate antioxidant constituents with antiproliferative effects in rat vascular smooth muscle cells (VSMC), broussoflavan A (36) [49], broussoflavonols F (45) [50] and G (46) [51], and broussoaurone A (48) [49] were found to inhibit the Fe2+-induced thiobarbituric acid-reactive substance formation in rat brain homogenate. Furthermore, broussoflavonols F (45) and G (46) inhibited fetal calf serum-, 5-hydroxytryptamine-, or ADP-induced [3H]thymidine incorporation into rat VSMC [45]. Antioxidant activities and inhibitory effects on proliferation of rat VSMC with potent antiplatelet activities of 45 and 46 may be useful for vascular diseases and atherosclerosis [43,45]. 

Fig. 1.5 Effect of iV-acetyl-L-cysteine (NAC) and diphenyleneiodonium (DPI) on Gia-2 and Gioc-3 protein expression in vascular smooth muscle cells (VSMC) from 12 week-old SHR and age-matched WKY rats. Confluent VSMC from SHR and WKY rats were treated with 20 mM NAC (A) or 10 pM DPI (B) for 24 hours at 37 °C. Membrane proteins (30 pg) were separated and transferred to nitrocellulose, which was immunoblotted with antibodies AS/7 and EC/1 against Gioc-2 (A) and Gioc-3 (B), respectively, as described earlier (Lappas et al. 2005). The blots are representative of five separate experiments. The graphs in the lower panel show quantification of protein bands by densitometric scanning. The results are expressed as percentage of WKY control which has been taken as 100%. Values are mean S.E.M of five separate experiments. P < 0.05 versus WKY, < 0.01 versus SHR.

Both PKC-pII and PKC-6 isoforms have been shown to be activated in aortic and vascular smooth muscle cells (VSMC) from diabetic rats, as well as in response to hyperglycemia (Koya and King 1998 Craven and DeRubertis 1989 Inoguchi et al. 1992 Kunisaki et al. 1994 Lee et al. 1999). Treatment of VSMCs with 22 mM glucose for 3 days increased the levels of DAG as well as PKC-pII by 50 and 110%,... 

NO and PGI2 produced by VEGF exhibit several other vascular protective effects. They inhibit vascular smooth muscle cell (VSMC) proliferation. The antiproliferative effect of NO and PGI2 on SMCs is mediated via the production of the intracellular messengers cGMP and cAMP, respectively (Asada et al. 1994 von der Leyen et al. 1995). 

Mechanochemical Transduction by Vascular Smooth Muscle Cells (VSMCs)... 

The in vitro experiments that utilize cultures of vascular smooth muscle cells (VSMC) require initial isolation of primary aortic VSMC from adult mice (5-8 weeks old). Because adult vascular cell culmres undergo significant phenotypic modulation with prolonged culture it is necessary to continuously generate and maintain low-passage cultures (<6). 

Vascular proliferative disease 235 Vascular re-endothelialization 319 Vascular smooth muscle cell (VSMC) 313 Vasoactive intestinal peptide (VIP)... 

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