| 1. |
- Pessah-Rasmussen, H, et al.
(författare)
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Glutathione transferase activity in human vessels and in cultured arterial smooth muscle cells
- 1993
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Ingår i: International Angiology. - 0392-9590. ; 12:4, s. 54-348
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Tidskriftsartikel (refereegranskat)abstract
- Glutathione transferases play an important role in the detoxification of many different endogeneous and exogenous compounds such as metabolites of polycyclic aromatic hydrocarbons (PAH) of cigarette tar. There is evidence that PAH may be atherogenic. The glutathione transferase activity towards trans-stilbene oxide (GST-tSBO) can be separated in blood in GST-positive and GST-negative phenotypes. We have previously suggested that the GST-negative phenotype may be associated with a higher morbidity in intermittent claudication among middle aged smokers. In the present study, GST-tSBO could easily be measured in human, rabbit and bovine arterial smooth muscle cells (SMC) in culture. The level of GST-tSBO was higher in rabbit than in bovine SMC. It was stable in bovine SMC during 5 cell passages and it could be induced twofold by long-time incubation with dimethylsulfoxide-soluble particulate matter from cigarette smoke or 3,4-benzo(a)pyrene. There was a positive correlation between the level of GST-tSBO in blood and in "healthy" arterial and venous tissue from individuals operated with coronary bypass. The enzyme levels in arterial tissue were lower than in venous tissue. GST-tSBO in atherosclerotic segments of human arteries was lower than in "healthy" segments from the same artery. These findings suggest that the arterial wall may have a low defense against toxic compounds that may decrease further as atherosclerosis proceeds. It is concluded that SMC are suitable for the study of the effects of PAH in relation to GST-tSBO and that the enzyme activity in blood will reflect the individual GST-tSBO phenotype also in vascular tissues.
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| 2. |
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| 3. |
- De Pergola, G, et al.
(författare)
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Amount of G-protein alpha-subunit in rat white adipocytes: lack of difference between subcutaneous and visceral fat.
- 1993
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Ingår i: Acta endocrinologica. - 0001-5598. ; 129:4, s. 366-70
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Tidskriftsartikel (refereegranskat)abstract
- It has been the purpose of this study to examine possible differences in the amount of stimulatory (Gs) and inhibitory (Gi) G-protein alpha-subunits (measured with a quantitative enzyme-linked immunosorbent assay in fat cell membrane preparation) between subcutaneous and intra-abdominal regions in rats. The lipolytic response to isoproterenol and the number of beta-adrenergic binding sites were also examined. These parameters were all evaluated simultaneously in subcutaneous (inguinal), epididymal and perirenal fat samples collected from six male Sprague-Dawley rats. The membrane contents of the Gs and Gi alpha-subunits were similar in the three depots. Moreover, no difference was found among the different regions with regard to isoproterenol-stimulated glycerol release and beta-adrenoceptor number, expressed per cell number. In conclusion, the present study shows for the first time in rats that the abundance of inhibitory and stimulatory G-protein alpha-subunits is similar in subcutaneous and in visceral adipocytes. Moreover, the number of beta-adrenoceptors and the lipolytic response to isoproterenol do not show significant variations with the anatomical site. As the present results are apparently in contrast with those obtained previously in human adipocytes, there is a possibility that the different results observed in rat and in human fat cells could be explained by species differences.
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| 4. |
- Pessah-Rasmussen, H, et al.
(författare)
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Increased smooth muscle cell proliferation by dimethylbenzanthracene is correlated to variations in activity of ornithine decarboxylase but not arylhydrocarbonhydroxylase
- 1991
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Ingår i: Artery. - 0098-6127. ; 18:5, s. 55-240
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Tidskriftsartikel (refereegranskat)abstract
- Polycyclic aromatic hydrocarbons of cigarette smoke have been suggested to be involved in atherogenesis. After being converted to epoxides by monooxidases in the arterial wall the hydrocarbons may exert toxic or mutagenic effects on the smooth muscle cells (SMC). In a previous study we found that dimethylbenzanthracene (DMBA), an inducer of arylhydrocarbonhydroxylase (AHH), increased SMC proliferation and viability. In the present work we intended to study whether these effects were mediated by AHH. Alpha-naphtoflavone (ANF), a non specific AHH inhibitor, decreased SMC proliferation. The effects of ANF were totally counteracted by serum, partially by albumin and not at all by platelet derived growth factor. AHH activity was not detectable nor basally nor after induction in SMC, and this made us conclude that the effects of DMBA and ANF on SMC proliferation were not mediated by AHH. On the other hand the activity of ornithine decarboxylase was influenced by DMBA and ANF in parallel to proliferation, suggesting the involvement of this enzyme in the described DMBA effects on SMC proliferation. This mechanism might be of relevance for the pathogenesis of atherosclerosis especially in relation to cigarette smoking.
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| 5. |
- Xu, C B, et al.
(författare)
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Interactions between cultured bovine arterial endothelial and smooth muscle cells : effects of injury on the release of growth stimulating and growth inhibiting substances
- 1991
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Ingår i: Pharmacology and Toxicology. - : Wiley. - 0901-9928 .- 1600-0773. ; 69:3, s. 195-200
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Tidskriftsartikel (refereegranskat)abstract
- Dimethylsulfoxide-soluble particles (DSP) from cigarette smoke and ultraviolet light caused a low degree (cell death less than 30%) and high degree (cell death 60-90%) injury to bovine arterial endothelial cells and smooth muscle cells in culture. Conditioned medium from low degree injured endothelial cells and smooth muscle cells generally inhibited DNA synthesis in new smooth muscle cells or endothelial cells while high degree injury increased DNA synthesis in new cells. Specifically, the growth stimulating activity from endothelial cells was decreased after low degree injury but increased after high degree. UV light released more growth stimulating substances from smooth muscle cells after both low and high degree injury. The release of growth inhibiting substances was dependent on both cell kind and degree of injury. In co-culture low and high degree DSP injury to endothelial cells inhibited smooth muscle cell proliferation, which was in contrast to the effect of conditioned medium from high degree injured endothelial cells. Conditioned medium from endothelial cells treated with LDL and glucose inhibited DNA synthesis in smooth muscle cells. It is concluded that injury to endothelial cells or smooth muscle cells will modify the release of growth inhibiting and growth stimulating activity and that this release will depend on cell kind as well as degree and kind of the injurious stimulus.
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| 6. |
- Xu, C B, et al.
(författare)
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Interactions between cultured bovine arterial endothelial and smooth muscle cells; further studies on the effects of injury and modification of the consequences of injury
- 1993
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Ingår i: Artery. - 0098-6127. ; 20:3, s. 79-163
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Tidskriftsartikel (refereegranskat)abstract
- The hypothesis that cells of the arterial wall might modify the consequences of arterial injury was tested. Bovine aortic endothelial cells (EC) or smooth muscle cells (SMC) were exposed to the two toxic stimuli 3,4-benzo(a)pyrene (BP) and dimethylsulfoxide-soluble particulate matter from cigarette smoke (DSP) or factors released from platelets. The modification of the injury caused by these substances on arterial cells was studied by using a conditioned medium from arterial cells or an EC-SMC co-culture model. Direct addition of BP or DSP to the EC or SMC cultures induced toxic effects on the cells. DSP caused a decreased release of prostacyclin by EC. Conditioned medium from EC and SMC modified these toxic effects, which resulted in a reduced cell death and a further decreased cell proliferation, while conditioned medium from SMC increased the release of prostacyclin by EC injured by DSP. In EC-SMC co-culture the same modifications were obtained. The modification of cell injury was not linked to cell proliferation but instead the results suggested that the effects were mediated by multiple substances released from arterial cells. It is concluded that interactions between different cells in the arterial wall, in the non-injured as well as in the injured state, could be modified by endogeneous substances. This might be of relevance for atherogenesis.
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| 7. |
- Xu, C B, et al.
(författare)
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Interactions between cultured bovine arterial endothelial and smooth muscle cells; studies on the release of prostacyclin by endothelial cells
- 1992
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Ingår i: Artery. - 0098-6127. ; 19:2, s. 94-111
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Tidskriftsartikel (refereegranskat)abstract
- The release of prostacyclin by endothelial cells (EC) in culture was studied after exposure to two toxic stimuli (UV light or dimethylsulfoxide-soluble smoke particles (DSP)) or to medium conditioned by smooth muscle cells (SMC), basically or after injury to the SMC. An activity stimulating the release of prostacyclin was found together with growth inhibiting activity from arterial SMC, but dissociated from growth stimulating activity. The prostacyclin stimulating activity was increased when SMC were exposed to UV light, while DSP caused a decrease. EC directly exposed to UV light or DSP generally released more prostacyclin than controls. One exception was very low concentrations of DSP. UV light induced a burst of release in contrast to DSP where a continuous release after a two hours lag period was seen. It is concluded that EC will increase the release of prostacyclin in response to injury but the release pattern will depend on the kind and doses of the stimulus. SMC release prostacyclin stimulating activity for EC, which can be modified by exposure to toxic stimuli. The results might have applications for atherogenesis.
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| 8. |
- Xu, X, et al.
(författare)
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Postreceptor events involved in the up-regulation of beta-adrenergic receptor mediated lipolysis by testosterone in rat white adipocytes.
- 1993
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Ingår i: Endocrinology. - 0013-7227. ; 132:4, s. 1651-7
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Tidskriftsartikel (refereegranskat)abstract
- In the previous studies we have shown that testosterone increases lipolytic responsiveness to catecholamines in rat white adipocytes, and that is associated with an up-regulation of beta-adrenergic receptor density. However, the postreceptor events involved in the testosterone induced enhancement of beta-adrenergic receptor activated lipolysis in these cells have not been adequately studied, and were therefore investigated in the present study. Male Sprague Dawley rats were divided into three groups: control, castrated, and castrated treated with testosterone. The beta-adrenergic receptor-mediated cAMP accumulation, measured with RIA after isoproterenol (a beta-adrenergic agonist) stimulation was decreased in castrated rats, and reversed by testosterone treatment, suggesting a testosterone effect at or proximal to adenylate cyclase. However, no differences between the groups were found in abundance of G alpha protein messenger RNAs (G alpha s, G alpha i-1, and G alpha i-2) as analyzed by Northern blot and a solution hybridization RNase protection assay, or in G protein mass measured with a quantitative enzyme-linked immunosorbent assay in fat cell membrane preparation. Lipolysis stimulated by N6-monobutyryl-cAMP was reduced in castrated rats and recovered by testosterone treatment, suggesting that components distal to the adenylate cyclase, i.e. protein kinase A (PKA) and/or hormone sensitive lipase (HSL) also are involved in testosterone regulation of lipolysis. In conclusion, these and previous results suggest that the testosterone-induced increase in lipolytic response to catecholamines in rat white adipocytes is mediated through several events including an increased beta-adrenergic receptor density, probably an increased adenylate cyclase activity and an increased protein kinase A/hormone sensitive lipase activity at the postreceptor level with apparent absence of effect on the expression of G-proteins.
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