The Experts below are selected from a list of 192 Experts worldwide ranked by ideXlab platform
Andrew C. Newby - One of the best experts on this subject based on the ideXlab platform.
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Neointima formation is promoted by surgical preparation and inhibited by cyclic nucleotides in human saphenous vein organ cultures
The Journal of thoracic and cardiovascular surgery, 1995Co-Authors: A.a. Soyombo, Gianni D. Angelini, Andrew C. NewbyAbstract:Abstract Intimal thickening is an important cause of late coronary vein graft occlusion, which no variation of surgical technique or pharmacologic intervention has been shown to reduce. We used a recently developed quantitative organ culture of human saphenous vein to investigate whether surgical preparative injury promotes neointima formation. We also investigated the effects on neointima formation of the lipid-soluble cyclic nucleotide analogs, 8-Br-cyclic adenosine monophosphate and 8-Br-cyclic guanosine monophosphate, and the phosphodiesterase inhibitor, Isobutylmethylxanthine. These agents are pharmacologic mimetics of endothelium-derived prostacyclin and nitric oxide, which elevate vascular smooth muscle cyclic adenosine monophosphate and cyclic guanosine monophosphate concentrations, respectively, and may normally suppress neointima formation. Surgical preparation was found to promote intimal thickening and neointimal smooth muscle cell proliferation by 42% and 48%, respectively. 8-Br-cyclic adenosine monophosphate, 8-Br-cyclic guanosine monophosphate, or Isobutylmethylxanthine (which elevated endogenous cyclic adenosine monophosphate concentrations) inhibited intimal thickening by 80%, 40%, and 72%, respectively, at a concentration of 0.1 mmol/L. The results imply that surgical techniques that avoid preparative injury and vasodilator drugs that act by elevating cyclic adenosine monophosphate or cyclic guanosine monophosphate concentrations may reduce neointima formation in vein grafts. (J Thoracic Cardiovasc Surg 1995;109:2-12)
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Inhibition of proliferation, but not of Ca2+ mobilization, by cyclic AMP and GMP in rabbit aortic smooth-muscle cells.
Biochemical Journal, 1992Co-Authors: J. W. Assender, K. M. Southgate, Maurice Bartlett Hallett, Andrew C. NewbyAbstract:The effects on cellular proliferation and Ca2+ mobilization of analogues of cyclic AMP (cAMP) and cyclic GMP (cGMP) and of agents that elevate the intracellular concentrations of cyclic nucleotides were compared in closely similar preparations of first-passage rabbit aortic vascular smooth-muscle cells. Proliferation induced by foetal-bovine serum was inhibited by 78% by 1 mM-8-bromo cAMP and by 42% by 1 mM-8-bromo cGMP. In the presence of 100 microM-Isobutylmethylxanthine, 100 microM-forskolin increased intracellular cAMP concentration 5-fold and inhibited proliferation by 87%, but did not affect cGMP concentration or cell viability (ATP concentration). Similarly in the presence of 100 microM-Isobutylmethylxanthine, 1 mM-SIN-1 (3-morpholinosydnonimine) elevated cGMP concentration 4-fold and inhibited proliferation by 48%, but did not affect cAMP or ATP concentration. Isobutylmethylxanthine (1 mM) elevated cAMP concentration by 3-fold and cGMP concentration by 20-fold and inhibited proliferation by 81%. Concentrations of 8-bromo cAMP, 8-bromo cGMP, forskolin or SIN-1 that inhibited proliferation did not affect the elevation of intracellular free Ca2+ concentration caused by 2% (v/v) foetal-bovine serum, 100 nM-5-hydroxytryptamine or 10 nM-angiotensin II. The results demonstrate that elevation of intracellular cAMP and cGMP concentrations both independently inhibit vascular smooth-muscle cell proliferation, but these effects on proliferation are not mediated by inhibition of Ca2+ mobilization.
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Does nitric oxide inhibit smooth muscle proliferation
Journal of Cardiovascular Pharmacology, 1991Co-Authors: J. W. Assender, K. M. Southgate, Andrew C. NewbyAbstract:The lipid-soluble analogue 8-bromocyclic GMP did not inhibit thymidine incorporation into rabbit aortic smooth muscle cells initially in the contractile state but tended to inhibit incorporation into passaged cells by approximately 30%. In passaged cells, the nitrovasodilator drug SIN-1 (0.1-1 mM) in the presence of the phosphodiesterase inhibitor Isobutylmethylxanthine produced a two- to fourfold increase in cyclic GMP concentration and an approximatively 50% reduction in [ 3 H]thymidine incorporation.
J S Fink - One of the best experts on this subject based on the ideXlab platform.
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calcium regulation of vasoactive intestinal polypeptide mrna abundance in sh sy5y human neuroblastoma cells
Journal of Neurochemistry, 2006Co-Authors: E M Adler, J S FinkAbstract:Second messenger regulation of gene expression provides a mechanism by which neurons can transduce environmental stimuli into long-term changes in the expression of molecules involved in neuronal signaling. We have investigated calcium-dependent induction of vasoactive intestinal polypeptide (VIP) mRNA and compared it with induction of VIP mRNA by cyclic AMP. Depolarization with 60 mM KCl or exposure to the calcium ionophore A23187 increases VIP mRNA levels in SH-SY5Y cells. The increase in VIP mRNA content in response to Ca2+ mobilization is slow, independent of adenylate cyclase activation, and requires de novo protein synthesis. The increase in VIP mRNA content in response to elevation of cyclic AMP levels by forskolin/Isobutylmethylxanthine is independent of Ca2+ influx and does not require new protein synthesis. The mRNA for the transcription factors ATF-3, c-fos, c-jun, junB, and zif/268 is induced by A23187. Of these, ATF-3 showed the greatest relative induction by A23187 compared with induction by forskolin/Isobutylmethylxanthine.
J. W. Assender - One of the best experts on this subject based on the ideXlab platform.
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Inhibition of proliferation, but not of Ca2+ mobilization, by cyclic AMP and GMP in rabbit aortic smooth-muscle cells.
Biochemical Journal, 1992Co-Authors: J. W. Assender, K. M. Southgate, Maurice Bartlett Hallett, Andrew C. NewbyAbstract:The effects on cellular proliferation and Ca2+ mobilization of analogues of cyclic AMP (cAMP) and cyclic GMP (cGMP) and of agents that elevate the intracellular concentrations of cyclic nucleotides were compared in closely similar preparations of first-passage rabbit aortic vascular smooth-muscle cells. Proliferation induced by foetal-bovine serum was inhibited by 78% by 1 mM-8-bromo cAMP and by 42% by 1 mM-8-bromo cGMP. In the presence of 100 microM-Isobutylmethylxanthine, 100 microM-forskolin increased intracellular cAMP concentration 5-fold and inhibited proliferation by 87%, but did not affect cGMP concentration or cell viability (ATP concentration). Similarly in the presence of 100 microM-Isobutylmethylxanthine, 1 mM-SIN-1 (3-morpholinosydnonimine) elevated cGMP concentration 4-fold and inhibited proliferation by 48%, but did not affect cAMP or ATP concentration. Isobutylmethylxanthine (1 mM) elevated cAMP concentration by 3-fold and cGMP concentration by 20-fold and inhibited proliferation by 81%. Concentrations of 8-bromo cAMP, 8-bromo cGMP, forskolin or SIN-1 that inhibited proliferation did not affect the elevation of intracellular free Ca2+ concentration caused by 2% (v/v) foetal-bovine serum, 100 nM-5-hydroxytryptamine or 10 nM-angiotensin II. The results demonstrate that elevation of intracellular cAMP and cGMP concentrations both independently inhibit vascular smooth-muscle cell proliferation, but these effects on proliferation are not mediated by inhibition of Ca2+ mobilization.
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Does nitric oxide inhibit smooth muscle proliferation
Journal of Cardiovascular Pharmacology, 1991Co-Authors: J. W. Assender, K. M. Southgate, Andrew C. NewbyAbstract:The lipid-soluble analogue 8-bromocyclic GMP did not inhibit thymidine incorporation into rabbit aortic smooth muscle cells initially in the contractile state but tended to inhibit incorporation into passaged cells by approximately 30%. In passaged cells, the nitrovasodilator drug SIN-1 (0.1-1 mM) in the presence of the phosphodiesterase inhibitor Isobutylmethylxanthine produced a two- to fourfold increase in cyclic GMP concentration and an approximatively 50% reduction in [ 3 H]thymidine incorporation.
Greti Aguilera - One of the best experts on this subject based on the ideXlab platform.
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cyclic adenosine 3 5 monophosphate regulation of corticotropin releasing hormone promoter activity in att 20 cells and in a transformed hypothalamic cell line
Endocrinology, 2003Co-Authors: Maria Nikodemova, John Kasckow, Vincent C Manganiello, Greti AguileraAbstract:The regulation of CRH promoter activity by cAMP was studied in two cell lines, the pituitary corticotroph cell line AtT-20 and the immortalized hypothalamic cell line 4B, which expresses CRH and vasopressin. In 4B cells transfected with a CRH promoter-luciferase construct, the adenylyl cyclase stimulator, forskolin, increased luciferase activity in parallel with increases in intracellular cAMP. In 4B cells, however, the phosphodiesterase inhibitor, Isobutylmethylxanthine, potentiated forskolin-stimulated cAMP without affecting further increases in luciferase activity. In AtT-20 cells, forskolin plus Isobutylmethylxanthine elevated cAMP only slightly, but increased luciferase activity to levels similar to those observed in 4B cells. AtT-20 cells were also unresponsive to 8-bromo-cAMP, due in part to higher phosphodiesterase (PDE) activities. Although both cells contained PDE1, -3, and -4, inhibition of either PDE4 or PDE1 potentiated luciferase activity stimulated by submaximal forskolin concentrations in ...
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Cyclic adenosine 3',5'-monophosphate regulation of corticotropin-releasing hormone promoter activity in AtT-20 cells and in a transformed hypothalamic cell line.
Endocrinology, 2003Co-Authors: Maria Nikodemova, John Kasckow, Vincent C Manganiello, Hanguan Liu, Greti AguileraAbstract:The regulation of CRH promoter activity by cAMP was studied in two cell lines, the pituitary corticotroph cell line AtT-20 and the immortalized hypothalamic cell line 4B, which expresses CRH and vasopressin. In 4B cells transfected with a CRH promoter-luciferase construct, the adenylyl cyclase stimulator, forskolin, increased luciferase activity in parallel with increases in intracellular cAMP. In 4B cells, however, the phosphodiesterase inhibitor, Isobutylmethylxanthine, potentiated forskolin-stimulated cAMP without affecting further increases in luciferase activity. In AtT-20 cells, forskolin plus Isobutylmethylxanthine elevated cAMP only slightly, but increased luciferase activity to levels similar to those observed in 4B cells. AtT-20 cells were also unresponsive to 8-bromo-cAMP, due in part to higher phosphodiesterase (PDE) activities. Although both cells contained PDE1, -3, and -4, inhibition of either PDE4 or PDE1 potentiated luciferase activity stimulated by submaximal forskolin concentrations in ...
Lars Bengtsson - One of the best experts on this subject based on the ideXlab platform.
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Serial cultivation of adult human endothelium from the great saphenous vein
Journal of vascular surgery, 1992Co-Authors: Anders Haegerstrand, C. Gillis, Lars BengtssonAbstract:The growth of endothelial cells from small segments of human great saphenous vein was investigated for possible functional studies of endothelial cell properties and endothelialization of cardiovascular prosthetic graft materials. Growth in medium containing fetal calf serum or human serum was compared, and the effects of adding compounds that increase intracellular cyclic adenosine monophosphate levels, that is, cholera toxin and Isobutylmethylxanthine, were also examined. It was shown that human serum was more efficient in stimulating cell growth than fetal calf serum at all concentrations tested. It was also shown that the addition of cholera toxin and Isobutylmethylxanthine significantly potentiated growth. Minimal Essential Medium with the addition of 40% human serum and cholera toxin (1 nmol/L) and Isobutylmethylxanthine (33 mumol/L) was shown to be optimal. From a single segment (3 to 5 cm), 20 x 10(6) human saphenous vein endothelial cells corresponding to 2000 cm2 or more could be achieved after 3 to 4 weeks in culture. The human saphenous vein endothelial cell cultures retained their cobblestone appearance, expression of von Willebrand Factor (vWF)-antigen, and capacity for prostacyclin production after six passages. We suggest that this provides a practically useful method for studies of cultured endothelium and possibly for pre-endothelialization of cardiovascular prosthetic materials.
