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  • Ovid Technologies (Wolters Kluwer Health)  (10)
  • 1
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    Critical Role of Rho-Kinase and MEK/ERK Pathways for Angiotensin II–Induced Plasminogen Activator Inhibitor Type-1 Gene Expression
    Ovid Technologies (Wolters Kluwer Health) ; 2001
    In:  Arteriosclerosis, Thrombosis, and Vascular Biology Vol. 21, No. 5 ( 2001-05), p. 868-873
    Details
    In: Arteriosclerosis, Thrombosis, and Vascular Biology, Ovid Technologies (Wolters Kluwer Health), Vol. 21, No. 5 ( 2001-05), p. 868-873
    Abstract: Abstract —Plasminogen activator inhibitor type-1 (PAI-1) plays an integral role not only in the regulation of fibrinolytic activity but also in the pathogenesis of atherosclerosis and hypertension. We investigated the signaling pathways of angiotensin II (Ang II) leading to PAI-1 gene expression. Ang II increased the PAI-1 mRNA and protein levels in a time- and dose-dependent manner through the Ang II type 1 receptor in vascular smooth muscle cells. PAI-1 gene promoter activity measured by luciferase assay was significantly increased by Ang II. PAI-1 mRNA stability was also increased by Ang II. Ang II–induced PAI-1 mRNA upregulation was inhibited by BAPTA-AM, genistein, and AG1478, suggesting that intracellular calcium, tyrosine kinase, and epidermal growth factor receptor transactivation are involved. Furthermore, PD98059, an inhibitor of extracellular signal–regulated kinase (ERK) kinase (MEK), almost completely suppressed Ang II–induced PAI-1 upregulation. Adenovirus-mediated overexpression of the dominant-negative form of Rho-kinase or Y27632, a Rho-kinase inhibitor, also completely prevented PAI-1 induction by Ang II without affecting Ang II–induced ERK activation. These data suggest that activation of MEK/ERK and Rho-kinase pathways plays a pivotal role in PAI-1 gene upregulation by Ang II. The Rho-kinase pathway may be a novel target to inhibit Ang II signaling, and its inhibition may be useful in the treatment of hypertension as well as atherosclerosis.
    Type of Medium: Online Resource
    ISSN: 1079-5642 , 1524-4636
    URL: Article
    DOI: 10.1161/01.ATV.21.5.868
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 2001
    detail.hit.zdb_id: 1494427-3
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  • 2
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    Online Resource
    Thrombin Induces Interleukin-6 Expression Through the cAMP Response Element in Vascular Smooth Muscle Cells
    Ovid Technologies (Wolters Kluwer Health) ; 2001
    In:  Arteriosclerosis, Thrombosis, and Vascular Biology Vol. 21, No. 11 ( 2001-11), p. 1759-1763
    Details
    In: Arteriosclerosis, Thrombosis, and Vascular Biology, Ovid Technologies (Wolters Kluwer Health), Vol. 21, No. 11 ( 2001-11), p. 1759-1763
    Abstract: The plasma level of interleukin-6 (IL-6) is elevated in patients with acute coronary syndromes and has prognostic value. Thrombin is a potent mitogen for vascular smooth muscle cells (VSMCs) and plays an important role in the progression of atherosclerosis. We examined the mechanism of thrombin-induced IL-6 expression in VSMCs. Thrombin induced IL-6 mRNA and protein expression in a dose-dependent manner. Pharmacological inhibition of extracellular signal-regulated protein kinase (ERK), p38 mitogen-activated protein kinase (MAPK), or epidermal growth factor receptor (EGF-R) suppressed the thrombin-induced IL-6 expression. Deletion and mutation analysis of the promoter region of the IL-6 gene by using luciferase as a reporter showed that the DNA segment between −228 and −150 bp containing the cAMP response element (CRE) site played a critical role. Thrombin also induced phosphorylation of CRE binding protein (CREB) in an ERK- and a p38 MAPK-dependent manner. Overexpression of the dominant-negative form of CREB inhibited thrombin-induced IL-6 mRNA expression. These results suggest that the CRE site and CREB play an important role in thrombin-induced IL-6 gene expression in VSMCs. Transactivation of EGF-R and activation of ERK and p38 MAPK are involved in this process. CREB may be a novel transcription factor that regulates thrombin-induced gene expression.
    Type of Medium: Online Resource
    ISSN: 1079-5642 , 1524-4636
    URL: Article
    DOI: 10.1161/hq1101.098489
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 2001
    detail.hit.zdb_id: 1494427-3
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  • 3
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    Apoptosis Induced by Inhibition of Cyclic AMP Response Element–Binding Protein in Vascular Smooth Muscle Cells
    Ovid Technologies (Wolters Kluwer Health) ; 2003
    In:  Circulation Vol. 108, No. 10 ( 2003-09-09), p. 1246-1252
    Details
    In: Circulation, Ovid Technologies (Wolters Kluwer Health), Vol. 108, No. 10 ( 2003-09-09), p. 1246-1252
    Abstract: Background— The balance between apoptosis and proliferation of vascular smooth muscle cells (VSMCs) is believed to contribute to the vascular remodeling process. Cyclic AMP response element–binding protein (CREB) is a critical transcription factor for the survival of neuronal cells and T lymphocytes. However, the role of CREB in blood vessels is incompletely characterized. Methods and Results— Nuclear staining with Hoechst 33258 or propidium iodine showed an increase in apoptotic cells with activation of caspase-3 in VSMCs infected with adenovirus expressing the dominant-negative form of CREB (AdCREBM1). Basal expression of Bcl-2 and Bcl-2 promoter activity were decreased by infection with AdCREBM1. Immunohistochemistry revealed that CREB was mainly induced and activated in the neointimal α-smooth muscle actin–positive cells of rat carotid artery after balloon injury. Infection with AdCREBM1 suppressed neointimal formation (intima-media ratio) by 33.8% after 14 days of injury, which was accompanied by an increase in apoptosis as indicated by terminal deoxynucleotidyl transferase–mediated dUTP nick end-labeling–positive cells and a decrease in bromodeoxyuridine incorporation. Conclusions— These results suggest that CRE-dependent gene transcription might play an important role in the survival and proliferation of VSMCs. CREB might be a novel transcription factor mediating the vascular remodeling process and a potential therapeutic target for atherosclerotic disease.
    Type of Medium: Online Resource
    ISSN: 0009-7322 , 1524-4539
    URL: Article
    DOI: 10.1161/01.CIR.0000085164.13439.89
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 2003
    detail.hit.zdb_id: 1466401-X
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  • 4
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    Cyclic AMP Response Element–Binding Protein Mediates Reactive Oxygen Species–Induced c- fos Expression
    Ovid Technologies (Wolters Kluwer Health) ; 2003
    In:  Hypertension Vol. 42, No. 2 ( 2003-08), p. 177-183
    Details
    In: Hypertension, Ovid Technologies (Wolters Kluwer Health), Vol. 42, No. 2 ( 2003-08), p. 177-183
    Abstract: Although the cyclic AMP response element–binding protein (CREB) plays an important role in the survival of neuronal cells and T lymphocytes, the role of CREB in vascular smooth muscle cells (VSMCs) is incompletely characterized. We examined the role of CREB in VSMCs stimulated with reactive oxygen species. Activation of CREB was examined by Western blot analysis with an antibody that specifically recognizes phosphorylation at serine 133 of CREB, which is a critical marker of activation. Hydrogen peroxide (H 2 O 2 ) time-dependently induced phosphorylation of CREB, with a peak at 15 minutes. The H 2 O 2 -induced phosphorylation of CREB was partially blocked by inhibition of either extracellular signal–regulated protein kinase kinase by PD98059 or of p38 mitogen-activated protein kinase (MAPK) by SB203580. AG1478, an epidermal growth factor receptor (EGFR) inhibitor, suppressed the H 2 O 2 -induced phosphorylation of CREB and tyrosine phosphorylation of EGFR. Overexpression of the dominant-negative form of CREB by an adenovirus vector suppressed H 2 O 2 -induced c- fos expression. These findings suggest that H 2 O 2 induces CREB phosphorylation through EGFR transactivation and mitogen-activated protein kinase pathways. CREB might be a novel redox-sensitive transcription factor involved in the regulation of VSMC gene expression.
    Type of Medium: Online Resource
    ISSN: 0194-911X , 1524-4563
    URL: Article
    DOI: 10.1161/01.HYP.0000079791.26014.04
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 2003
    detail.hit.zdb_id: 2094210-2
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  • 5
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    Downregulation of Angiotensin II Type 1 Receptor by Hydrophobic 3-Hydroxy-3-Methylglutaryl Coenzyme A Reductase Inhibitors in Vascular Smooth Muscle Cells
    Ovid Technologies (Wolters Kluwer Health) ; 2001
    In:  Arteriosclerosis, Thrombosis, and Vascular Biology Vol. 21, No. 12 ( 2001-12), p. 1896-1901
    Details
    In: Arteriosclerosis, Thrombosis, and Vascular Biology, Ovid Technologies (Wolters Kluwer Health), Vol. 21, No. 12 ( 2001-12), p. 1896-1901
    Abstract: Abstract — 3-Hydroxy-3-methylglutaryl coenzyme A (HMG CoA) reductase inhibitors, so-called statins, reduce the relative risk of a major coronary event by lowering the serum cholesterol level. In addition, statins may confer beneficial effects by cholesterol-lowering independent mechanisms, which are incompletely characterized. Because angiotensin II (Ang II) plays crucial roles in the pathogenesis of cardiovascular diseases, we examined the effect of statins on the expression of the Ang II type 1 receptor (AT 1 -R) in cultured vascular smooth muscle cells (VSMCs). Cerivastatin and fluvastatin reduced the AT 1 -R mRNA and the AT 1 -R protein levels; however, pravastatin lacked this effect. Cerivastatin and fluvastatin suppressed the AT 1 -R promoter activity measured by luciferase assay but did not affect AT 1 -R mRNA stability, suggesting that the suppression occurs at the transcriptional level. Coincubation of VSMCs with mevalonate or geranylgeranyl pyrophosphate but not with farnesyl pyrophosphate reversed the cerivastatin-induced AT 1 -R downregulation. Overexpression of dominant-negative Rho A also suppressed AT 1 -R mRNA expression. Treatment with cerivastatin for 24 hours reduced the calcium response of VSMCs to Ang II. Taken together, statins downregulate AT 1 -R expression through a mevalonate-dependent, geranylgeranyl pyrophosphate-dependent, and Rho A-dependent manner and attenuate the biological function of Ang II. Downregulation of AT 1 -R may contribute to the cholesterol-independent beneficial effect of statins on the cardiovascular system.
    Type of Medium: Online Resource
    ISSN: 1079-5642 , 1524-4636
    URL: Article
    DOI: 10.1161/hq1201.099430
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 2001
    detail.hit.zdb_id: 1494427-3
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  • 6
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    Reactive Oxygen Species–Mediated Homologous Downregulation of Angiotensin II Type 1 Receptor mRNA by Angiotensin II
    Ovid Technologies (Wolters Kluwer Health) ; 2001
    In:  Hypertension Vol. 37, No. 2 ( 2001-02), p. 535-540
    Details
    In: Hypertension, Ovid Technologies (Wolters Kluwer Health), Vol. 37, No. 2 ( 2001-02), p. 535-540
    Abstract: Recent studies suggest a crucial role of reactive oxygen species (ROS) for the signaling of angiotensin (Ang) II through Ang II type 1 receptor (AT 1 -R). However, the role of ROS in the regulation of AT 1 -R expression has not been explored. In this study, we examined the effect of an antioxidant on the homologous downregulation of AT 1 -R by Ang II. Ang II (10 −6 mol/L) decreased AT 1 -R mRNA with a peak suppression at 6 hours of stimulation in rat aortic vascular smooth muscle cells. Preincubation of vascular smooth muscle cells with N -acetylcysteine (NAC), a potent antioxidant, almost completely inhibited the Ang II–induced downregulation of AT 1 -R mRNA. The effect of NAC was due to stabilization of the AT 1 -R mRNA that was destabilized by Ang II. The Ang II–induced AT 1 -R mRNA downregulation was also blocked by PD98059, an extracellular signal–regulated protein kinase (ERK) kinase inhibitor. Ang II–induced ERK activation was inhibited by NAC as well as by PD98059. Exogenous H 2 O 2 also suppressed AT 1 -R mRNA. These results suggest that the production of ROS and the activation of ERK are critical for the downregulation of AT 1 -R mRNA. The generation of ROS through stimulation of AT 1 -R not only mediates signaling of Ang II but also may play a crucial role in the adaptation process of AT 1 -R to the sustained stimulation of Ang II.
    Type of Medium: Online Resource
    ISSN: 0194-911X , 1524-4563
    URL: Article
    DOI: 10.1161/01.HYP.37.2.535
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 2001
    detail.hit.zdb_id: 2094210-2
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  • 7
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    Downregulation of Vascular Angiotensin II Type 1 Receptor by Thyroid Hormone
    Ovid Technologies (Wolters Kluwer Health) ; 2003
    In:  Hypertension Vol. 41, No. 3 ( 2003-03), p. 598-603
    Details
    In: Hypertension, Ovid Technologies (Wolters Kluwer Health), Vol. 41, No. 3 ( 2003-03), p. 598-603
    Abstract: Thyroid hormone has a broad effect on cardiovascular system. 3,3′,5-triiodo- l -thyronine (T3), a biologically active form of thyroid hormone, increases cardiac contractility. T3 causes arterial relaxation and reduction of systemic vascular resistance, resulting in an increase in cardiac output. However, the molecular mechanisms of vascular relaxation by T3 are incompletely characterized. We studied the effect of T3 on the angiotensin (Ang) II type 1 receptor (AT 1 R) expression in vascular smooth muscle cells. T3 dose-dependently decreased expression levels of AT 1 R mRNA, with a peak at 6 hours of stimulation. Binding assay using [ 125 I]Sar 1 -Ile 8 -Ang II revealed that AT 1 R number was decreased by stimulation with T3 without changing the affinity to Ang II. T3 reduced calcium response of vascular smooth muscle cells to Ang II by 26%. AT 1 R promoter activity measured by luciferase assay was reduced by 50% after 9 hours of T3 administration. mRNA stability was also decreased by T3. Real-time quantitative reverse transcription–polymerase chain reaction and Western blot analysis revealed that AT 1 R mRNA and protein were downregulated in the aorta of T3-treated rats. These results suggest that T3 downregulates AT 1 R expression both at transcriptional and posttranscriptional levels, and attenuates biological function of Ang II. Our results suggest that downregulation of AT 1 R gene expression may play an important role for T3-induced vascular relaxation.
    Type of Medium: Online Resource
    ISSN: 0194-911X , 1524-4563
    URL: Article
    DOI: 10.1161/01.HYP.0000056524.35294.80
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 2003
    detail.hit.zdb_id: 2094210-2
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  • 8
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    Peroxisome Proliferator-Activated Receptor γ Activators Downregulate Angiotensin II Type 1 Receptor in Vascular Smooth Muscle Cells
    Ovid Technologies (Wolters Kluwer Health) ; 2000
    In:  Circulation Vol. 102, No. 15 ( 2000-10-10), p. 1834-1839
    Details
    In: Circulation, Ovid Technologies (Wolters Kluwer Health), Vol. 102, No. 15 ( 2000-10-10), p. 1834-1839
    Abstract: Background —Peroxisome proliferator-activated receptor γ (PPARγ) activators, such as troglitazone (Tro), not only improve insulin resistance but also suppress the neointimal formation after balloon injury. However, the precise mechanisms have not been determined. Angiotensin II (Ang II) plays crucial roles in the pathogenesis of atherosclerosis, hypertension, and neointimal formation after angioplasty. We examined the effect of PPARγ activators on the expression of Ang II type 1 receptor (AT 1 -R) in cultured vascular smooth muscle cells (VSMCs). Methods and Results —AT 1 -R mRNA and AT 1 -R protein levels were determined by Northern blot analysis and radioligand binding assay, respectively. Natural PPARγ ligand 15-deoxy-Δ 12,14 -prostaglandin J 2 , as well as Tro, reduced the AT 1 -R mRNA expression and the AT 1 -R protein level. The PPARγ activators also reduced the calcium response of VSMCs to Ang II. PPARγ activators suppressed the AT 1 -R promoter activity measured by luciferase assay but did not affect the AT 1 -R mRNA stability, suggesting that the suppression occurs at the transcriptional level. Conclusions —PPARγ activators reduced the AT 1 -R expression and calcium response to Ang II in VSMCs. Downregulation of AT 1 -R may contribute to the inhibition of neointimal formation by PPARγ activators.
    Type of Medium: Online Resource
    ISSN: 0009-7322 , 1524-4539
    URL: Article
    DOI: 10.1161/01.CIR.102.15.1834
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 2000
    detail.hit.zdb_id: 1466401-X
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  • 9
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    cAMP-Response Element-Binding Protein Mediates Tumor Necrosis Factor-α–Induced Vascular Smooth Muscle Cell Migration
    Ovid Technologies (Wolters Kluwer Health) ; 2004
    In:  Arteriosclerosis, Thrombosis, and Vascular Biology Vol. 24, No. 9 ( 2004-09), p. 1634-1639
    Details
    In: Arteriosclerosis, Thrombosis, and Vascular Biology, Ovid Technologies (Wolters Kluwer Health), Vol. 24, No. 9 ( 2004-09), p. 1634-1639
    Abstract: Migration of vascular smooth muscle cells (VSMCs) contributes to formation of vascular stenotic lesions. TNF-α, a potent migration factor for VSMCs, activated CREB through p38 mitogen-activated protein kinase (p38-MAPK). CREB inhibition suppressed TNF-α–induced VSMC migration and Rac1 expression. These results suggest p38-MAPK/CREB/Rac1 pathway mediates TNF-α–induced VSMC migration.
    Type of Medium: Online Resource
    ISSN: 1079-5642 , 1524-4636
    URL: Article
    DOI: 10.1161/01.ATV.0000138052.86051.0d
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 2004
    detail.hit.zdb_id: 1494427-3
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  • 10
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    cAMP Response Element-Binding Protein Mediates Thrombin-Induced Proliferation of Vascular Smooth Muscle Cells
    Ovid Technologies (Wolters Kluwer Health) ; 2001
    In:  Arteriosclerosis, Thrombosis, and Vascular Biology Vol. 21, No. 11 ( 2001-11), p. 1764-1769
    Details
    In: Arteriosclerosis, Thrombosis, and Vascular Biology, Ovid Technologies (Wolters Kluwer Health), Vol. 21, No. 11 ( 2001-11), p. 1764-1769
    Abstract: Thrombin is a potent mitogen for vascular smooth muscle cells (VSMCs) and plays an important role in the progression of atherosclerosis. Although recent reports have suggested that cAMP response element-binding protein (CREB) is necessary for the survival of neuronal cells, the role of CREB in VSMC proliferation is not determined. We examined the role of CREB in thrombin-induced VSMC proliferation and the effect of thrombin on phosphorylation of CREB at Ser133, which is a critical marker for activation by Western blot analysis. Thrombin induced phosphorylation of CREB in a dose-dependent manner. An oligopeptide, SFLLRN, which activates the thrombin receptor, also induced the phosphorylation of CREB. Inhibition of extracellular signal-regulated protein kinase or inhibition of p38 mitogen-activated protein kinase suppressed the thrombin-induced CREB phosphorylation. Inhibition of the epidermal growth factor receptor by AG1478 also inhibited the thrombin-induced CREB phosphorylation. Overexpression of the dominant-negative form of CREB inhibited thrombin-induced c- fos mRNA expression and incorporation of [ 3 H]thymidine and [ 3 H]leucine. These results suggest that CREB-dependent gene transcription plays a critical role in thrombin-induced proliferation and hypertrophy of VSMCs. Transactivation of the epidermal growth factor receptor and 2 mitogen-activated protein kinase pathways are involved in this process. CREB may be a novel transcription factor mediating the vascular remodeling process induced by thrombin.
    Type of Medium: Online Resource
    ISSN: 1079-5642 , 1524-4636
    URL: Article
    DOI: 10.1161/hq2112.098770
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 2001
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