The Notch Pathway Attenuates Interleukin 1β (IL1β)-mediated Induction of Adenylyl Cyclase 8 (AC8) Expression during Vascular Smooth Muscle Cell (VSMC) Trans-differentiation

Keuylian, Zela; Baaij, Jeroen H. F. de; Glorian, Martine; Rouxel, Clotilde; Merlet, Elise; Lipskaia, Larissa; Blaise, Régis; Mateo, Véronique; Limon, Isabelle

doi:10.1074/jbc.m111.292516

Cited by 20 publications

(13 citation statements)

References 38 publications

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“…Future studies using both electrophysiological and biomolecular techniques will be needed in studying in-depth some of these aspects. We cannot rule out the possibility that this form of sustained anxiety could trigger a de novo expression of AC8, a process present in the inflammatory context of atherosclerosis [ 35 ].…”

Section: Discussionmentioning

confidence: 99%

Calcium activated adenylyl cyclase AC8 but not AC1 is required for prolonged behavioral anxiety

Bernabucci

Zhuo

2016

Mol Brain

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BackgroundAnxiety disorder is a state of mental discomfort while acute anxiety induces an enhancement of vigilance/arousal or increased anxious responses. Most of the previous studies investigated basic mechanisms for acute anxiety, while less information is available for prolonged or repetitive anxiety.ResultsIn the present study, we wanted to examine possible molecular mechanisms for behavioral anxiety after repeated exposures. Performing a paradigm of five sessions of the elevated plus-maze (EPM), we show that the repeated exposure to the EPM induces a long-lasting anxiety causing a gradual increase of anxiolytic activity, which is maintained for at least 21 days. Genetic deletion of AC8 (adenylyl cyclase 8) but not AC1 abolished long-lasting anxiety.ConclusionsOur results suggest that calcium-stimulated AC8 is required to sustain the long-lasting anxiety caused by repeated EPM testing, and we can identify in AC8 a novel target for treating anxiety-related mood disorders.

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Section: Discussionmentioning

confidence: 99%

Calcium activated adenylyl cyclase AC8 but not AC1 is required for prolonged behavioral anxiety

Bernabucci

Zhuo

2016

Mol Brain

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“…The dynamic process of VSMC phenotype transition involves numerous molecular signaling cascades that regulate VSMC growth, differentiation, and fate. Several studies suggest a role for the Notch and Wnt/β‐catenin signaling pathways in pathophysiological remodeling during vascular injury [Wang et al., ; Morrow et al., ; Keuylian et al., ; Mill and George, ]. For Notch signaling, ligands of the Jagged‐1 and ‐2 and Delta‐like families interact with Notch family receptors (Notch‐1 to 4) on an adjacent/same cell [Morrow et al., ].…”

Section: Discussionmentioning

confidence: 99%

Curcumin Regulates VSMC Phenotype Transition via Modulation of Notch and Wnt Signaling Pathways

Chen

et al. 2013

Drug Development Research

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In the development of cardiovascular diseases, vascular smooth muscle cells (VSMCs) undergo transition from a contractile to a synthetic phenotype. Notch-and Wnt-dependent signaling pathways play a critical role during this process. Curcumin has potential for clinical use including anti-inflammatory and antitumor actions. However, the effect of curcumin on VSMC phenotype transition remains unclear. In VSMCs isolated from the thoracic aorta of Sprague Dawley rats, curcumin (5-20 mM) produced a concentration-dependent inhibition of serum-elicited VSMC migration. Furthermore, curcumin, at the dose of 20 mM, partially reversed the repression of VSMC markers induced by serum stimulation, an effect associated with attenuation of Jagged-1 and Notch-1 levels and downregulation of the downstream gene Hey-1. Downregulation of Wnt-4 was also observed after curcumin treatment in the presence of serum, which was followed by inhibition of nuclear b-catenin translocation and cyclin D1 expression. These data suggest that curcumin is a potent regulator of VSMCs phenotype transition and may play a critical role in regulating these events after vascular injury. Drug Dev Res 74 : 252-258, 2013.

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“…To characterize rat aortic VSMCs we used smooth muscle myosin heavy chain 1&2, smooth muscle alpha-actin, SM22, calponin, and caldesmon, as preiously described 8,61 . Cells were infected with rAAV at100 pfu/cell.…”

Section: Methodsmentioning

confidence: 99%

Efficient transduction of vascular smooth muscle cells with a translational AAV2.5 vector: a new perspective for in-stent restenosis gene therapy

et al. 2013

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Coronary artery disease represents the leading cause of mortality in the developed world. Percutaneous coronary intervention (PCI) involving stent placement remains disadvantaged by restenosis or thrombosis. Vascular gene-therapy-based methods may be approached, but lack a vascular gene delivery vector. We report a safe and efficient long-term transduction of rat carotid vessels after balloon-injury intervention with a translational optimized AAV2.5 vector. Compared to other known AAV serotypes, AAV2.5 demonstrated the highest transduction efficiency of human coronary artery vascular smooth muscle cells (VSMC) in vitro. Local delivery of AAV2.5-driven transgenes in injured carotid arteries resulted in transduction as soon as day 2 after surgery and persisted for at least 30 days. In contrast to adenovirus 5 vector, inflammation was not detected in AAV2.5-transduced vessels. The functional effects of AAV2.5-mediated gene transfer on neointimal thickening were assessed using the sarco/endoplasmic reticulum Ca2+ ATPase (SERCA2a) human gene, known to inhibit VSMC proliferation. At 30 days, human SERCA2a mRNA was detected in transduced arteries. Morphometric analysis revealed a significant decrease of neointimal hyperplasia in AAV2.5-SERCA2a transduced arteries: 28.36±11.30 (n=8) vs 77.96±24.60 (n=10) μm2, in AAV2.5-GFP-infected, p<0.05. In conclusion, AAV2.5 vector can be considered as a promising safe and effective vector for vascular gene therapy.

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The Notch Pathway Attenuates Interleukin 1β (IL1β)-mediated Induction of Adenylyl Cyclase 8 (AC8) Expression during Vascular Smooth Muscle Cell (VSMC) Trans-differentiation

Cited by 20 publications

References 38 publications

Calcium activated adenylyl cyclase AC8 but not AC1 is required for prolonged behavioral anxiety

Calcium activated adenylyl cyclase AC8 but not AC1 is required for prolonged behavioral anxiety

Curcumin Regulates VSMC Phenotype Transition via Modulation of Notch and Wnt Signaling Pathways

Efficient transduction of vascular smooth muscle cells with a translational AAV2.5 vector: a new perspective for in-stent restenosis gene therapy

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