Apoptosis Induced by Inhibition of Cyclic AMP Response Element–Binding Protein in Vascular Smooth Muscle Cells

Tokunou, Tomotake; Shibata, Rei; Kai, Hisashi; Ichiki, Toshihiro; Morisaki, T.; Fukuyama, Kae; Ono, Hiroki; Iino, Naoko; Masuda, Shinya; Shimokawa, Hiroaki; Egashira, Kensuke; Imaizumi, Tsutomu; Takeshita, Akira

doi:10.1161/01.cir.0000085164.13439.89

Cited by 68 publications

(71 citation statements)

References 45 publications

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“…10 In vivo labeling with BrdU (0.5 mg/kg), a thymidine analogue that was injected intraperitoneally 3 hours before preparation of the artery, was performed to identify replicating cells by detection of DNA synthesis. The incorporated BrdU was detected immunohistochemically with an anti-BrdU antibody (Cell proliferation kit, Amersham Pharmacia Biotech) as described previously.…”

Section: Detection Of Apoptosis and Dna Synthesis In Vivomentioning

confidence: 99%

“…The incorporated BrdU was detected immunohistochemically with an anti-BrdU antibody (Cell proliferation kit, Amersham Pharmacia Biotech) as described previously. 10 …”

Section: Detection Of Apoptosis and Dna Synthesis In Vivomentioning

confidence: 99%

“…10 We assumed that T3 might show the same effect if T3 inhibits CREB function in vivo. We treated rats with T3 after balloon injury (Table).…”

Section: Neointimal Formation Of Balloon-injured Artery Was Suppressementioning

confidence: 99%

“…Overexpression of dominant negative CREB, of which serine 133 is replaced with alanine, attenuated neointimal formation after balloon injury of rat carotid artery. 10 A recent study showed a physical interaction between TR and CREB 11 in fibroblasts. However, it is not clear whether this novel signaling cross talk affects the vascular remodeling process.…”

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confidence: 99%

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Thyroid Hormone Inhibits Vascular Remodeling Through Suppression of cAMP Response Element Binding Protein Activity

Fukuyama

Ichiki

Imayama

et al. 2006

ATVB

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Objective-Although accumulating evidences suggest that impaired thyroid function is a risk for ischemic heart disease, the molecular mechanism of anti-atherosclerotic effects of thyroid hormone is poorly defined. We examined whether thyroid hormone affects signaling pathway of angiotensin II (Ang II), which is critically involved in a broad aspect of cardiovascular disease process. Methods and Results-3,3Ј,5-triiodo-L-thyronine (T3) did not show a significant effect on Ang II-induced activation of extracellular signal-regulated protein kinase or p38 mitogen-activated protein kinase in vascular smooth muscle cells (VSMCs), whereas T3 inhibited Ang II-induced activation of cAMP response element (CRE) binding protein (CREB), a nuclear transcription factor involved in the vascular remodeling process. Coimmunoprecipitaion assay revealed the protein-protein interaction between thyroid hormone receptor and CREB. T3 reduced an expression level of interleukin (IL)-6 mRNA, CRE-dependent promoter activity, and protein synthesis induced by Ang II. Administration of T3 (100 g/100 g for 14 days) to rats attenuated neointimal formation after balloon injury of carotid artery with reduced CREB activation and BrdU incorporation. Conclusion-These results suggested that T3 inhibits CREB/CRE signaling pathway and suppresses cytokine expression and VSMCs proliferation, which may account for, at least in part, an anti-atherosclerotic effect of thyroid hormone.

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Section: Detection Of Apoptosis and Dna Synthesis In Vivomentioning

confidence: 99%

“…The incorporated BrdU was detected immunohistochemically with an anti-BrdU antibody (Cell proliferation kit, Amersham Pharmacia Biotech) as described previously. 10 …”

Section: Detection Of Apoptosis and Dna Synthesis In Vivomentioning

confidence: 99%

“…10 We assumed that T3 might show the same effect if T3 inhibits CREB function in vivo. We treated rats with T3 after balloon injury (Table).…”

Section: Neointimal Formation Of Balloon-injured Artery Was Suppressementioning

confidence: 99%

mentioning

confidence: 99%

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Thyroid Hormone Inhibits Vascular Remodeling Through Suppression of cAMP Response Element Binding Protein Activity

Fukuyama

Ichiki

Imayama

et al. 2006

ATVB

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“…ATF5, encoded by ATF5 gene, belongs to the ATF/cyclic adenosine monophosphate response-element binding (CREB) protein family (40). CREB has been reported to serve a role in modulating the apoptosis and proliferation of vascular smooth muscle cells (41,42).…”

Section: Discussionmentioning

confidence: 99%

A comprehensive analysis of differentially expressed genes and pathways in abdominal aortic aneurysm

Yuan

Liang

Zhang

2015

Molecular Medicine Reports

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Abstract. The current study aimed to investigate the molecular mechanism underlying abdominal aortic aneurysm (AAA) via various bioinformatics techniques. Gene expression profiling analysis of differentially expressed genes (DEGs) between AAA samples and normal controls was conducted. The Database for Annotation, Visualization and Integrated Discovery tool was utilized to perform Gene ontology (GO) and Kyoto Encyclopedia of Genes and Genomes analyses for DEGs and clusters from the protein-protein interaction (PPI) network, which was constructed using the Search Tool for the Retrieval of Interacting Genes. In addition, important transcription factors (TFs) that regulated DEGs were investigated. A total of 346 DEGs were identified between AAA samples and healthy controls. Additionally, four clusters were identified from the PPI network. Cluster 1 was associated with sensory perception of smell and the olfactory transduction subpathway. The most significant GO function terms for cluster 2 and 3 were response to virus and defense response, respectively. Cluster 4 was associated with mitochondria-associated functions and the oxidative phosphorylation subpathway. Early growth response-1 (EGR-1), Myc, activating transcription factor 5 (ATF5) and specificity protein (SP) 1:SP3 were identified to be critical TFs in this disease. The present study suggested that the olfactory transduction subpathway, mitochondria and oxidative phosphorylation pathways were involved in AAA, and TFs, such as EGR-1, Myc, ATF5 and SP1:SP3, may be potential candidate molecular targets for this disease.

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Induction of endothelial cell apoptosis by heat‐shock protein 60–reactive antibodies from anti–endothelial cell autoantibody–positive systemic lupus erythematosus patients

Dieudé¹,

Senécal²,

Raymond³

2004

Arthritis & Rheumatism

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Objective. To determine whether anti-endothelial cell autoantibodies (AECAs) from systemic lupus erythematosus (SLE) patients with the antiphospholipid syndrome are involved in the initial endothelial cell (EC) membrane perturbation effect that is postulated to provide a target for antiphospholipid antibody (aPL) binding and, hence, to trigger the thrombotic cascade. To identify the AECA antigenic target on ECs and to determine the mechanism whereby the EC membrane is disrupted.Methods. AECAs from SLE patients were assayed for binding to ECs by flow cytometry. Positive AECAs were assayed by immunoblotting, and a consensus antigen was identified by mass spectrometry. This candidate antigen was tested in recombinant form for AECA recognition. AECAs were affinity-purified on this antigen and incubated with ECs to determine their physiologic effects. Anti-Hsp60 antibody titers were determined by enzyme-linked immunosorbent assay. The relationship of anti-Hsp60 status and lupus anticoagulant (LAC) status to thrombotic manifestations between disease onset and the last followup visit were analyzed.Results. Most of the SLE sera (73%) possessed IgG that bound to the surface of ECs. These positive IgG shared reactivity against a 60-kd EC surface polypeptide that was identified as human Hsp60. The presence of Hsp60 at the EC surface was established using anti-Hsp60 antibodies from commercial sources or affinity-purified from SLE sera that bound ECs. Incubation of ECs with these anti-Hsp60 antibodies induced apoptosis in a time-and dose-dependent manner, as determined by Hoechst 33342 dye staining of condensed nuclei and by annexin V binding to surface phosphatidylserine. Anti-Hsp60 antibodies were not restricted to SLE patients, but were found in patients with other autoimmune diseases. However, anti-Hsp60 antibodies were significantly associated with an increased frequency of thrombosis when present in combination with LAC in the SLE patients.Conclusion. The presence of Hsp60 at the surface of ECs serves as a target for the anti-Hsp60 antibodies in SLE sera. These anti-Hsp60 antibodies bind to ECs and induce apoptosis, particularly phosphatidylserine exposure, thus providing a target for the binding of aPL and inducing the subsequent thrombotic cascade.

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Apoptosis Induced by Inhibition of Cyclic AMP Response Element–Binding Protein in Vascular Smooth Muscle Cells

Cited by 68 publications

References 45 publications

Thyroid Hormone Inhibits Vascular Remodeling Through Suppression of cAMP Response Element Binding Protein Activity

Thyroid Hormone Inhibits Vascular Remodeling Through Suppression of cAMP Response Element Binding Protein Activity

A comprehensive analysis of differentially expressed genes and pathways in abdominal aortic aneurysm

Induction of endothelial cell apoptosis by heat‐shock protein 60–reactive antibodies from anti–endothelial cell autoantibody–positive systemic lupus erythematosus patients

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