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  • 1
    Online Resource
    Online Resource
    Interferon Regulatory Factor 4 Inhibits Neointima Formation by Engaging Krüppel-Like Factor 4 Signaling
    Ovid Technologies (Wolters Kluwer Health) ; 2017
    In:  Circulation Vol. 136, No. 15 ( 2017-10-10), p. 1412-1433
    Details
    In: Circulation, Ovid Technologies (Wolters Kluwer Health), Vol. 136, No. 15 ( 2017-10-10), p. 1412-1433
    Abstract: The mechanisms underlying neointima formation remain unclear. Interferon regulatory factors (IRFs), which are key innate immune regulators, play important roles in cardiometabolic diseases. However, the function of IRF4 in arterial restenosis is unknown. Methods: IRF4 expression was first detected in human and mouse restenotic arteries. Then, the effects of IRF4 on neointima formation were evaluated with universal IRF4-deficient mouse and rat carotid artery injury models. We performed immunostaining to identify IRF4-expressing cells in the lesions. Smooth muscle cell (SMC)–specific IRF4-knockout (KO) and -transgenic (TG) mice were generated to evaluate the effects of SMC-IRF4 on neointima formation. We used microarray, bioinformatics analysis, and chromatin immunoprecipitation assay to identify the downstream signals of IRF4 and to verify the targets in vitro. We compared SMC-IRF4-KO/Krüppel-like factor 4 (KLF4)–TG mice with SMC-IRF4-KO mice and SMC-specific IRF4-TG/KLF4-KO mice with SMC-specific IRF4-TG mice to investigate whether the effect of IRF4 on neointima formation is KLF4-dependent. The effect of IRF4 on SMC phenotype switching was also evaluated. Results: IRF4 expression in both the human and mouse restenotic arteries is eventually downregulated. Universal IRF4 ablation potentiates neointima formation in both mice and rats. Immunostaining indicated that IRF4 was expressed primarily in SMCs in restenotic arteries. After injury, SMC-IRF4-KO mice developed a thicker neointima than control mice. This change was accompanied by increased SMC proliferation and migration. However, SMC-specific IRF4-TG mice exhibited the opposite phenotype, demonstrating that IRF4 exerts protective effects against neointima formation. The mechanistic study indicated that IRF4 promotes KLF4 expression by directly binding to its promoter. Genetic overexpression of KLF4 in SMCs largely reversed the neointima-promoting effect of IRF4 ablation, whereas ablation of KLF4 abolished the protective function of IRF4, indicating that the protective effects of IRF4 against neointima formation are KLF4-dependent. In addition, IRF4 promoted SMC dedifferentiation. Conclusions: IRF4 protects arteries against neointima formation by promoting the expression of KLF4 by directly binding to its promoter. Our findings suggest that this previously undiscovered IRF4-KLF4 axis plays a key role in vasculoproliferative pathology and may be a promising therapeutic target for the treatment of arterial restenosis.
    Type of Medium: Online Resource
    ISSN: 0009-7322 , 1524-4539
    URL: Article
    DOI: 10.1161/CIRCULATIONAHA.116.026046
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 2017
    detail.hit.zdb_id: 1466401-X
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  • 2
    Online Resource
    Online Resource
    The Ubiquitin E3 Ligase TRAF6 Exacerbates Ischemic Stroke by Ubiquitinating and Activating Rac1
    Society for Neuroscience ; 2017
    In:  The Journal of Neuroscience Vol. 37, No. 50 ( 2017-12-13), p. 12123-12140
    Details
    In: The Journal of Neuroscience, Society for Neuroscience, Vol. 37, No. 50 ( 2017-12-13), p. 12123-12140
    Abstract: Stroke is one of the leading causes of morbidity and mortality worldwide. Inflammation, oxidative stress, apoptosis, and excitotoxicity contribute to neuronal death during ischemic stroke; however, the mechanisms underlying these complicated pathophysiological processes remain to be fully elucidated. Here, we found that the expression of tumor necrosis factor receptor-associated factor 6 (TRAF6) was markedly increased after cerebral ischemia/reperfusion (I/R) in mice. TRAF6 ablation in male mice decreased the infarct volume and neurological deficit scores and decreased proinflammatory signaling, oxidative stress, and neuronal death after cerebral I/R, whereas transgenic overexpression of TRAF6 in male mice exhibited the opposite effects. Mechanistically, we demonstrated that TRAF6 induced Rac1 activation and consequently promoted I/R injury by directly binding and ubiquitinating Rac1. Either functionally mutating the TRAF6 ubiquitination site on Rac1 or inactivating Rac1 with a specific inhibitor reversed the deleterious effects of TRAF6 overexpression during I/R injury. In conclusion, our study demonstrated that TRAF6 is a key promoter of ischemic signaling cascades and neuronal death after cerebral I/R injury. Therefore, the TRAF6/Rac1 pathway might be a promising target to attenuate cerebral I/R injury. SIGNIFICANCE STATEMENT Stroke is one of the most severe and devastating neurological diseases globally. The complicated pathophysiological processes restrict the translation of potential therapeutic targets into medicine. Further elucidating the molecular mechanisms underlying cerebral ischemia/reperfusion injury may open a new window for pharmacological interventions to promote recovery from stroke. Our study revealed that ischemia-induced tumor necrosis factor receptor-associated factor 6 (TRAF6) upregulation binds and ubiquitinates Rac1 directly, which promotes neuron death through neuroinflammation and neuro-oxidative signals. Therefore, precisely targeting the TRAF6-Rac1 axis may provide a novel therapeutic strategy for stroke recovery.
    Type of Medium: Online Resource
    ISSN: 0270-6474 , 1529-2401
    URL: Article
    DOI: 10.1523/JNEUROSCI.1751-17.2017
    Language: English
    Publisher: Society for Neuroscience
    Publication Date: 2017
    detail.hit.zdb_id: 1475274-8
    SSG: 12
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  • 3
    Online Resource
    Online Resource
    Restoration of Circulating MFGE8 (Milk Fat Globule-EGF Factor 8) Attenuates Cardiac Hypertrophy Through Inhibition of Akt Pathway
    Ovid Technologies (Wolters Kluwer Health) ; 2017
    In:  Hypertension Vol. 70, No. 4 ( 2017-10), p. 770-779
    Details
    In: Hypertension, Ovid Technologies (Wolters Kluwer Health), Vol. 70, No. 4 ( 2017-10), p. 770-779
    Abstract: Cardiac hypertrophy occurs in response to numerous stimuli like neurohumoral stress, pressure overload, infection, and injury, and leads to heart failure. Mfge8 (milk fat globule-EGF factor 8) is a secreted protein involved in various human diseases, but its regulation and function during cardiac hypertrophy remain unexplored. Here, we found that circulating MFGE8 levels declined significantly in failing hearts from patients with dilated cardiomyopathy. Correlation analyses revealed that circulating MFGE8 levels were negatively correlated with the severity of cardiac dysfunction and remodeling in affected patients. Deleting Mfge8 in mice maintained normal heart function at basal level but substantially exacerbated the hypertrophic enlargement of cardiomyocytes, reprogramming of pathological genes, contractile dysfunction, and myocardial fibrosis after aortic banding surgery. In contrast, cardiac-specific Mfge8 overexpression in transgenic mice significantly blunted aortic banding–induced cardiac hypertrophy. Whereas MAPK (mitogen-activated protein kinase) pathways were unaffected in either Mfge8 -knockout or Mfge8 -overexpressing mice, the activated Akt/PKB (protein kinase B)–Gsk-3β (glycogen synthase kinase-3β)/mTOR (mammalian target of rapamycin) pathway after aortic banding was significantly potentiated by Mfge8 deficiency but suppressed by Mfge8 overexpression. Inhibition of Akt with MK-2206 blocked the prohypertrophic effects of Mfge8 deficiency in angiotensin II–treated neonatal rat cardiomyocytes. Finally, administering a recombinant human MFGE8 in mice in vivo alleviated cardiac hypertrophy induced by aortic banding. Our findings indicate that Mfge8 is an endogenous negative regulator of pathological cardiac hypertrophy and may, thus, have potential both as a novel biomarker and as a therapeutic target for treatment of cardiac hypertrophy.
    Type of Medium: Online Resource
    ISSN: 0194-911X , 1524-4563
    URL: Article
    DOI: 10.1161/HYPERTENSIONAHA.117.09465
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 2017
    detail.hit.zdb_id: 2094210-2
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  • 4
    Online Resource
    Online Resource
    Dickkopf‐3 Ablation Attenuates the Development of Atherosclerosis in ApoE‐Deficient Mice
    Ovid Technologies (Wolters Kluwer Health) ; 2017
    In:  Journal of the American Heart Association Vol. 6, No. 2 ( 2017-02-02)
    Details
    In: Journal of the American Heart Association, Ovid Technologies (Wolters Kluwer Health), Vol. 6, No. 2 ( 2017-02-02)
    Abstract: Dickkopf‐3 ( DKK 3) is a negative regulator of the Wnt/β‐catenin signaling pathway, which is involved in inflammation. However, little is known about the relationship between DKK 3 expression and the progression of atherosclerosis. The aim of the present study was to define the role of DKK 3 and its potential mechanism in the development of atherosclerosis. Methods and Results Immunofluorescence analysis showed that DKK 3 was strongly expressed in macrophages of atherosclerotic plaques from patients with coronary heart disease and in hyperlipidemic mice. The expression level was significantly increased in atherogenesis. DKK 3 −/− ApoE −/− mice exhibited a significant decrease in atherosclerotic lesions in the entire aorta, aortic sinus, and brachiocephalic arteries. Transplantation of bone marrow from DKK 3 −/− ApoE −/− mice into lethally irradiated ApoE −/− recipients resulted in a reduction of atherosclerotic lesions, compared with the lesions in recipients transplanted with ApoE −/− donor cells, suggesting that the effect of DKK 3 deficiency was largely mediated by bone marrow–derived cells. A reduction in the necrotic core size, accompanied by increased collagen content and smooth muscle cells and decreased accumulation of macrophages and lipids, contributed to the stability of plaques in DKK 3 −/− ApoE −/− mice. Furthermore, multiple proinflammatory cytokines exhibited marked decreases in DKK 3 −/− ApoE −/− mice. Finally, we observed that DKK 3 ablation increased β‐catenin expression in the nuclei of macrophages both in vivo and in vitro. Conclusions DKK 3 expression in macrophages is involved in the pathogenesis of atherosclerosis through modulation of inflammation and inactivation of the Wnt/β‐catenin pathway.
    Type of Medium: Online Resource
    ISSN: 2047-9980
    URL: Article
    DOI: 10.1161/JAHA.116.004690
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 2017
    detail.hit.zdb_id: 2653953-6
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  • 5
    Online Resource
    Online Resource
    Spatiotemporal characteristics of pain-associated neuronal activities in primary somatosensory cortex induced by peripheral persistent nociception
    Elsevier BV ; 2008
    In:  Neuroscience Letters Vol. 448, No. 1 ( 2008-12), p. 134-138
    Details
    In: Neuroscience Letters, Elsevier BV, Vol. 448, No. 1 ( 2008-12), p. 134-138
    Type of Medium: Online Resource
    ISSN: 0304-3940
    URL: Article
    DOI: 10.1016/j.neulet.2008.08.090
    Language: English
    Publisher: Elsevier BV
    Publication Date: 2008
    detail.hit.zdb_id: 1498535-4
    SSG: 12
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  • 6
    Online Resource
    Online Resource
    MiR-122 knockdown regulates vascular smooth muscle cells phenotypic switching through enhanced FOXO3 expression
    Canadian Science Publishing ; 2023
    In:  Canadian Journal of Physiology and Pharmacology
    Details
    In: Canadian Journal of Physiology and Pharmacology, Canadian Science Publishing
    Abstract: Vascular smooth muscle cells (VSMCs) phenotypic switching is identified as enhanced dedifferentiation, proliferation, and migration ability of VSMCs, in which microRNAs have been identified as important regulators of the process. The present study is aimed to explore the pathophysiological effect of miR-122 on VSMC phenotypic modulation. Here, the result showed that the decreased miR-122 expression was found in VSMCs subjected to platelet-derived growth factor-BB (PDGF-BB) treatment. Next, we investigated the response of miR-122 knockdown in VSMCs with PDGF-BB stimulation. MiR-122 silencing showed increased proliferation and migration capability, whereas attenuated the differentiation markers expression. The above results were reversed by miR-122 overexpression. Finally, we further demonstrated that FOXO3 was an important target for miR-122. Collectively, we demonstrated that miR-122 silencing promoted VSMC phenotypic modulation partially through upregulated FOXO3 expression that indicated miR-122 may be a novel therapeutic target for neointimal formation.
    Type of Medium: Online Resource
    ISSN: 0008-4212 , 1205-7541
    URL: Article
    DOI: 10.1139/cjpp-2022-0549
    Language: English
    Publisher: Canadian Science Publishing
    Publication Date: 2023
    detail.hit.zdb_id: 2004356-9
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  • 7
    Online Resource
    Online Resource
    Background noise of satellite-to-ground quantum key distribution
    IOP Publishing ; 2005
    In:  New Journal of Physics Vol. 7 ( 2005-10-10), p. 215-215
    Details
    In: New Journal of Physics, IOP Publishing, Vol. 7 ( 2005-10-10), p. 215-215
    Type of Medium: Online Resource
    ISSN: 1367-2630
    URL: Article
    DOI: 10.1088/1367-2630/7/1/215
    Language: Unknown
    Publisher: IOP Publishing
    Publication Date: 2005
    detail.hit.zdb_id: 1464444-7
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  • 8
    Online Resource
    Online Resource
    RIP2 Knockdown Attenuates Vascular Smooth Muscle Cells Activation via Negative Regulating Myocardin Expression
    Oxford University Press (OUP) ; 2022
    In:  American Journal of Hypertension Vol. 35, No. 5 ( 2022-05-10), p. 454-461
    Details
    In: American Journal of Hypertension, Oxford University Press (OUP), Vol. 35, No. 5 ( 2022-05-10), p. 454-461
    Abstract: RIP2 is an adaptor protein contributing to the activation of nuclear factor-κB induced by TNF receptor-associated factor (TRAF) and nucleotide oligomerization domain (NOD)-dependent signaling implicated in innate and adaptive immune response. Beyond regulation of immunity, we aimed to elucidate the role of RIP2 in vascular smooth muscle cell (VSMC) phenotypic modulation. Methods and results In the current study, we observed that RIP2 showed an increased expression in VSMCs with PDGF-BB stimulation in a dose-dependent manner. Knockdown of RIP2 expression mediated by adenovirus dramatically accelerated the expression of VSMC-specific differentiation genes induced by PDGF-BB. Silencing of RIP2 inhibited proliferative and migratory ability of VSMCs. Additionally, we demonstrated that RIP2 knockdown can promoted myocardin expression. Furthermore, RIP2 inhibition also can attenuate the formation of intimal hyperplasia. Conclusions These findings suggested that RIP2 played an important role in regulation of VSMCs differentiation, migration, and proliferation that may due to affect myocardin expression. Our results indicated that RIP2 may be a novel therapeutic target for intimal hyperplasia.
    Type of Medium: Online Resource
    ISSN: 0895-7061 , 1941-7225
    URL: Article
    DOI: 10.1093/ajh/hpac009
    Language: English
    Publisher: Oxford University Press (OUP)
    Publication Date: 2022
    detail.hit.zdb_id: 1479505-X
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  • 9
    Online Resource
    Online Resource
    Oncostatin M receptor β deficiency attenuates atherogenesis by inhibiting JAK2/STAT3 signaling in macrophages
    Elsevier BV ; 2017
    In:  Journal of Lipid Research Vol. 58, No. 5 ( 2017-05), p. 895-906
    Details
    In: Journal of Lipid Research, Elsevier BV, Vol. 58, No. 5 ( 2017-05), p. 895-906
    Type of Medium: Online Resource
    ISSN: 0022-2275
    URL: Article
    DOI: 10.1194/jlr.M074112
    Language: English
    Publisher: Elsevier BV
    Publication Date: 2017
    detail.hit.zdb_id: 1466675-3
    SSG: 12
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  • 10
    Online Resource
    Online Resource
    Association between unstable angina and CXCL17: a new potential biomarker
    Walter de Gruyter GmbH ; 2019
    In:  Open Medicine Vol. 14, No. 1 ( 2019-12-08), p. 939-944
    Details
    In: Open Medicine, Walter de Gruyter GmbH, Vol. 14, No. 1 ( 2019-12-08), p. 939-944
    Abstract: Atherosclerosis and chemokines are strongly related, but the role of the chemokine CXCL17 in atherogenesis is still poorly understood. We aim to investigate the serum CXCL17 levels in different stages of patients with coronary heart disease and explore whether these differences contribute to atherosclerosis. In the current prospective study, we enrolled 48 patients with unstable angina (UA), 51 patients with stable angina (SA) and 41 patients for the control group (CG). All subjects were diagnosed by coronary angiography and Gensini score was used to evaluate the severity of coronary artery disease. The CXCL17 levels were determined using ELISA, while lipid metabolism indicators and high sensitivity C-reactive protein (hs-CRP) were detected by automatic biochemical analyzer. We observed that the unstable angina group had higher CXCL17 levels compared with the stable angina and the control group. The logistic regression analysis showed that CXCL17 was an independent risk factor for unstable angina. Our results showed that CXCL17 was also statistically correlated with hs-CRP, while it was irrelevant with Gensini score. CXCL17 levels were associated with activity of inflammatory response and the instability of atherosclerotic plaques. These results suggest that CXCL17 elevation may be a potential new biomarker of unstable angina.
    Type of Medium: Online Resource
    ISSN: 2391-5463
    URL: Article
    DOI: 10.1515/med-2019-0080
    Language: English
    Publisher: Walter de Gruyter GmbH
    Publication Date: 2019
    detail.hit.zdb_id: 2829380-0
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