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1.
ESC Heart Fail ; 10(2): 1077-1089, 2023 04.
Artigo em Inglês | MEDLINE | ID: mdl-36578105

RESUMO

AIM: The progression of atherosclerosis can lead to the occurrence of multiple cardiovascular diseases (coronary heart disease, etc.). E prostanoid receptor-3 (EP3) is known to participate in the progression of atherosclerosis. This study aimed to investigate the mechanism by which EP3 modulates the development of atherosclerosis. METHODS AND RESULTS: ApoE-/- mice were used to construct in vivo model of atherosclerosis. Human aortic smooth muscle cells (HASMCs) were stimulated with oxidized low-density lipoprotein (ox-LDL) to construct in vitro model of atherosclerosis. mRNA expressions were assessed by qRT-PCR, and western blot was applied to assess the protein levels. CCK-8 assay was applied to assess the cell viability. The inflammatory cytokines levels were assessed by enzyme-linked immunosorbent assay, and flow cytometry was applied to assess cell apoptosis. In vivo experiment was constructed to investigate the impact of EP3 in atherosclerosis development. L-798106 (EP3 inhibitor) significantly inhibited the levels of pro-inflammatory cytokines in atherosclerosis in vivo. EP3 inhibitor (L-798106) significantly reversed ox-LDL-caused HASMCs injury via inhibiting the apoptosis and inflammatory responses (P < 0.05). The levels of interleukin-17 (IL-17) and intercellular adhesion molecule-1 (ICAM-1) in HASMCs were elevated by ox-LDL, whereas L-798106 or knockdown of cyclic AMP (cAMP) response element-binding protein (CREB) notably restored this phenomenon (P < 0.05). EP3 overexpression further aggravated ox-LDL-induced inflammation in HASMCs, and EP3 up-regulated the levels of IL-17 and ICAM-1 in ox-LDL-treated HASMCs (P < 0.05). EP3 up-regulation promoted the inflammatory responses in ox-LDL-treated HASMCs through mediation of cAMP/protein kinase A (PKA)/CREB/IL-17/ICAM-1 axis (P < 0.05). CONCLUSIONS: EP3 inhibitor alleviates ox-LDL-induced HASMC inflammation via mediation of cAMP/PKA/CREB/IL-17/ICAM-1 axis. Our study might shed new lights on discovering novel strategies against atherosclerosis.


Assuntos
Aterosclerose , Molécula 1 de Adesão Intercelular , Animais , Humanos , Camundongos , Aterosclerose/genética , Moléculas de Adesão Celular/metabolismo , Citocinas/metabolismo , Inflamação/metabolismo , Molécula 1 de Adesão Intercelular/metabolismo , Interleucina-17/metabolismo , Lipoproteínas LDL/metabolismo , Miócitos de Músculo Liso/metabolismo , Prostaglandinas/metabolismo
2.
Medicine (Baltimore) ; 99(27): e20994, 2020 Jul 02.
Artigo em Inglês | MEDLINE | ID: mdl-32629716

RESUMO

INTRODUCTION: Acute myocardial infarction with simultaneous coronary thrombosis has been rarely reported. This combination induces various arrhythmias and is a high-risk factor for cardiogenic shock. PATIENT CONCERNS: A 65-year-old man presented with sweating and a 3-h abrupt persistent back pain that radiated to the anterior. DIAGNOSIS: Multisite myocardial infarction, coronary thrombosis with and complex malignant arrhythmia INTERVENTIONS:: Prompt intervention includes cardiac pacing, percutaneous coronary intervention (PCI), thrombus aspiration and intra-aortic balloon pump (IABP). OUTCOMES: The patient was successfully rescued after PCI and thrombus aspiration. CONCLUSIONS: Recognition of dynamic electrocardiographic changes enhances our understanding of the pathogenesis of myocardial infarction.


Assuntos
Arritmias Cardíacas/complicações , Trombose Coronária/complicações , Infarto do Miocárdio/complicações , Idoso , Arritmias Cardíacas/cirurgia , Trombose Coronária/cirurgia , Eletrocardiografia , Humanos , Masculino , Intervenção Coronária Percutânea/métodos , Choque Cardiogênico/etiologia
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