Interleukin-1Β Induces Intracellular Serum Amyloid A1 Expression In Human Coronary Endothelial Cells And Promotes Its Intercellular Exchange

Abstract Purpose Endothelial dysfunction is central to the pathogenesis of acute coronary syndrome. The study of diseased endothelium is very challenging due to inherent difficulties in isolating endothelial cells from the coronary vascular bed. We sought to isolate and characterise coronary endothelial cells from patients undergoing thrombectomy for myocardial infarction to develop a patient-specific in vitro model of endothelial dysfunction. Methods In a prospective cohort study, 49 patients underwent percutaneous coronary intervention with thrombus aspiration. Specimens were cultured, and coronary endothelial outgrowth (CEO) cells were isolated. CEO cells, endothelial cells isolated from peripheral blood, explanted coronary arteries, and umbilical veins were phenotyped and assessed functionally in vitro and in vivo. Results CEO cells were obtained from 27/37 (73%) atherothrombotic specimens and gave rise to cells with cobblestone morphology expressing CD146 (94 ± 6%), CD31 (87 ± 14%), and von Willebrand factor (100 ± 1%). Proliferation of CEO cells was impaired compared to both coronary artery and umbilical vein endothelial cells (population doubling time, 2.5 ± 1.0 versus 1.6 ± 0.3 and 1.2 ± 0.3 days, respectively). Cell migration was also reduced compared to umbilical vein endothelial cells (29 ± 20% versus 85±19%). Importantly, unlike control endothelial cells, dysfunctional CEO cells did not incorporate into new vessels or promote angiogenesis in vivo. Conclusions CEO cells can be reliably isolated and cultured from thrombectomy specimens in patients with acute coronary syndrome. Compared to controls, patient-derived coronary endothelial cells had impaired capacity to proliferate, migrate, and contribute to angiogenesis. CEO cells could be used to identify novel therapeutic targets to enhance endothelial function and prevent acute coronary syndromes.

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Effect of atorvastatin on the angiogenic responsiveness of coronary endothelial cells in normal and streptozotocin (STZ) induced diabetic rats

Canadian Journal of Physiology and Pharmacology ◽

10.1139/cjpp-2013-0391 ◽

2014 ◽

Vol 92 (4) ◽

pp. 338-349 ◽

Cited By ~ 7

Author(s):

Kiranj K. Chaudagar ◽

Anita A. Mehta

Keyword(s):

Endothelial Cells ◽

Low Dose ◽

Ischemia Reperfusion ◽

Late Phase ◽

Diabetic Rats ◽

Lipid Lowering ◽

Diabetic Rat ◽

High Dose ◽

Atorvastatin Treatment ◽

Coronary Endothelial Cells

Atorvastatin, a lipid lowering agent, possesses various pleiotropic vasculoprotective effects, but its role in coronary angiogenesis is still controversial. Our objective was to study the effects of atorvastatin on the angiogenic responsiveness of coronary endothelial cells (cEC) from normal and diabetic rats. Male Wistar rats were distributed among 9 groups; (i) normal rats, (ii) 30 day diabetic rats, (iii) 60 day diabetic rats, (iv) normal rats administered a low dose of atorvastatin (1 mg/kg body mass, per oral (p.o.), for 15 days); (v) 30 day diabetic rats administered a low dose of atorvastatin; (vi) 60 day diabetic rats administered a low dose of atorvastatin; (vii) normal rats administered a high dose of atorvastatin (5 mg/kg, p.o., for 15 days); (viii) 30 day diabetic rats administered a high dose of atorvastatin; (ix) 60 day diabetic rats administered a high dose of atorvastatin. Each group was further divided into 2 subgroups, (i) sham ischemia–reperfusion and (ii) rats hearts that underwent ischemia–reperfusion. Angiogenic responsiveness the and nitric oxide (NO) releasing properties of the subgroups of cECs were studied using a chorioallantoic membrane assay and the Griess method, respectively. Atorvastatin treatment significantly increased VEGF-induced angiogenic responsiveness and the NO-releasing properties of cECs from all of the subgroups, compared with their respective non-treated subgroups except for the late-phase diabetic rat hearts that underwent ischemia–reperfusion, and the high dose of atorvastatin treatment groups. These effects of atorvastatin were significantly inhibited by pretreatment of cECs with l-NAME, wortmannin, and chelerythrine. Thus, treatment with a low dose of atorvastatin improves the angiogenic responsiveness of the cECs from normal and diabetic rats, in the presence of VEGF, via activation of eNOS–NO release.

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Serum Amyloid A, Serum Amyloid A1 and Haptoglobin in pregnant mares and their fetuses after experimental induction of placentitis

Animal Reproduction Science ◽

10.1016/j.anireprosci.2021.106766 ◽

2021 ◽

pp. 106766

Author(s):

Y. Linhares Boakari ◽

A. Esteller-Vico ◽

S. Loux ◽

H. El-Sheikh Ali ◽

C. Barbosa Fernandes ◽

...

Keyword(s):

Serum Amyloid A ◽

Serum Amyloid ◽

Amyloid A ◽

Experimental Induction ◽

Serum Amyloid A1

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Serum Amyloid A1/Toll-Like Receptor-4 Axis, an Important Link between Inflammation and Outcome of TBI Patients

Biomedicines ◽

10.3390/biomedicines9060599 ◽

2021 ◽

Vol 9 (6) ◽

pp. 599

Author(s):

Víctor Farré-Alins ◽

Alejandra Palomino-Antolín ◽

Paloma Narros-Fernández ◽

Ana Belen Lopez-Rodriguez ◽

Céline Decouty-Perez ◽

...

Keyword(s):

Injury Severity ◽

White Blood Cells ◽

Serum Amyloid ◽

Toll Like Receptor ◽

Toll Like Receptor 4 ◽

Important Link ◽

Tlr4 Mrna ◽

Serum Amyloid A1

Traumatic brain injury (TBI) is one of the leading causes of mortality and disability worldwide without any validated biomarker or set of biomarkers to help the diagnosis and evaluation of the evolution/prognosis of TBI patients. To achieve this aim, a deeper knowledge of the biochemical and pathophysiological processes triggered after the trauma is essential. Here, we identified the serum amyloid A1 protein-Toll-like receptor 4 (SAA1-TLR4) axis as an important link between inflammation and the outcome of TBI patients. Using serum and mRNA from white blood cells (WBC) of TBI patients, we found a positive correlation between serum SAA1 levels and injury severity, as well as with the 6-month outcome of TBI patients. SAA1 levels also correlate with the presence of TLR4 mRNA in WBC. In vitro, we found that SAA1 contributes to inflammation via TLR4 activation that releases inflammatory cytokines, which in turn increases SAA1 levels, establishing a positive proinflammatory loop. In vivo, post-TBI treatment with the TLR4-antagonist TAK242 reduces SAA1 levels, improves neurobehavioral outcome, and prevents blood–brain barrier disruption. Our data support further evaluation of (i) post-TBI treatment in the presence of TLR4 inhibition for limiting TBI-induced damage and (ii) SAA1-TLR4 as a biomarker of injury progression in TBI patients.

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Liraglutide reduces coronary endothelial cells no-reflow damage through activating MAPK/ERK signaling pathway

Journal of Receptors and Signal Transduction ◽

10.1080/10799893.2020.1833921 ◽

2020 ◽

pp. 1-5

Author(s):

Yi Chen ◽

Chen Liu ◽

Peng Zhou ◽

Jiannan Li ◽

Xiaoxiao Zhao ◽

...

Keyword(s):

Endothelial Cells ◽

Signaling Pathway ◽

Erk Signaling ◽

No Reflow ◽

Coronary Endothelial Cells

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A nanoscale fluorocarbon coating on PET surfaces improves the adhesion and growth of cultured coronary endothelial cells

Nanotechnology ◽

10.1088/0957-4484/19/27/275101 ◽

2008 ◽

Vol 19 (27) ◽

pp. 275101 ◽

Cited By ~ 6

Author(s):

S Pezzatini ◽

L Morbidelli ◽

R Gristina ◽

P Favia ◽

M Ziche

Keyword(s):

Endothelial Cells ◽

Coronary Endothelial Cells

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NEAT1/miR-140-3p/MAPK1 mediates the viability and survival of coronary endothelial cells and affects coronary atherosclerotic heart disease

Acta Biochimica et Biophysica Sinica ◽

10.1093/abbs/gmaa087 ◽

2020 ◽

Vol 52 (9) ◽

pp. 967-974

Author(s):

Hui Zhang ◽

Ningning Ji ◽

Xinyan Gong ◽

Shimao Ni ◽

Yu Wang

Keyword(s):

Cell Proliferation ◽

Endothelial Cells ◽

Heart Disease ◽

Cell Viability ◽

Mitogen Activated Protein Kinase ◽

Expression Level ◽

Luciferase Reporter ◽

Coronary Endothelial Cells ◽

Induced Apoptosis ◽

Lncrna Neat1

Abstract Studies have shown that long non-coding RNAs (lncRNA) play critical roles in coronary atherosclerotic heart disease (CAD). However, the function of lncRNA nuclear enriched abundant transcript 1 (NEAT1) in CAD is unclear. In this study, we aimed to investigate the functions of lncRNA NEAT1 in CAD. RT-PCR and western blot analysis were carried out to examine the expressions of related RNAs. Colony formation assay, cell proliferation assay, apoptosis assay, and dual-luciferase reporter assay were conducted to investigate the abilities of colony migration, cell proliferation, apoptosis, and targeting. The results showed that NEAT1 was up-regulated in CAD blood samples and in human coronary endothelial cells (HCAECs). Transfection of pcNEAT1 significantly inhibited the survival rate of HCAECs and induced apoptosis of HCAECs. MiR-140-3p was down-regulated in HCAECs. NEAT1 directly targeted miR-140-3p, and the expression of miR-140-3p was inversely correlated with the expression of NEAT1 in CAD patients. In addition, co-transfection of NEAT1 with miR-140-3p mimic reversed the effect of pcNEAT1 on cell viability and apoptosis. mitogen-activated protein kinase 1 (MAPK1) was proved to be a target gene of miR-140-3p, and the miR-140-3p mimic was shown to reduce the expression of MAPK1 in HCAECs. pcNEAT1 significantly increased the expression level of MAPK1, while shNEAT1 significantly reduced the expression level of MAPK1. Our results revealed that lncRNA NEAT1 increased cell viability and inhibited CAD cell apoptosis possibly by activating the miR-140-3p/MAPK1 pathway, and lncRNA NEAT1 might serve as a potential therapeutic target for CAD.

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