scholarly journals The role of neutrophils in the pathogenesis of atherosclerosis

2018 ◽  
Vol 17 (6) ◽  
pp. 110-116
Author(s):  
Yu. V. Saranchina ◽  
S. V. Dutova ◽  
O. Yu. Kilina ◽  
N. V. Khanarin ◽  
T. S. Kulakova
Keyword(s):  
Clinical Symptoms ◽  
Protein Complexes ◽  
Endothelial Damage ◽  
Current Data ◽  
Vascular Endothelial ◽  
Coronary Syndrome ◽  
Physiological Processes ◽  
Atherosclerotic Lesions ◽  
Structure And Functions

Atherosclerosis (AS) is one of the causes of cardiovascular disease. The formation of atherosclerotic lesions of the arteries is a long process, and clinical symptoms appear already at the stage of atherosclerotic plaque (ASB), which prevents blood flow and can cause coronary heart disease, as well as acute coronary syndrome. The study of atherosclerosis mechanisms at the subclinical level is relevant. This article provides a summary of current data on the structure and functions of neutrophils (NF) in physiological processes. Particular attention is paid to the participation of neutrophils in the damage and formation of vascular endothelial dysfunction. Discusses several mechanisms of involvement of neutrophils in atherogenesis: the production of reactive oxygen species, which cause direct endothelial damage; the synthesis of cytokines that trigger the migration of leukocytes in inflammation; the formation of protein complexes with cholesterol, contributing to their deposition in the vessels, and neutrophil traps, triggering destructive-alterative reactions.

New insights into the role of imaging in polymyalgia rheumatica

Rheumatology ◽  
2020 ◽  
Author(s):  
Dario Camellino ◽  
Christina Duftner ◽  
Christian Dejaco
Keyword(s):  
Fdg Pet ◽  
Clinical Symptoms ◽  
Imaging Techniques ◽  
Diagnostic Value ◽  
Current Data ◽  
Acute Phase Reactants ◽  
Anatomical Basis ◽  
Positron Emission ◽  
Diagnostic Values

Abstract PMR is an inflammatory rheumatic disease of elderly people characterized by pain and stiffness in the neck, shoulder and pelvic girdles. No specific diagnostic confirmatory tests exist and clinical symptoms, as well as increased acute phase reactants, are unspecific. The diagnostic value of imaging including ultrasound, MRI and 18F-fluorodeoxyglucose positron emission tomography (FDG-PET) with/without CT for PMR is increasingly studied. These techniques, particularly FDG-PET/CT, may help to detect underlying GCA in PMR patients with an incomplete response to glucocorticoids and/or recurrent relapses. Recent imaging studies provide novel insights into the anatomical basis of inflammation in PMR, particularly at hip and spine, which may help to distinguish this disease from other mimicking conditions. In this review, we discuss novel insights into the pathoanatomy of PMR, compare the diagnostic values of different imaging techniques and summarize current data on the role of imaging for monitoring and outcome prediction.

scholarly journals Acute lung injury in TBI patients with SIRS: role of vascular endothelial damage

Critical Care ◽  
2010 ◽  
Vol 14 (Suppl 1) ◽  
pp. P191 ◽  
Author(s):  
T Saito ◽  
H Kushi ◽  
T Miki ◽  
J Sato ◽  
A Yoshino ◽  
...  
Keyword(s):  
Acute Lung Injury ◽  
Lung Injury ◽  
Endothelial Damage ◽  
Vascular Endothelial

scholarly journals Vascular Endothelial Damage: The Role of Syndecan-1 and Hyaluronan as Severity Indicators in COVID-19

2021 ◽  
Vol 2 (5) ◽  
Author(s):  
Azwar Anas ◽  
Arie Utariani ◽  
Bambang Pujo Semedi
Keyword(s):  
Distress Syndrome ◽  
Cell Damage ◽  
Organ Damage ◽  
Endothelial Damage ◽  
Vascular Endothelial ◽  
Vascular Integrity ◽  
Mural Cells ◽  
Coagulation Inhibitors ◽  
Hypoxic Respiratory Failure

SARS-CoV-2 was firstly found in bronchoalveloar lavage (BAL) of three suspected COVID-19 patients at Jinyintan Hospital, Wuhan, Hubei Province, China. The cases are still raisingwith2,12% global mortality rate. Hypoxic respiratory failure due to acute respiratory distress syndrome (ARDS) is the main cause of COVID-19 death. Endothelial cell damage has an important role in the pathogenesis of ARDS and multi-organ dysfuntion of COVID-19 patients. The endothelium is protected by mural cells, which keep vascular integrity. Inflammation is prevented by these cells by inhibiting the interaction of immune cells and platelets with endothelial cells. These cells also prevent coagulation by producing glycocalyx, coagulation inhibitors, and blood-clotting enzyme. Vascular glycocalyx has an important role to maintain endothelial function and is disrupted systemically in elderly and patients with various comorbidities, which can be a probable mechanism for the serious complications of COVID-19. Glycocalyx disruption in severe and critical COVID-19 patients causes increased levels of its components such assyndecan-1 and hyaluronan in the serum. Previous studies showed the significant increase ofsyndecan-1 and hyaluronan levels in septic, and severe Kawasaki and dengue patients. These biomarkers are also markers of organ damage. Therefore, hyaluronan and syndecan-1can be significant prognostic factors for morbidity and survival in patients with COVID-19.

The Role of microRNAs Identified in the Amniotic Fluid

MicroRNA ◽  
2019 ◽  
Vol 9 (1) ◽  
pp. 8-16 ◽  
Author(s):  
Fasoulakis Zacharias ◽  
Theodora Marianna ◽  
Tsirkas Ioannis ◽  
Tsirka Theodora ◽  
Kalagasidou Sofia ◽  
...  
Keyword(s):  
Amniotic Fluid ◽  
Fetal Development ◽  
Current Knowledge ◽  
Current Data ◽  
Adverse Outcomes ◽  
Many Body ◽  
Kidney Fibrosis ◽  
Physiological Processes ◽  
Fetal Nutrition

Aim:The study aimed to provide an overall view of current data considering the presence of microRNAs in amniotic fluid.Methods:The available literature in MEDLINE, regarding the role of the amniotic fluid in pregnancy and fetal development, was searched for related articles including terms such as “microRNA”, “Amniotic fluid”, “Adverse outcome” and others.Results:The amniotic fluid has an undoubtedly significant part in fetal nutrition, with a protecting and thermoregulatory role alongside. MicroRNAs have proven to be highly expressed during pregnancy in many body liquids including amniotic fluid and are transferred between cells loaded in exosomes, while they are also implicated in many processes during fetal development and could be potential biomarkers for early prediction of adverse outcomes.Conclusion:Current knowledge reveals that amniotic fluid microRNAs participate in many developmental and physiological processes of pregnancy including proliferation of fibroblasts, fetal development, angiogenesis, cardioprotection, activation of signaling pathways, differentiation and cell motility, while the expression profile of specific microRNAs has a potential prognostic role in the prediction of Down syndrome, congenital hydronephrosis and kidney fibrosis.

scholarly journals Insight into the Key Points of Preeclampsia Pathophysiology: Uterine Artery Remodeling and the Role of MicroRNAs

2021 ◽  
Vol 22 (6) ◽  
pp. 3132
Author(s):  
Katarzyna Pankiewicz ◽  
Anna Fijałkowska ◽  
Tadeusz Issat ◽  
Tomasz M. Maciejewski
Keyword(s):  
Uterine Artery ◽  
Clinical Symptoms ◽  
Multiorgan Failure ◽  
Endothelial Damage ◽  
Disease Stage ◽  
Stage Model ◽  
Two Stage ◽  
Placental Perfusion ◽  
Artery Remodeling

Preeclampsia affects about 3–8% of all pregnancies. It represents a complex and multifaceted syndrome with at least several potential pathways leading to the development of disease. The main dogma in preeclampsia is the two-stage model of disease. Stage 1 (placental stage) takes place in early pregnancy and is thought to be impaired placentation due to inadequate trophoblastic invasion of the maternal spiral arteries that leads to reduced placental perfusion and release of numerous biological factors causing endothelial damage and development of acute maternal syndrome with systemic multiorgan failure (stage 2—the onset of maternal clinical symptoms, maternal stage). Recently, in the light of the vast body of evidence, two-stage model of preeclampsia has been updated with a few novel pathways leading to clinical manifestation in the second part of pregnancy. This paper reviews current state of knowledge about pathophysiology of preeclampsia and places particular focus on the recent advances in understanding of uterine artery remodeling alterations, as well as the role of microRNAs in preeclampsia.

scholarly journals The Protective Effect of Dabigatran and Rivaroxaban on DNA Oxidative Changes in a Model of Vascular Endothelial Damage with Oxidized Cholesterol

2020 ◽  
Vol 21 (6) ◽  
pp. 1953 ◽  
Author(s):  
Ewelina Woźniak ◽  
Marlena Broncel ◽  
Bożena Bukowska ◽  
Paulina Gorzelak-Pabiś
Keyword(s):  
Oxidative Damage ◽  
Oxidative Dna Damage ◽  
Vascular Endothelial Cells ◽  
Endothelial Damage ◽  
Vascular Endothelial ◽  
Coronary Syndrome ◽  
Oxidized Cholesterol ◽  
Endonuclease Iii ◽  
Single Strand Breaks ◽  
Repairing Effect

Background: Atherosclerotic plaques are unstable, and their release may result in thrombosis; therefore, currently, antiplatelet therapy with anticoagulants is recommended for the treatment of acute coronary syndrome. The aim of this study was to assess the effect of oxidized cholesterol on human umbilical vascular endothelial cells (HUVECs). The study also examines the protective and repairing effect of dabigatran and rivaroxaban in a model of vascular endothelial damage with 25-hydroxycholesterol (25-OHC). Methods: HUVECs were treated with compounds induce DNA single-strand breaks (SSBs) using the comet assay. Oxidative DNA damage was detected using endonuclease III (Nth) or human 8 oxoguanine DNA glycosylase (hOOG1). Reactive oxygen species (ROS) formation was determined using flow cytometry. Results: 25-hydroxycholesterol caused DNA SSBs, induced oxidative damage and increased ROS in the HUVECs; ROS level was lowered by dabigatran and rivaroxaban. Only dabigatran was able to completely repair the DNA SSBs induced by oxysterol. Dabigatran was able to reduce the level of oxidative damage of pyrimidines induced by oxysterol to the level of control cells. Conclusions: Observed changes strongly suggest that the tested anticoagulants induced indirect repair of DNA by inhibiting ROS production. Furthermore, dabigatran appears to have a higher antioxidant activity than rivaroxaban.

scholarly journals Exosomes: Future Perspective in Neurodegenerative Diseases

2020 ◽  
Vol 6 (4) ◽  
pp. 251-258
Author(s):  
Leila Alidoust ◽  
◽  
Adele Jafari ◽  
Keyword(s):  
Neurodegenerative Diseases ◽  
Future Perspective ◽  
Therapeutic Tool ◽  
Irreversible Loss ◽  
Physiological Processes ◽  
Potential Applications ◽  
And Function ◽  
The Brain ◽  
Structure And Functions

Neurodegeneration is a progressive and irreversible loss of neuronal cells in specific regions of the brain. Alzheimer Diseases (AD) Parkinson Disease (PD) are the most common forms of neurodegenerative diseases in older people. Exosomes are extracellular nanovesicles that have a key role in physiological processes such as intercellular communication, cell migration, angiogenesis, and anti-tumor immunity. Mounting evidence indicates the role of exosomes in neurodegenerative disorders as possible carriers of disease particles. They have several different potential applications thanks to their unique structure and functions. The present review summarizes recent studies on exosome potentials as a biomarker and therapeutic tool in neurodegenerative diseases. It also provides an overview of the structure and function of exosomes.

scholarly journals MECHANISMS OF ATHEROGENESIS AND ITS INTENSIFICATION IN PATIENTS WITH RHEUMATOID ARTHRITIS

2020 ◽  
pp. 8-24
Author(s):  
V. K. Kazymyrko ◽  
L. N. Ivanitska ◽  
T. S. Silantyeva ◽  
A. G. Dubkova ◽  
V. V. Kutovoy
Keyword(s):  
Immune Complexes ◽  
Protein Complexes ◽  
Cell Damage ◽  
Cholesterol Crystals ◽  
Atherosclerotic Lesions ◽  
Arterial Lesions ◽  
Tnf Α ◽  
Traditional Risk Factors ◽  
Mechanisms Of Development

The article describes the role of cholesterol crystals (CS) in the mechanisms of development in the inner lining of arteries of inflammation – granulomatosis, induced by foreign bodies. The smallest CS crystals are found already in early atherosclerotic lesions. They are a factor in the initiation and exacerbation of atherosclerosis (At), cause cell damage and apoptosis. The formation of crystals within the necrotic nuclei of plaques can lead to an increase in their volume and to rupture. It has been shown that damage to the membranes of macrophages phagolysosomes by absorbed CS crystals leads to the inclusion of protein complexes – inflammasomes – in the inflammatory process, which trigger the inflammatory signaling cascade and are responsible for the secretion of pro-inflammatory cytokines. Inflammasomes NLRP3 are necessary for the process of atherogenesis; their activation is a link between the metabolism of cholesterol and inflammation involving macrophages. Unlike At, RA is manifested by autoimmune inflammation and immunocomplex vasculitis. When these diseases are combined, the effects of proinflammatory cytokines add up, an increase in the severity of inflammation, increased tissue damage and progression of atherosclerotic arterial lesions. The accelerated development of At in RA patients is facilitated by a combination of the action of traditional risk factors for atherogenesis and damage to the walls (endothelium) of arteries by immune complexes, complement, neutrophils and lymphocytes with an increase in their permeability to the lipid factor. The deposition of immune complexes in the capillaries of plaques leads to damage to their walls, destabilization of plaques and the development of acute cardiovascular events. The intensification of lipid accumulation and inflammation in the plaques of RA patients is confirmed in the section. Anticytokine drugs, primarily TNF-α and IL-1β antagonists, are pathogenetically substantiated agents for the progression of At in patients with RA. Statins remain a widely used class of drugs. They, in addition to hypolipidemic, immunomodulatory and anti-inflammatory effects, affect the crystallization of cholesterol, dissolve crystals and stabilize plaques.

The distribution and expression of vascular endothelial growth factor A (VEGFA) during follicular development and atresia in the pig

2020 ◽  
Vol 32 (3) ◽  
pp. 259 ◽  
Author(s):  
Xiaomeng Gao ◽  
Jinbi Zhang ◽  
Zengxiang Pan ◽  
Qifa Li ◽  
Honglin Liu
Keyword(s):  
Vascular Endothelial Growth Factor ◽  
Growth Factor ◽  
Granulosa Cells ◽  
Molecular Level ◽  
Follicular Development ◽  
Vascular Endothelial ◽  
Antral Follicles ◽  
Physiological Processes ◽  
Endothelial Growth Factor

The involvement of vascular endothelial growth factor A (VEGFA) in ovarian physiological processes has been widely reported, but the location and role of VEGFA during follicular atresia remain unknown. This study investigated the distribution and expression of VEGFA during porcine follicular development and atresia. Pig ovaries were obtained, individual medium-sized (3–5mm in diameter) antral follicles were separated and classified into healthy, early atretic or progressively atretic groups. Immunobiology and quantitative techniques were used to investigate the varied follicular distribution of VEGFA at both the morphological and molecular level. The results indicated that VEGFA protein expression peaked in tertiary follicles, mostly distributed in the thecal and inner granulosa layers, during follicular development while VEGFA mRNA was mainly expressed in the inner granulosa layers. Additionally, healthy antral follicles showed a significantly higher expression of VEGFA than atretic follicles in both theca and granulosa cells. Knockdown of VEGFA using siRNA revealed an antiapoptosis effect of VEGFA in cultured pig granulosa cells. Our results increase the knowledge of VEGFA functions in follicles.

scholarly journals Hyperthrombotic Milieu in COVID-19 Patients

Cells ◽  
2020 ◽  
Vol 9 (11) ◽  
pp. 2392
Author(s):  
Mohamed Hassan Kamel ◽  
Wenqing Yin ◽  
Chris Zavaro ◽  
Jean M. Francis ◽  
Vipul C. Chitalia
Keyword(s):  
Cell Damage ◽  
Anticoagulation Therapy ◽  
Endothelial Damage ◽  
Coagulation Cascade ◽  
Thromboembolic Events ◽  
Coronary Syndrome ◽  
Venous Thromboembolic Events ◽  
Venous Thromboembolic ◽  
Systemic Manifestations

COVID-19 infection has protean systemic manifestations. Experience from previous coronavirus outbreaks, including the current SARS-CoV-2, has shown an augmented risk of thrombosis of both macrovasculature and microvasculature. The former involves both arterial and venous beds manifesting as stroke, acute coronary syndrome and venous thromboembolic events. The microvascular thrombosis is an underappreciated complication of SARS-CoV-2 infection with profound implications on the development of multisystem organ failure. The telltale signs of perpetual on-going coagulation and fibrinolytic cascades underscore the presence of diffuse endothelial damage in the patients with COVID-19. These parameters serve as strong predictors of mortality. While summarizing the alterations of various components of thrombosis in patients with COVID-19, this review points to the emerging evidence that implicates the prominent role of the extrinsic coagulation cascade in COVID-19-related coagulopathy. These mechanisms are triggered by widespread endothelial cell damage (endotheliopathy), the dominant driver of macro- and micro-vascular thrombosis in these patients. We also summarize other mediators of thrombosis, clinically relevant nuances such as the occurrence of thromboembolic events despite thromboprophylaxis (breakthrough thrombosis), current understanding of systemic anticoagulation therapy and its risk–benefit ratio. We conclude by emphasizing a need to probe COVID-19-specific mechanisms of thrombosis to develop better risk markers and safer therapeutic targets.

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