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Article ; Online: Significance of sphingosine-1-phosphate in cardiovascular physiology and pathology.

Jozefczuk, E / Guzik, T J / Siedlinski, M

2020 Volume 156, Page(s) 104793

Abstract: Sphingosine-1-phosphate (S1P) is a signaling lipid, synthetized by sphingosine kinases (SPHK1 and SPHK2), that affects cardiovascular function in various ways. S1P signaling is complex, particularly since its molecular action is reliant on the ... ...

Abstract	Sphingosine-1-phosphate (S1P) is a signaling lipid, synthetized by sphingosine kinases (SPHK1 and SPHK2), that affects cardiovascular function in various ways. S1P signaling is complex, particularly since its molecular action is reliant on the differential expression of its receptors (S1PR1, S1PR2, S1PR3, S1PR4, S1PR5) within various tissues. Significance of this sphingolipid is manifested early in vertebrate development as certain defects in S1P signaling result in embryonic lethality due to defective vasculo- or cardiogenesis. Similar in the mature organism, S1P orchestrates both physiological and pathological processes occurring in the heart and vasculature of higher eukaryotes. S1P regulates cell fate, vascular tone, endothelial function and integrity as well as lymphocyte trafficking, thus disbalance in its production and signaling has been linked with development of such pathologies as arterial hypertension, atherosclerosis, endothelial dysfunction and aberrant angiogenesis. Number of signaling mechanisms are critical - from endothelial nitric oxide synthase through STAT3, MAPK and Akt pathways to HDL particles involved in redox and inflammatory balance. Moreover, S1P controls both acute cardiac responses (cardiac inotropy and chronotropy), as well as chronic processes (such as apoptosis and hypertrophy), hence numerous studies demonstrate significance of S1P in the pathogenesis of hypertrophic/fibrotic heart disease, myocardial infarction and heart failure. This review presents current knowledge concerning the role of S1P in the cardiovascular system, as well as potential therapeutic approaches to target S1P signaling in cardiovascular diseases.
MeSH term(s)	Animals ; Cardiovascular Diseases/metabolism ; Cardiovascular Diseases/pathology ; Cardiovascular Diseases/physiopathology ; Cardiovascular System/embryology ; Cardiovascular System/metabolism ; Cardiovascular System/physiopathology ; Embryonic Development ; Hemodynamics ; Humans ; Lysophospholipids/metabolism ; Neovascularization, Physiologic ; Receptors, Lysosphingolipid/metabolism ; Signal Transduction ; Sphingosine/analogs & derivatives ; Sphingosine/metabolism
Chemical Substances	Lysophospholipids ; Receptors, Lysosphingolipid ; sphingosine 1-phosphate (26993-30-6) ; Sphingosine (NGZ37HRE42)
Language	English
Publishing date	2020-04-08
Publishing country	Netherlands
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	1003347-6
ISSN	1096-1186 ; 0031-6989 ; 1043-6618
ISSN (online)	1096-1186
ISSN	0031-6989 ; 1043-6618
DOI	10.1016/j.phrs.2020.104793
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Article ; Online: Acute daily exposure to ambient air pollution impairs endothelium-dependent vasodilator responses in young, healthy individuals.

Jasiewicz-Honkisz, B / Osmenda, G / Wilk, G / Urbanski, K / Luc, K / Guzik, B / Mikołajczyk, T P / Guzik, T J

Journal of physiology and pharmacology : an official journal of the Polish Physiological Society

2023 Volume 74, Issue 4

Abstract: Exposure to ambient air pollution influences cardiovascular (CV) morbidity and mortality. The differential effects of changing particulate or gaseous air pollution on endothelial function in young healthy individuals remain unclear. The aim of this study ...

Abstract	Exposure to ambient air pollution influences cardiovascular (CV) morbidity and mortality. The differential effects of changing particulate or gaseous air pollution on endothelial function in young healthy individuals remain unclear. The aim of this study was to evaluate the relationships between exposures to different pollutants and vascular function in a group of 39 young (33±11 years old) subjects with low CV risk. Flow-mediated dilatation (FMD) and nitroglycerin-mediated dilatation (NMD) were performed, when air pollution reached highest levels (heating period) and repeated in a subgroup of 18 participants a few months later (just before the heating period starts). Daily mean concentrations of PM2.5 and PM10 were inversely correlated with FMD, and this relationship remained significant after adjusting for factors known to affect vascular dysfunction. Endothelial function did not differ between the two time points studied. However, we observed a strong inverse association between the change in the concentration of particulate matter (deltaPM2.5 and deltaPM10) and the change in FMD (deltaFMD) between the two visits (R= -0.65, p= 0.02; R= -0.64, p= 0.02, respectively). In summary, we provide evidence that the concentration of PM2.5 and PM10, but not SO
MeSH term(s)	Humans ; Young Adult ; Adult ; Air Pollutants/adverse effects ; Air Pollutants/analysis ; Endothelium-Dependent Relaxing Factors ; Vasodilator Agents ; Air Pollution/adverse effects ; Air Pollution/analysis ; Particulate Matter/adverse effects ; Particulate Matter/analysis
Chemical Substances	Air Pollutants ; Endothelium-Dependent Relaxing Factors ; Vasodilator Agents ; Particulate Matter
Language	English
Publishing date	2023-10-16
Publishing country	Poland
Document type	Journal Article
ZDB-ID	1125221-2
ISSN	1899-1505 ; 0867-5910 ; 0044-6033
ISSN (online)	1899-1505
ISSN	0867-5910 ; 0044-6033
DOI	10.26402/jpp.2023.4.03
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Article ; Online: Oxidative stress and inflammatory markers in prediabetes and diabetes.

Luc, K / Schramm-Luc, A / Guzik, T J / Mikolajczyk, T P

Journal of physiology and pharmacology : an official journal of the Polish Physiological Society

2020 Volume 70, Issue 6

Abstract: Prediabetes is a state of elevated plasma glucose in which the threshold for diabetes has not yet been reached and can predispose to the development of type 2 diabetes and cardiovascular diseases. Insulin resistance and impaired beta-cell function are ... ...

Abstract	Prediabetes is a state of elevated plasma glucose in which the threshold for diabetes has not yet been reached and can predispose to the development of type 2 diabetes and cardiovascular diseases. Insulin resistance and impaired beta-cell function are often already present in prediabetes. Hyperglycemia can upregulate markers of chronic inflammation and contribute to increased reactive oxygen species (ROS) generation, which ultimately cause vascular dysfunction. Conversely, increased oxidative stress and inflammation can lead to insulin resistance and impaired insulin secretion. Proper treatment of hyperglycemia and inhibition of ROS overproduction is crucial for delaying onset of diabetes and for prevention of cardiovascular complications. Thus, it is imperative to determine the mechanisms involved in the progression from prediabetes to diabetes including a clarification of how old and new medications affect oxidative and immune mechanisms of diabetes. In this review, we discuss the relationship between oxidative stress and hyperglycemia along with links between inflammation and prediabetes. Additionally, the effects of hyperglycemic memory, microvesicles, micro-RNA, and epigenetic regulation on inflammation, oxidative state, and glycemic control are highlighted. Adipose tissue and their influence on chronic inflammation are also briefly reviewed. Finally, the role of immune-targeted therapies and anti-diabetic medication on glycemic control and oxidative stress are discussed.
MeSH term(s)	Animals ; Biomarkers/metabolism ; Blood Glucose/metabolism ; Cardiovascular Diseases/etiology ; Diabetes Mellitus, Type 2/physiopathology ; Epigenesis, Genetic ; Humans ; Hyperglycemia/physiopathology ; Inflammation/physiopathology ; Insulin Resistance ; Oxidative Stress/physiology ; Prediabetic State/physiopathology ; Reactive Oxygen Species/metabolism
Chemical Substances	Biomarkers ; Blood Glucose ; Reactive Oxygen Species
Language	English
Publishing date	2020-02-19
Publishing country	Poland
Document type	Journal Article ; Review
ZDB-ID	1125221-2
ISSN	1899-1505 ; 0867-5910 ; 0044-6033
ISSN (online)	1899-1505
ISSN	0867-5910 ; 0044-6033
DOI	10.26402/jpp.2019.6.01
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Article ; Online: Nox1/4 inhibition exacerbates age dependent perivascular inflammation and fibrosis in a model of spontaneous hypertension.

Nosalski, R / Mikolajczyk, T / Siedlinski, M / Saju, B / Koziol, J / Maffia, P / Guzik, T J

Pharmacological research

2020 Volume 161, Page(s) 105235

Abstract: Hypertension is associated with oxidative stress and perivascular inflammation, critical contributors to perivascular fibrosis and accelerated vascular ageing. Oxidative stress can promote vascular inflammation, creating options for potential use of ... ...

Abstract	Hypertension is associated with oxidative stress and perivascular inflammation, critical contributors to perivascular fibrosis and accelerated vascular ageing. Oxidative stress can promote vascular inflammation, creating options for potential use of NADPH oxidase inhibitors in pharmacological targeting of perivascular inflammation and its consequences. Accordingly, we characterized age-related changes in oxidative stress and immune cell infiltration in normotensive (WKY) and spontaneously hypertensive rats (SHRs). Subsequently, we used pharmacological inhibitors of Nox1 (ML171) and Nox1/Nox4 (GKT137831; 60 mg/kg), to modulate NADPH oxidase activity at the early stage of spontaneous hypertension and investigated their effects on perivascular inflammation and fibrosis. RESULTS: Ageing was associated with a progressive increase of blood pressure as well as an elevation of the total number of leukocytes, macrophages and NK cells infiltrating perivascular adipose tissue (PVAT) in SHRs but not in WKY. At 1 month of age, when blood pressure was not yet different, only perivascular NK cells were significantly higher in SHR. Spontaneous hypertension was also accompanied by the higher perivascular T cell accumulation, although this increase was age independent. Aortic Nox1 and Nox2 mRNA expression increased with age only in SHR but not in WKY, while age-related increase of Nox4 mRNA in the vessels has been observed in both groups, it was more pronounced in SHRs. At early stage of hypertension (3-months) the most pronounced differences were observed in Nox1 and Nox4. Surprisingly, GKT137831, dual inhibitor of Nox1/4, therapy increased both blood pressure and perivascular macrophage infiltration. Mechanistically, this was linked to increased expression of proinflammatory chemokines expression (CCL2 and CCL5) in PVAT. This inflammatory response translated to increased perivascular fibrosis. This effect was likely Nox4 dependent as the Nox1 inhibitor ML171 did not affect the development of spontaneous hypertension, perivascular macrophage accumulation, chemokine expression nor adventitial collagen deposition. In summary, spontaneous hypertension promotes ageing-associated perivascular inflammation which is exacerbated by Nox4 but not Nox1 pharmacological inhibition.
MeSH term(s)	Adipose Tissue/drug effects ; Adipose Tissue/enzymology ; Adipose Tissue/immunology ; Adipose Tissue/pathology ; Age Factors ; Animals ; Aorta/drug effects ; Aorta/enzymology ; Aorta/immunology ; Aorta/pathology ; Blood Pressure ; Disease Models, Animal ; Enzyme Inhibitors/toxicity ; Fibrosis ; Hypertension/complications ; Hypertension/physiopathology ; Inflammation Mediators/metabolism ; Killer Cells, Natural/drug effects ; Killer Cells, Natural/immunology ; Killer Cells, Natural/metabolism ; Macrophages/drug effects ; Macrophages/immunology ; Macrophages/metabolism ; Male ; NADPH Oxidase 1/antagonists & inhibitors ; NADPH Oxidase 1/metabolism ; NADPH Oxidase 4/antagonists & inhibitors ; NADPH Oxidase 4/metabolism ; Pyrazolones/toxicity ; Pyridones/toxicity ; Rats, Inbred SHR ; Rats, Inbred WKY ; Signal Transduction ; T-Lymphocytes/drug effects ; T-Lymphocytes/immunology ; T-Lymphocytes/metabolism ; Vasculitis/chemically induced ; Vasculitis/enzymology ; Vasculitis/immunology ; Vasculitis/pathology
Chemical Substances	Enzyme Inhibitors ; Inflammation Mediators ; Pyrazolones ; Pyridones ; setanaxib (45II35329V) ; NADPH Oxidase 1 (EC 1.6.3.-) ; NADPH Oxidase 4 (EC 1.6.3.-) ; NOX1 protein, rat (EC 1.6.3.-) ; Nox4 protein, rat (EC 1.6.3.-)
Language	English
Publishing date	2020-10-22
Publishing country	Netherlands
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	1003347-6
ISSN	1096-1186 ; 0031-6989 ; 1043-6618
ISSN (online)	1096-1186
ISSN	0031-6989 ; 1043-6618
DOI	10.1016/j.phrs.2020.105235
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Article ; Online: Is systemic inflammation a missing link between periodontitis and hypertension? Results from two large population-based surveys.

Muñoz Aguilera, E / Leira, Y / Miró Catalina, Q / Orlandi, M / Czesnikiewicz-Guzik, M / Guzik, T J / Hingorani, A D / Nart, J / D'Aiuto, F

Journal of internal medicine

2020 Volume 289, Issue 4, Page(s) 532–546

Abstract: Objective: The primary objective was to investigate the relationship between periodontitis and hypertension in two independent large surveys. The secondary objective was to ascertain whether systemic inflammation had a mediation effect in the ... ...

Abstract	Objective: The primary objective was to investigate the relationship between periodontitis and hypertension in two independent large surveys. The secondary objective was to ascertain whether systemic inflammation had a mediation effect in the association. Methods: This cross-sectional study analysed representative samples of the US (n = 3460; NHANES 2009/10) and Korean (n = 4539; 2015 KNHANES VI-3) populations. The association between periodontitis (exposure), hypertension (outcome) and inflammatory markers [C-reactive protein (CRP) and white blood cell counts (WBC)] (mediators) was assessed using multivariate linear and logistic regression models and mediation analysis. Results: Participants with periodontitis were more likely to have hypertension (NHANES: OR = 1.3, 95% CI: 1.0-1.6, P = 0.025; KNHANES: OR = 1.2, 95% CI: 1.0-1.4, P = 0.041) and actual systolic blood pressure ≥ 140 mmHg (NHANES: OR = 1.6, 95% CI: 1.1-2.3, P < 0.001; KNHANES: OR = 1.3, 95% CI :1.0-1.6, P < 0.031) than those without the disease. These associations were independent of age, gender, BMI, education level, smoking, alcohol consumption, creatinine, physical activity, presence of other comorbidities and confirmed in participants not taking antihypertensive medications. Diagnosis of periodontitis was directly associated with WBC (in both surveys: NHANES: β ± SE = 0.3 ± 0.1, P < 0.004; KNHANES: β ± SE = 0.3 ± 0.1, P < 0.001) and with CRP levels (in one survey: NHANES: β ± SE = 0.1 ± 0.03, P < 0.007; KNHANES: β ± SE = 0.1 ± 0.04, P > 0.213). Mediation analyses confirmed that CRP acted as a mediator in the association between periodontitis and hypertension in both populations (mediated effect: NHANES: β ± SE = 0.010 ± 0.003, P < 0.001; KNHANES: β ± SE = 0.003 ± 0.001, P = 0.015). WBC acted as a mediator in the KNHANES (mediated effect: β ± SE = 0.004 ± 0.001, P = 0.004) whilst in the NHANES, its effect was dependent of CRP inclusion in the model (mediated effect WBC + CRP: β ± SE = 0.002 ± 0.001, P = 0.001). Conclusions: These findings suggest that periodontitis is closely linked to hypertension and systemic inflammation is, in part, a mediator of this association.
MeSH term(s)	C-Reactive Protein/analysis ; Cross-Sectional Studies ; Humans ; Hypertension/epidemiology ; Inflammation/epidemiology ; Nutrition Surveys ; Periodontitis/epidemiology ; Republic of Korea/epidemiology ; United States/epidemiology
Chemical Substances	C-Reactive Protein (9007-41-4)
Language	English
Publishing date	2020-11-19
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	96274-0
ISSN	1365-2796 ; 0954-6820
ISSN (online)	1365-2796
ISSN	0954-6820
DOI	10.1111/joim.13180
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Article ; Online: Effects of controlled physical activity on immune cell phenotype in peripheral blood in prehypertension - studies in preclinical model and randomised crossover study.

Mazur, M / Glodzik, J / Szczepaniak, P / Nosalski, R / Siedlinski, M / Skiba, D / Rewiuk, K / Salakowski, A / Czesnikiewicz-Guzik, M / Grodzicki, T / Guzik, T J / Mikolajczyk, T P

Journal of physiology and pharmacology : an official journal of the Polish Physiological Society

2019 Volume 69, Issue 6

Abstract: Hypertension (HT) is a global public health issue. There are many behavioural risk factors including unhealthy diet, tobacco use and alcohol consumption as well physical inactivity that contribute to the development of high blood pressure (BP) and its ... ...

Abstract	Hypertension (HT) is a global public health issue. There are many behavioural risk factors including unhealthy diet, tobacco use and alcohol consumption as well physical inactivity that contribute to the development of high blood pressure (BP) and its complications. Favourable effect of regular physical activity on treatment or prevention of hypertension by improvement of endothelial function is widely accepted however little is known about its relationship with immune system. Thus, the aim of this study was to assess the role of moderate regular physical activity on immune cell phenotype. T cell and monocyte subsets were characterised in 31 subjects with prehypertension (130 - 139 mmHg systolic and 85 - 89 mmHg diastolic blood pressure) who participated in moderate training (3 times/week) on cyclometers for 3 months in crossover study design. Complementary study was performed in murine model of Ang II-induced hypertension and ten-week-old animals were trained on a treadmill (5 times/week, 1 hour) for 2 weeks before and 1.5 weeks after minipumps implantation. In the context of elevated blood pressure regular physical activity had modest influence on immune cell phenotype. Both in human study and murine model we did not observe effects of applied exercise that can explain the mechanism of BP reduction after short-term regular training. Twelve-weeks regular training did not affect the activation status of T lymphocytes measured as expression of CD69, CD25 and CCR5 in human study. Physical activity resulted in higher expression of adhesion molecule CD11c on CD16+ monocytes (especially CD14 high) without any changes in leukocytes subpopulation counts. Similar results were observed in murine model of hypertension after the training. However the training caused significant decrease of CCR5 and CD25 expressions (measured as a mean fluorescence intensity) on CD8+ T cells infiltrating perivascular adipose tissue. Our studies show modest regulatory influence of moderate training on inflammatory markers in prehypertensive subjects and murine model of Ang II induced hypertension.
MeSH term(s)	Adult ; Animals ; Antigens, CD/immunology ; Biomarkers/metabolism ; Blood Pressure/immunology ; Blood Pressure/physiology ; Cross-Over Studies ; Disease Models, Animal ; Exercise/physiology ; Exercise Test/methods ; Female ; Humans ; Hypertension/immunology ; Hypertension/physiopathology ; Inflammation/immunology ; Inflammation/metabolism ; Inflammation/physiopathology ; Male ; Mice ; Mice, Inbred C57BL ; Monocytes/immunology ; Monocytes/metabolism ; Monocytes/physiology ; Phenotype ; Prehypertension/immunology ; Prehypertension/physiopathology ; T-Lymphocytes/immunology ; T-Lymphocytes/metabolism ; T-Lymphocytes/physiology
Chemical Substances	Antigens, CD ; Biomarkers
Language	English
Publishing date	2019-03-18
Publishing country	Poland
Document type	Journal Article
ZDB-ID	1125221-2
ISSN	1899-1505 ; 0867-5910 ; 0044-6033
ISSN (online)	1899-1505
ISSN	0867-5910 ; 0044-6033
DOI	10.26402/jpp.2018.6.12
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Article: Mechanisms of superoxide production in human blood vessels: relationship to endothelial dysfunction, clinical and genetic risk factors.

Channon, K M / Guzik, T J

Journal of physiology and pharmacology : an official journal of the Polish Physiological Society

2003 Volume 53, Issue 4 Pt 1, Page(s) 515–524

Abstract: Common vascular disease states including diabetes, hypertension and atherosclerosis are associated with endothelial dysfunction, characterised by reduced bioactivity of nitric oxide (NO). Loss of the vasculoprotective effects of NO contributes to disease ...

Abstract	Common vascular disease states including diabetes, hypertension and atherosclerosis are associated with endothelial dysfunction, characterised by reduced bioactivity of nitric oxide (NO). Loss of the vasculoprotective effects of NO contributes to disease progression, but the mechanisms underlying endothelial dysfunction remain unclear. Increased superoxide production in animal models of vascular disease contributes to reduced NO bioavailability, endothelial dysfunction and oxidative stress. In human blood vessels, the NAD(P)H oxidase system is the principal source of superoxide, and is functionally related to clinical risk factors and systemic endothelial dysfunction. Furthermore, the C242T polymorphism in the NAD(P)H oxidase p22phox subunit is associated with significantly reduced superoxide production in patients carrying the 242T allele, suggesting a role for genetic variation in modulating vascular superoxide production. In vessels from patients with diabetes mellitus, endothelial dysfunction, NAD(P)H oxidase activity and protein subunits are significantly increased compared with matched non-diabetic vessels. Furthermore, the vascular endothelium in diabetic vessels is a net source of superoxide rather than NO production, due to dysfunction of endothelial NO synthase (eNOS). This deficit is dependent on the eNOS cofactor, tetrahydrobiopterin, and is in part mediated by protein kinase C signalling. These studies suggest an important role for both the NAD(P)H oxidases and endothelial NOS in the increased vascular superoxide production and endothelial dysfunction in human vascular disease states.
MeSH term(s)	Alleles ; Arteriosclerosis/physiopathology ; Biopterins/analogs & derivatives ; Biopterins/metabolism ; Blood Vessels/metabolism ; Endothelium, Vascular/physiopathology ; Genetic Predisposition to Disease ; Humans ; Membrane Transport Proteins ; NADPH Dehydrogenase/genetics ; NADPH Oxidases ; Nitric Oxide Synthase/metabolism ; Nitric Oxide Synthase Type III ; Phosphoproteins/genetics ; Polymorphism, Genetic ; Superoxides/metabolism ; Vascular Diseases/etiology ; Vascular Diseases/physiopathology
Chemical Substances	Membrane Transport Proteins ; Phosphoproteins ; Superoxides (11062-77-4) ; Biopterins ; NOS3 protein, human (EC 1.14.13.39) ; Nitric Oxide Synthase (EC 1.14.13.39) ; Nitric Oxide Synthase Type III (EC 1.14.13.39) ; NADPH Oxidases (EC 1.6.3.-) ; CYBA protein, human (EC 1.6.3.1) ; NADPH Dehydrogenase (EC 1.6.99.1) ; sapropterin (EGX657432I)
Language	English
Publishing date	2003-01-02
Publishing country	Poland
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	1125221-2
ISSN	1899-1505 ; 0867-5910 ; 0044-6033
ISSN (online)	1899-1505
ISSN	0867-5910 ; 0044-6033
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Article ; Online: Heterogeneity of peripheral blood monocytes, endothelial dysfunction and subclinical atherosclerosis in patients with systemic lupus erythematosus.

Mikołajczyk, T P / Osmenda, G / Batko, B / Wilk, G / Krezelok, M / Skiba, D / Sliwa, T / Pryjma, J R / Guzik, T J

Lupus

2015 Volume 25, Issue 1, Page(s) 18–27

Abstract: Background: Systemic lupus erythematosus (SLE) is characterized by increased cardiovascular morbidity and mortality. SLE patients have increased prevalence of subclinical atherosclerosis, although the mechanisms of this observation remain unclear. ... ...

Abstract	Background: Systemic lupus erythematosus (SLE) is characterized by increased cardiovascular morbidity and mortality. SLE patients have increased prevalence of subclinical atherosclerosis, although the mechanisms of this observation remain unclear. Considering the emerging role of monocytes in atherosclerosis, we aimed to investigate the relationship between subclinical atherosclerosis, endothelial dysfunction and the phenotype of peripheral blood monocytes in SLE patients. Methods: We characterized the phenotype of monocyte subsets defined by the expression of CD14 and CD16 in 42 patients with SLE and 42 non-SLE controls. Using ultrasonography, intima-media thickness (IMT) of carotid arteries and brachial artery flow-mediated dilation (FMD) as well as nitroglycerin-induced dilation (NMD) were assessed. Results: Patients with SLE had significantly, but only modestly, increased IMT when compared with non-SLE controls (median (25th/75th percentile) 0.65 (0.60/0.71) mm vs 0.60 (0.56/0.68) mm; p < 0.05). Importantly, in spite of early atherosclerotic complications in the studied SLE group, marked endothelial dysfunction was observed. CD14dimCD16+proinflammatory cell subpopulation was positively correlated with IMT in SLE patients. This phenomenon was not observed in control individuals. Interestingly, endothelial dysfunction assessed by FMD was not correlated with any of the studied monocyte subsets. Conclusions: Our observations suggest that CD14dimCD16+monocytes are associated with subclinical atherosclerosis in SLE, although the mechanism appears to be independent of endothelial dysfunction.
MeSH term(s)	Adult ; Aged ; Asymptomatic Diseases ; Atherosclerosis/blood ; Atherosclerosis/diagnostic imaging ; Atherosclerosis/etiology ; Atherosclerosis/physiopathology ; Biomarkers/blood ; Brachial Artery/diagnostic imaging ; Brachial Artery/physiopathology ; Carotid Arteries/diagnostic imaging ; Carotid Artery Diseases/blood ; Carotid Artery Diseases/diagnostic imaging ; Carotid Artery Diseases/etiology ; Carotid Intima-Media Thickness ; Case-Control Studies ; Endothelium, Vascular/physiopathology ; Female ; Flow Cytometry ; GPI-Linked Proteins/blood ; Humans ; Lipopolysaccharide Receptors/blood ; Lupus Erythematosus, Systemic/blood ; Lupus Erythematosus, Systemic/complications ; Lupus Erythematosus, Systemic/diagnosis ; Male ; Middle Aged ; Monocytes/metabolism ; Phenotype ; Predictive Value of Tests ; Receptors, IgG/blood ; Risk Factors ; Vasodilation ; Young Adult
Chemical Substances	Biomarkers ; FCGR3B protein, human ; GPI-Linked Proteins ; Lipopolysaccharide Receptors ; Receptors, IgG
Language	English
Publishing date	2015-08-06
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	1154407-7
ISSN	1477-0962 ; 0961-2033
ISSN (online)	1477-0962
ISSN	0961-2033
DOI	10.1177/0961203315598014
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Article ; Online: Prolactin--not only lactotrophin. A "new" view of the "old" hormone.

Ignacak, A / Kasztelnik, M / Sliwa, T / Korbut, R A / Rajda, K / Guzik, T J

Journal of physiology and pharmacology : an official journal of the Polish Physiological Society

2012 Volume 63, Issue 5, Page(s) 435–443

Abstract: Prolactin (PRL) is a hormone mainly secreted by the anterior pituitary. Recent studies have shown that it may also be produced by many extrapituitary cells. The PRL gene expression is controlled by two independent promoter regions, which may be ... ...

Abstract	Prolactin (PRL) is a hormone mainly secreted by the anterior pituitary. Recent studies have shown that it may also be produced by many extrapituitary cells. The PRL gene expression is controlled by two independent promoter regions, which may be differentially regulated in the pituitary and extrapituitary organs. Proteolytic modifications of PRL generate variants of the hormone. A16 kDa PRL fragment, acting through a specific receptor, has both an antiangiogenic activity as well as an inhibitory effect on tumor growth. Stimulation of the PRL receptor involves many signal transduction pathways, for example JAK2/STAT, MAPK, c-src and Fyn kinase cascade, and these pathways may vary in different tissues. PRL synthesis and secretion is mainly regulated by the inhibitory influence of dopamine but other hormones are also involved in these mechanisms. The essential biological action of PRL is the stimulation of lactogenesis and galactopoesis. Apart from its classical functions, PRL affects other aspects of human body function including osmoregulation, metabolism and regulation of the immune and the central nervous system. Hyperprolactinemia is a common syndrome affecting both men and women. It is manifested by the presence of galactorrhoea and through the symptoms of hypogonadotrophic hypogonadism. Following on from the fact that PRL has so many pleiotropic tissue specific effects it is not surprising to learn that hyperprolactinaemia is a systemic condition which may predispose to numerous cardiovascular and immune-mediated reactions. The exact effects of PRL on both immune and cardiovascular systems are being currently unraveled and may lead to the introduction of novel therapeutic approaches in the future.
MeSH term(s)	Animals ; Cardiovascular Physiological Phenomena ; Central Nervous System/physiology ; Humans ; Hyperprolactinemia/etiology ; Immune System/physiology ; Prolactin/physiology ; Receptors, Prolactin/physiology
Chemical Substances	Receptors, Prolactin ; Prolactin (9002-62-4)
Language	English
Publishing date	2012-10
Publishing country	Poland
Document type	Journal Article ; Review
ZDB-ID	1125221-2
ISSN	1899-1505 ; 0867-5910 ; 0044-6033
ISSN (online)	1899-1505
ISSN	0867-5910 ; 0044-6033
Database	MEDical Literature Analysis and Retrieval System OnLINE

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Article: Adipocytokines - novel link between inflammation and vascular function?

Guzik, T J / Mangalat, D / Korbut, R

Journal of physiology and pharmacology : an official journal of the Polish Physiological Society

2006 Volume 57, Issue 4, Page(s) 505–528

Abstract: Obesity and obesity related diseases are a major public health problem. Recent studies have shown that fat tissue is not a simple energy storage organ, but exerts important endocrine and immune functions. These are achieved predominantly through release ... ...

Abstract	Obesity and obesity related diseases are a major public health problem. Recent studies have shown that fat tissue is not a simple energy storage organ, but exerts important endocrine and immune functions. These are achieved predominantly through release of adipocytokines, which include several novel and highly active molecules released abundantly by adipocytes like leptin, resistin, adiponectin or visfatin, as well as some more classical cytokines released possibly by inflammatory cells infiltrating fat, like TNF-alpha, IL-6, MCP-1 (CCL-2), IL-1. All of those molecules may act on immune cells leading to local and generalized inflammation and may also affect vascular (endothelial) function by modulating vascular nitric oxide and superoxide release and mediating obesity related vascular disorders (including hypertension, diabetes, atherosclerosis, and insulin resistance) but also cancer or non-alcoholic fatty liver diseases. Present review, in a concise form, focuses on the effects of major adipocytokines, characteristic for adipose tissue like leptin, adiponectin, resistin and visfatin on the immune system, particularly innate and adaptive immunity as well as on blood vessels. Macrophages and T cells are populating adipose tissue which develops into almost an organized immune organ. Activated T cells further migrate to blood vessels, kidney, brain and other organs surrounded by infiltrated fat leading to their damage, thus providing a link between metabolic syndrome, inflammation and cardiovascular and other associated disorders. Ceretain treatments may lead to significant changes in adipocytokine levels. For example include beta-2 adrenoreceptor agonists, thiazolidinediones as well as androgens lead to decrease of plasma leptin levels. Moreover future treatments of metabolic system associated disorders should focus on the regulation of adipocytokines and their modes of action.
MeSH term(s)	Adipocytes/immunology ; Adipocytes/metabolism ; Adipose Tissue/immunology ; Adipose Tissue/metabolism ; Cytokines/immunology ; Cytokines/metabolism ; Humans ; Inflammation/immunology ; Inflammation/metabolism ; Vascular Diseases/immunology ; Vascular Diseases/metabolism
Chemical Substances	Cytokines
Language	English
Publishing date	2006-12
Publishing country	Poland
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	1125221-2
ISSN	1899-1505 ; 0867-5910 ; 0044-6033
ISSN (online)	1899-1505
ISSN	0867-5910 ; 0044-6033
Database	MEDical Literature Analysis and Retrieval System OnLINE

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