Immune-Inflammatory Responses in Atherosclerosis: The Role of Myeloid Cells.

Inflammation plays a key role in the initiation and progression of atherosclerosis and can be caused by multiple agents, including increased concentration of circulating low-density lipoprotein (LDL) cholesterol. Areas of the arterial wall affected by atherosclerosis are enriched with lymphocytes and dendritic cells (DCs). Atherosclerotic plaques contain a variety of proinflammatory immune cells, such as macrophages, DCs, T cells, natural killer cells, neutrophils and others.

Novel Approaches to Anti-atherosclerotic Therapy: Cell-based Models and Herbal Preparations (Review of Our Own Data).

Atherosclerosis is a chronic arterial disease characterized by vascular inflammation, accumulation of lipids in the arterial wall, and formation and growth of atherosclerotic plaques followed by ischemia. In subclinical atherosclerosis, cholesterol retention in subendothelial cells leads to induction of local inflammation, generation of foam cells and lesion formation, followed by a chain of other pathogenic events. Atherosclerotic progression can frequently be fatal, since plaque rupture may lead to thrombosis and acute events, such as myocardial infarction, stroke and sudden death.

Role of androgens in cardiovascular pathology.

Cardiovascular effects of android hormones in normal and pathological conditions can lead to either positive or negative effects. The reason for this variation is unknown, but may be influenced by gender-specific effects of androids, heterogeneity of the vascular endothelium, differential expression of the androgen receptor in endothelial cells (ECs) and route of androgen administration. Generally, androgenic hormones are beneficial for ECs because these hormones induce nitric oxide production, proliferation, motility, and growth of ECs and inhibit inflammatory activation and induction of procoagulant, and adhesive properties in ECs.

Matrix metalloproteinases in pro-atherosclerotic arterial remodeling.

Matrix metalloproteinases (MMPs) is a family of Zn endopeptidases that process various components of the extracellular matrix. These enzymes are also involved in activation and inhibition of signaling cascades through proteolytic cleavage of surface receptors. Moreover, MMPs play a key role in tissue remodeling and and repair.

Circulating tumor cells and their advances to promote cancer metastasis and relapse, with focus on glioblastoma multiforme.

In the late stages of their development, cancers can form metastases. Formation of metastases was found to be associated with the capacity of cancer cells to quit the tumor mass and journey through the circulation to distant organs. This cell population is called circulating tumor cells (CTCs).

Glioma Cell and Astrocyte Co-cultures As a Model to Study Tumor-Tissue Interactions: A Review of Methods.

Astrocytes are a dominant cell type that envelopes the glioma bed. Typically, that is followed by formation of contacts between astrocytes and glioma cells and accompanied by change in astrocyte phenotype, a phenomenon known as a 'reactive astrogliosis.' Generally considered glioma-promoting, astrocytes have many controversial peculiarities in communication with tumor cells, which need thorough examination in vitro.

Potential of anti-inflammatory agents for treatment of atherosclerosis.

Chronic inflammation is a central pathogenic mechanism of atherosclerosis induction and progression. Vascular inflammation is associated with accelerated onset of late atherosclerosis complications. Atherosclerosis-related inflammation is mediated by a complex cocktail of pro-inflammatory cytokines, chemokines, bioactive lipids, and adhesion molecules, and blocking the key pro-atherogenic inflammatory mechanisms can be beneficial for treatment of atherosclerosis.

The role of monocytosis and neutrophilia in atherosclerosis.

Monocytosis and neutrophilia are frequent events in atherosclerosis. These phenomena arise from the increased proliferation of hematopoietic stem and multipotential progenitor cells (HSPCs) and HSPC mobilization from the bone marrow to other immune organs and circulation. High cholesterol and inflammatory signals promote HSPC proliferation and preferential differentiation to the myeloid precursors (i.

New biomarkers for diagnosis and prognosis of localized prostate cancer.

The diagnostics and management of localized prostate cancer is complicated because of cancer heterogeneity and differentiated progression in various subgroups of patients. As a prostate cancer biomarker, FDA-approved detection assay for serum prostate specific antigen (PSA) and its derivatives are not potent enough to diagnose prostate cancer, especially high-grade disease (Gleason ≥7). To date, a collection of new biomarkers was developed.

Calcifying Matrix Vesicles and Atherosclerosis.

Artery calcification is a well-recognized predictor of late atherosclerotic complications. In the intima media, calcification starts with apoptosis of vascular smooth muscle cells (VSMCs) and the release of calcifying matrix vesicles with diameter of 0.5-15 m that can be observed microscopically.

The role of mitochondrial dysfunction in cardiovascular disease: a brief review.

Cardiovascular disease (CVD) is a leading cause of mortality worldwide. Proper mitochondrial function is necessary in tissues and organs that are of high energy demand, including the heart. Mitochondria are very sensitive to nutrient and oxygen supply and undergo metabolic adaptation to the changing environment.

Epigenetic Alterations in DNA and Histone Modifications Caused by Depression and Antidepressant Drugs: Lessons from the Rodent Models.

Epigenetic modifications regulate chromatin folding and function. Epigenetic mechanisms regulate transcription mediating effects of various stimuli on gene expression. These mechanisms are involved in transcriptional control in various physiological and pathological conditions including neuropsychiatric disorders and behavioral abnormalities such as depression.

Engineered Nanoparticles: Their Properties and Putative Applications for Therapeutic Approaches Utilizing Stem Cells for the Repair of Atherosclerotic Disease.

Background: Stem cell therapy was established as a promising approach for regenerative medicine applications such as cardiac repair. However, current stem cell-based therapeutic strategies have serious challenges such as low retention and viability of transplanted stem cells in the injured myocardium. This significantly limits efficiency of stem cell therapy.

The impact of interferon-regulatory factors to macrophage differentiation and polarization into M1 and M2.

The mononuclear phagocytes control the body homeostasis through the involvement in resolving tissue injury and further wound healing. Indeed, local tissue microenvironmental changes can significantly influence the functional behavior of monocytes and macrophages. Such microenvironmental changes for example occur in an atherosclerotic plaque during all progression stages.

Role of lipids and intraplaque hypoxia in the formation of neovascularization in atherosclerosis.

According to the current paradigm, chronic vascular inflammation plays a central role in the pathogenesis of atherosclerosis. The plaque progression is typically completed with rupture and subsequent acute cardiovascular complications. Previously, the role of adventitial vasa vasorum in atherogenesis was underestimated.

Mechanisms of foam cell formation in atherosclerosis.

Low-density lipoprotein (LDL) and cholesterol homeostasis in the peripheral blood is maintained by specialized cells, such as macrophages. Macrophages express a variety of scavenger receptors (SR) that interact with lipoproteins, including SR-A1, CD36, and lectin-like oxLDL receptor-1 (LOX-1). These cells also have several cholesterol transporters, including ATP-binding cassette transporter ABCA1, ABCG1, and SR-BI, that are involved in reverse cholesterol transport.

The impact of FOXO-1 to cardiac pathology in diabetes mellitus and diabetes-related metabolic abnormalities.

Diabetic heart pathology has a serious social impact due to high prevalence worldwide and significant mortality/invalidation of diabetic patients suffered from cardiomyopathy. The pathogenesis of diabetic and diabetes-related cardiomyopathy is associated with progressive loss and impairment of cardiac function due to adverse effects of metabolic, prooxidant, proinflammatory, and pro-apoptotic stress factors. In the adult heart, the transcriptional factor forkhead box-1 (FOXO-1) is involved in maintaining cardiomyocytes in the homeostatic state and induction of their adaptation to metabolic and pro-oxidant stress stimuli.

Thrombospondins: A Role in Cardiovascular Disease.

Thrombospondins (TSPs) represent extracellular matrix (ECM) proteins belonging to the TSP family that comprises five members. All TSPs have a complex multidomain structure that permits the interaction with various partners including other ECM proteins, cytokines, receptors, growth factors, etc. Among TSPs, TSP1, TSP2, and TSP4 are the most studied and functionally tested.

Impact of the cardiovascular system-associated adipose tissue on atherosclerotic pathology.

Cardiac obesity makes an important contribution to the pathogenesis of cardiovascular disease. One of the important pathways of this contribution is the inflammatory process that takes place in the adipose tissue. In this review, we consider the role of the cardiovascular system-associated fat in atherosclerotic cardiovascular pathology and a non-atherosclerotic cause of coronary artery disease, such as atrial fibrillation.

The EGFR variant III mutant as a target for immunotherapy of glioblastoma multiforme.

In epithelial tumors, the epidermal growth factor receptor (EGFR) controls key signaling pathways responsible for growth, proliferation, migration, and survival of tumor cells. The epidermal growth factor receptor variant III (EGFRvIII) is the most common EGFR mutation that occurs in up to 30% of high-grade gliomas especially glioblastoma multiforme (GBM). EGFRvIII arises from the deletion of exon 2-7 that leads to the formation of the constitutively activated mutant receptor incapable of binding any known ligand.

Early-life adversity-induced long-term epigenetic programming associated with early onset of chronic physical aggression: Studies in humans and animals.

To examine whether chronic physical aggression (CPA) in adulthood can be epigenetically programmed early in life due to exposure to early-life adversity. Literature search of public databases such as PubMed/MEDLINE and Scopus. Children/adolescents susceptible for CPA and exposed to early-life abuse fail to efficiently cope with stress that in turn results in the development of CPA later in life.