ABSTRACT
The expression profiling analysis of inflammatory chemokines and their receptors in newly formed lymph nodes in breast cancer was carried out. The analysis revealed the increase in expression of the genes CCL16, XCR1, CYFIP2, TNFSF14 and the reduction in expression of chemokine ligands CXCL5 and CXCL12 in tertiary lymphoid organs. The obtained results allow us to suggest that the process of induction of lymph nodes neogenesis is identical (in its key mechanisms) to the process of lymphoid tissue neogenesis in autoimmune diseases and in some infections, but may have different triggers.
Subject(s)
Breast Neoplasms/metabolism , Chemokines/metabolism , Lymph Nodes/metabolism , Receptors, Chemokine/metabolism , Adult , Aged , Breast Neoplasms/pathology , Chemokines/genetics , Female , Gene Expression Profiling , Humans , Inflammation/metabolism , Inflammation/pathology , Inflammation Mediators/metabolism , Lymphoid Tissue/metabolism , Middle Aged , Organogenesis/physiology , Receptors, Chemokine/geneticsABSTRACT
The goal of this work was to determine a correlation between the VE-cadherin and circulating endothelial cells (CECs) blood levels at hemorrhagic fever with renal syndrome (HFRS) of different severity and research association between the VE-cadherin gene c. 1550T>C missense mutation and HRFS severity. Significant decreasing of the VE-cadherin and increasing of CECs blood levels in the course of the disease in all studied groups was established. Most prominent changes were found at severe type with complications. There was found a strong negative correlation between these two indexes. There was significant high frequency of homozygotic genotype *T/*T at severe type with complications. It was concluded that there was increased endothelium desquamation due to the VE-cadherin internalization at moderate and severe uncomplicated types of HFRS and as a result ofVE-cadherin gene c. 1550T>C missense mutation at severe type with complications.
Subject(s)
Antigens, CD , Cadherins , Endothelium, Vascular/pathology , Gene Frequency/genetics , Hemorrhagic Fever with Renal Syndrome , Adult , Antigens, CD/blood , Antigens, CD/genetics , Cadherins/blood , Cadherins/genetics , Endothelial Cells/cytology , Endothelial Cells/metabolism , Gene Expression , Genetic Association Studies , Genotype , Hemorrhagic Fever with Renal Syndrome/blood , Hemorrhagic Fever with Renal Syndrome/genetics , Hemorrhagic Fever with Renal Syndrome/pathology , Hemorrhagic Fever with Renal Syndrome/virology , Homozygote , Humans , Male , Middle Aged , Mutation, Missense , Puumala virus/genetics , Puumala virus/pathogenicityABSTRACT
The dynamics of plasma level of plasminogen-1 activator inhibitor (PAI-1) and frequency distribution of PAI-1 gene polymorphic locus 4G/5G genotypes and alleles were studied in male and female patients of different age with hemorrhagic fever complicated by renal syndrome of different severity. A significant elevation of PAI-1 level was recorded during fever in adult patients of mature age groups I and II with medium severe and severe uncomplicated disease, the elevation being followed by a significant reduction, except the oliguric and polyuric periods of medium severe form. In complicated disease, the concentration of PAI-1 was low during fever in patients of mature age group I, after which it increased significantly until the period of diuresis recovery; in patients of mature age group II it remained low, except the polyuria period. No appreciable age- or gender-related differences in frequency distributions of PAI-1 gene polymorphic locus 4G/5G genotypes and alleles in patients with disease of different severity were found; no differences from the control group by these parameters were revealed. The dynamics of PAI-1 plasma level in different forms of hemorrhagic fever with renal syndrome were not genetically determined and represented an adequate metabolic response to endotheliotropic virus.
Subject(s)
Hemorrhagic Fever with Renal Syndrome/genetics , Plasminogen Activator Inhibitor 1/genetics , Polymorphism, Genetic , Adult , Age Factors , Alleles , Case-Control Studies , Female , Gene Frequency , Genetic Loci , Genotype , Hemorrhagic Fever with Renal Syndrome/blood , Humans , Kidney , Male , Middle Aged , Plasminogen Activator Inhibitor 1/blood , Polymerase Chain Reaction , Promoter Regions, Genetic , Severity of Illness IndexABSTRACT
MicroRNAs (miRNAs) are a class of RNA which controls gene expression at the posttranscription level. Binding with the target RNA, a miRNA can supress translation and/or induce degradation of mRNA. The studies of miRNAs have already shown that miRNA were essential to switch the programs of gene expression during embryo development as well as to control cell functioning of the adult organism. Alteration of the miRNA expression profile may appear not less important in development of pathology than better known structural variations of the proteins. The role of miRNA has been confirmed for a range of common diseases connected to impaired balance of cell proliferation, differentiation and programmed death. This review discusses specific features of miRNA-mediated regulation of gene expression and its role in normal and pathological development of muscle, immune, and nervous systems. The evidence of miRNA involvent in neurodegenerative disorders and mental disorders is demonstrated.
