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1.
BMC Musculoskelet Disord ; 13: 259, 2012 Dec 23.
Article in English | MEDLINE | ID: mdl-23259508

ABSTRACT

BACKGROUND: VDR may be considered as a candidate gene potentially related to idiopathic scoliosis susceptibility and natural history. Transcriptional profile of VDR mRNA isoforms might be changed in the structural tissues of the scoliotic spine and potentially influence the expression of VDR responsive genes. The purpose of the study was to determine differences in mRNA abundance of VDR isoforms in bone, cartilage and paravertebral muscles between tissues from curve concavity and convexity, between JIS and AIS and to identify VDR responsive genes differentiating juvenile and adolescent idiopathic scoliosis in paravertebral muscles. METHODS: In a group of 29 patients with JIS and AIS, specimens of bone, cartilage, paravertebral muscles were harvested at the both sides of the curve apex together with peripheral blood samples. Extracted total RNA served as a matrix for VDRs and VDRl mRNA quantification by QRT PCR. Subsequent microarray analysis of paravertebral muscular tissue samples was performed with HG U133A chips (Affymetrix). Quantitative data were compared by a nonparametric Mann Whitney U test. Microarray results were analyzed with GeneSpring 11GX application. Matrix plot of normalized log-intensities visualized the degree of differentiation between muscular tissue transcriptomes of JIS and AIS group. Fold Change Analysis with cutoff of Fold Change ≥2 identified differentially expressed VDR responsive genes in paravertebral muscles of JIS and AIS. RESULTS: No significant differences in transcript abundance of VDR isoforms between tissues of the curve concavity and convexity were found. Statistically significant difference between JIS and AIS group in mRNA abundance of VDRl isoform was found in paravertebral muscles of curve concavity. Higher degree of muscular transcriptome differentiation between curve concavity and convexity was visualized in JIS group. In paravertebral muscles Tob2 and MED13 were selected as genes differentially expressed in JIS and AIS group. CONCLUSIONS: In Idiopathic Scolioses transcriptional activity and alternative splicing of VDR mRNA in osseous, cartilaginous, and paravertebral muscular tissues are tissue specific and equal on both sides of the curve. The number of mRNA copies of VDRl izoform in concave paravertebral muscles might be one of the factors differentiating JIS and AIS. In paravertebral muscles Tob2 and Med13 genes differentiate Adolescent and Juvenile type of Idiopathic Scoliosis.


Subject(s)
Bone and Bones/chemistry , Cartilage/chemistry , Gene Expression Profiling/methods , Muscle, Skeletal/chemistry , Oligonucleotide Array Sequence Analysis , RNA, Messenger/blood , Receptors, Calcitriol/genetics , Scoliosis/genetics , Adolescent , Age of Onset , Cell Cycle Proteins/genetics , Child , Child, Preschool , Disease Progression , Female , Gene Expression Regulation , Genetic Markers , Genetic Predisposition to Disease , Humans , Male , Mediator Complex/genetics , Phenotype , Poland/epidemiology , Real-Time Polymerase Chain Reaction , Reverse Transcriptase Polymerase Chain Reaction , Scoliosis/blood , Scoliosis/classification , Scoliosis/diagnostic imaging , Scoliosis/epidemiology , Severity of Illness Index , Spine/diagnostic imaging , Tomography, X-Ray Computed
2.
Pol Merkur Lekarski ; 26(151): 9-13, 2009 Jan.
Article in Polish | MEDLINE | ID: mdl-19391499

ABSTRACT

UNLABELLED: Cardiovascular diseases including myocardial infarction cause 50 percent of all deaths cases and range before cancer as the cause of death. The term 'ischemic heart disease' covers wide range of diseases including all ischemic conditions of myocardium. It's the most common reason (98%) is atherosclerosis, which causes a restriction or occlusion of a coronary artery lumen resulting in myocardial ischemia. Acute coronary syndromes are caused by the rupture of unstable atherosclerotic plaque resulting in clot formation which blocks the blood vessel. In this process an important role play adhesion molecules triggering adhesion, aggregation and the whole blood coagulation cascade. AIM OF THE STUDY: The aim of the study was to assess PECAM-1 gene expression in peripheral blood mononuclear cells in patients with acute coronary syndrome during first 24 hours of hospitalization in comparison with healthy individuals. MATERIAL AND METHODS: There were 80 subjects included to the study divided into two groups. First group, consecutive patients admitted to the Department of Cardiology due to acute coronary syndrome and the second group, 20 healthy subjects. The total RNA was extracted from peripheral blood mononuclear cell (PBMC) using Chomczynski and Scchaci method. Transcription activity was assessed using commercially available TaqMan Gene Expression Assays. The PECAM-1 gene PCR reaction was preformed with ABI PRISM 7000 Sequence Detector (Applied Biosystems, USA). RESULTS: The comparison of PECAM-1 gene expression revealed statistically significant difference, between increased level of PECAM-1 in patients with acute coronary syndrome and it's lower level in healthy individuals. CONCLUSION: Observed in peripherial blood mononuclear cells increase of PECAM-1 protein gene expression may be responsible for increased adhesion and aggregation process and acute coronary syndrome occurrence.


Subject(s)
Acute Coronary Syndrome/blood , Acute Coronary Syndrome/genetics , Leukocytes, Mononuclear/metabolism , Vascular Cell Adhesion Molecule-1/genetics , Gene Expression , Humans
3.
Adv Clin Exp Med ; 22(2): 209-17, 2013.
Article in English | MEDLINE | ID: mdl-23709377

ABSTRACT

BACKGROUND: The inflammatory process underlying nasal polyposis is induced and perpetuated by the enhanced activity of several agents including transcription factors. It has recently been demonstrated that one of them, named nuclear factor-kappa B (NF-κB), is implicated in the regulation of multiple pro-inflammatory genes. OBJECTIVES: The aim of the study was to identify using microarray technology which NF-κB-dependent genes are activated in nasal polyp (NP) samples compared to the control mucosa. MATERIAL AND METHODS: The transcriptional activity of genes was analyzed using an oligonucleotide microarray on 15 NPs and 8 cases of normal nasal mucosa. RESULTS: Gene expression patterns obtained in NPs were significantly different from those in normal mucosa. NPs and control cases clustered separately, each of them with large homogeneity in gene expression. Among 582 human NF-κB-dependent genes 25 showed a significantly higher expression in NPs compared to the control. The largest increase focused on gene encoding TFF3 (a 5-fold higher expression) followed by NOS2A (5x), SERPINA1 (4x), UCP2 (4x), OXTR (4x) and IL8 (3x) (p<0.05). In healthy mucosa 19 genes presented increased transcription activity compared to NPs. The most significantly enhanced levels were shown LTF gene (20 fold) followed by KRT6B (7x), LYZ (7x), SD11B2 (5x) and MMP3 (4x) (p<0.05). CONCLUSIONS: DNA microarray technology highlights the involvement of many unsuspected pathologic pathways which could be involved in NP growth. The identification of novel disease-related genes may help to understand the biology of NPs and elaborate new targeted therapy.


Subject(s)
NF-kappa B/genetics , Nasal Polyps/genetics , Rhinitis/genetics , Sinusitis/genetics , Transcriptome , Adult , Aged , Chronic Disease , Female , Humans , Male , Middle Aged , NF-kappa B/metabolism , Oligonucleotide Array Sequence Analysis , Transcription, Genetic/physiology
4.
Inflammation ; 33(6): 398-407, 2010 Dec.
Article in English | MEDLINE | ID: mdl-20306290

ABSTRACT

Cardiovascular diseases, including acute coronary syndrome (ACS), are the leading cause of death among humans. Adhesion proteins, owing to their involvement in the initiation and progression of atherosclerotic lesions, contribute to the progression of coronary disease and ACS occurrence. Considering ambiguosity of results reported to date, we decided to conduct a preliminary investigation of adhesion protein gene expression in ACS patients as well as in healthy subjects by making use of oligonucleotide microarray technology. Analysis of eight microarrays revealed ten upregulated genes differentiating between the two groups: intercellular adhesion molecule-2, platelet/endothelial cell adhesion molecule-1, zyxin, integrin-linked kinase, calcium and integrin binding protein-1 (calmyrin), integrin beta 2, integrin beta 3 (ITGB3), integrin beta 7, integrin alpha 2b, and selectin P ligand. The expression of ITGB3 was found to have been downregulated.


Subject(s)
Acute Coronary Syndrome/genetics , Gene Expression Regulation , Acute Coronary Syndrome/blood , Acute Coronary Syndrome/metabolism , Aged , Antigens, CD/blood , Antigens, CD/genetics , Biomarkers/blood , CD18 Antigens/blood , CD18 Antigens/genetics , Calcium-Binding Proteins/blood , Calcium-Binding Proteins/genetics , Cell Adhesion , Cell Adhesion Molecules/blood , Cell Adhesion Molecules/genetics , Cytoskeletal Proteins/blood , Cytoskeletal Proteins/genetics , Endothelium, Vascular/metabolism , Female , Glycoproteins/blood , Glycoproteins/genetics , Humans , Integrin alpha2/blood , Integrin alpha2/genetics , Integrin beta Chains/blood , Integrin beta Chains/genetics , Integrin beta3/blood , Integrin beta3/genetics , Male , Membrane Glycoproteins/blood , Membrane Glycoproteins/genetics , Middle Aged , Myocardial Infarction/blood , Myocardial Infarction/genetics , Myocardial Infarction/metabolism , Oligonucleotide Array Sequence Analysis , Platelet Endothelial Cell Adhesion Molecule-1/blood , Platelet Endothelial Cell Adhesion Molecule-1/genetics , Polymerase Chain Reaction , Protein Serine-Threonine Kinases/blood , Protein Serine-Threonine Kinases/genetics , Risk Factors , Zyxin
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