Dataset Information

Genetic basis of keloid formation in wounds after cardiac surgery.

ABSTRACT: Keloid disease is the abnormal formation of scar tissue in genetically predisposed people. Among many genes which may be related to the development of keloids, transforming growth factor ?1 (TGF-?1) is one of the most mentioned. It encodes cytokinin, which is responsible for the production of extracellular matrix and takes part in healing. Any abnormalities which arise during synthesis of the protein as a result of polymorphism or gene mutation may be the cause of healing disorders (scarring of the body); thus it is responsible for the development of keloids. The objective of this study is to determine the single nucleotide polymorphism of the gene TGF-?1, at the position -509(rs1800469)509, to compare the obtained results in the form of three different genotypes within the analysed group (keloids) and within the control group (healthy scars), and to analyse the correlation between obtained genotypes and the occurrence of keloid disease. Seventy-three patients after cardiac surgery with scars on their sternums were examined (22 women and 51 men) in the age group from 38 to 84 years. Two groups of patients were distinguished: 37 with keloids and 36 with healthy scars. DNA taken from patients was analysed and polymorphism C(-509)T of the gene TGF-?1 was determined. On the basis of the study it was found that the allele T in the position -509 of the gene TGF-?1 is associated with a lower risk of keloid formation regardless of age and gender.

SUBMITTER: Kulawczuk P

PROVIDER: S-EPMC4283882 | biostudies-literature | 2014 Sep

REPOSITORIES: biostudies-literature

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Genetic basis of keloid formation in wounds after cardiac surgery.

Kulawczuk Przemysław P Czapla Norbert N Bińczak-Kuleta Agnieszka A Safranow Krzysztof K Jaworska-Kulawczuk Anna A Gajewska Dominika D Agata Karolina K Brykczyński Miłosz M Bargiel Piotr P

Kardiochirurgia i torakochirurgia polska = Polish journal of cardio-thoracic surgery 20140928 3

Keloid disease is the abnormal formation of scar tissue in genetically predisposed people. Among many genes which may be related to the development of keloids, transforming growth factor β1 (TGF-β1) is one of the most mentioned. It encodes cytokinin, which is responsible for the production of extracellular matrix and takes part in healing. Any abnormalities which arise during synthesis of the protein as a result of polymorphism or gene mutation may be the cause of healing disorders (scarring of ...[more]

PMID: 26336434

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Project description:Sheep are routinely used in experimental cardiac electrophysiology and surgery.The purpose of this study was to (1) ascertain the topography and architecture of the ovine epicardial neural plexus (ENP), (2) determine the relationships of ENP with vagal and sympathetic cardiac nerves and ganglia, and (3) evaluate gross anatomic differences and similarities of ENP in humans, sheep, and other species.Ovine ENP and extrinsic sympathetic and vagal nerves were stained histochemically for acetylcholinesterase in whole heart and/or thorax-dissected preparations from 23 newborn lambs, with subsequent examination by stereomicroscope.Intrinsic cardiac nerves extend from the venous part of the ovine heart hilum along the roots of the cranial (superior) caval and left azygos veins to both atria and ventricles via five epicardial routes: dorsal right atrial, middle dorsal, left dorsal, right ventral, and ventral left atrial nerve subplexuses. Intrinsic nerves proceeding from the arterial part of the heart hilum along the roots of the aorta and pulmonary trunk extend exclusively into the ventricles as the right and left coronary subplexuses. The dorsal right atrial, right ventral, and middle dorsal subplexuses receive the main extrinsic neural input from the right cervicothoracic and right thoracic sympathetic T(2) and T(3) ganglia as well as from the right vagal nerve. The left dorsal is supplied by sizeable extrinsic nerves from the left thoracic T(4)-T(6) sympathetic ganglia and the left vagal nerve. Sheep hearts contained an average of 769 +/- 52 epicardial ganglia. Cumulative areas of epicardial ganglia on the root of the cranial vena cava and on the wall of the coronary sinus were the largest of all regions (P <.05).Despite substantial interindividual variability in the morphology of ovine ENP, right-sided epicardial neural subplexuses supplying the sinoatrial and atrioventricular nodes are mostly concentrated at a fat pad between the right pulmonary veins and the cranial vena cava. This finding is in sharp contrast with a solely left lateral neural input to the human atrioventricular node, which extends mainly from the left dorsal and middle dorsal subplexuses. The abundance of epicardial ganglia distributed widely along the ovine ventricular nerves over respectable distances below the coronary groove implies a distinctive neural control of the ventricles in human and sheep hearts.

Project description:BackgroundKeloid is a benign fibro-proliferative dermal tumor formed by an abnormal scarring response to injury and characterized by excessive collagen accumulation and invasive growth. The mechanism of keloid formation has not been fully elucidated, especially during abnormal scarring. Here, we investigated the regulatory genes, micro-RNAs (miRNAs) and transcription factors (TFs) that influence keloid development by comparing keloid and normal scar as well as keloid and normal skin.MethodsGene expression profiles (GSE7890, GSE92566, GSE44270 and GSE3189) of 5 normal scar samples, 10 normal skin samples and 18 keloid samples from the Gene Expression Omnibus (GEO) database were interrogated. Differentially expressed genes (DEGs) were identified between keloid and normal skin samples as well as keloid and normal scar samples with R Project for Statistical Computing. Gene Ontology (GO) functional enrichment analysis was also performed with R software. DEG-associated protein-protein interaction (PPI) network was constructed by STRING, followed by module selection from the PPI network based on the MCODE analysis. Regulatory relationships between TF/miRNA and target genes were predicted with miRnet and cytoscape. Core regulatory genes were verified by RT-qPCR.ResultsWe identified 628 DEGs, of which 626 were up-regulated and 2 were down-regulated. Seven core genes [neuropeptide Y(NPY), 5-hydroxytryptamine receptor 1A(HTR1A), somatostatin (SST), adenylate cyclase 8 (ADCY8), neuromedin U receptor 1 (NMUR1), G protein subunit gamma 3 (GNG3), and G protein subunit gamma 13 (GNG13)] all belong to MCODE1 and were enriched in the "G protein coupled receptor signaling pathway" of the GO biological process category. Furthermore, nine core miRNAs (hsa-mir-124, hsa-let-7, hsa-mir-155, hsa-mir-26a, hsa-mir-941, hsa-mir-10b, hsa-mir-20, hsa-mir-31 and hsa-mir-372), and two core TFs (SP1 and TERT) were identified to play important roles in keloid formation. In the TF/miRNA-target gene network, both hsa-mir-372 and hsa-mir-20 had a regulatory effect on GNG13, ADCY8 was predicted to be target by hsa-mir-10b, and HTR1A and NPY were potentially by SP1. Furthermore, the expression of core regulatory genes (GNG13, ADCY8, HTR1A and NPY) was validated in clinical samples.ConclusionsGNG13, ADCY8, NPY and HTR1A may act as core genes in keloid formation and these core genes establish relationship with SP1 and miRNA (hsa-mir-372, hsa-mir-20, hsa-mir-10b), which may influence multiple signaling pathways in the pathogenesis of keloid.

Dataset Information

Genetic basis of keloid formation in wounds after cardiac surgery.

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Genetic basis of keloid formation in wounds after cardiac surgery.

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