Journal Title
Title of Journal: Protein J
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Abbravation: The Protein Journal
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Authors: Pawel Burchardt Witold Nowak Jakub Zurawski Anna GozdzickaJozefiak Tomasz Siminiak
Publish Date: 2010/09/25
Volume: 29, Issue: 7, Pages: 524-529
Abstract
Increased plasma levels of insulinlike growth factor 1 IGF1 are observed in advanced arteriosclerosis but the reasons for these elevated levels remain unknown One possibility to explain them is variation in the sequences that control IGF1 gene expression The goal of this study was to determine the effect of molecular variants of the IGF1 P1 promoter on IGF1 serum levels and to determine the impact of IGF1 levels on the severity of coronary atherosclerosis Methods Blood samples were collected from 101 consecutive patients undergoing routine angiography Genomic DNA was isolated from the nucleated cells of the blood plasma as described 2 Based on the presence of conformational differences in the DNA strand and on the absence of single nucleotide polymorphisms the DNA from 38 patients was further analyzed by the “allelic ladder” method to determine the number of repeated GC dinucleotides in the P1 promoter of the IGF1 gene In addition we analyzed serum growth hormone levels in order to examine the effect on systemic IGF1 synthesis Results Conformational differences in the P1 promoter of the IGF1 gene were observed in 38 out of the 101 patients Several genotypes depending on the number of GC repeats were observed 11/1917/1918/1918/2119/1919/2019/21 Interestingly a family history of coronary artery disease was seen less often among individuals heterozygous for the GC repeats A lower IGF1 levels were seen in nonvariant carriers homozygous genotypes for 19 or 21 repeats of GC or heterozygous genotype 19/21 when compared to the variant group other heterozygous genotypes then 19/21 1816 ± 479 ng/mL vs 2277 ± 737 p = 0026 A correlation between IGF1 IGFbinding protein number 3 and growth hormone levels p = ns was not observed and there were no significant differences in the growth hormone levels in the studied group of patients p = ns
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