RESUMO
This study aimed to use gene chips to investigate differential gene expression profiles in the occurrence and development of acute myocardial infarction (AMI). The study included 12 AMI patients and 12 healthy individuals. Total mRNA of peripheral bloodwas extracted and reversed-transcribed to cDNA for microarray analysis. After establishing two pools with three subjects each (3 AMI patients and 3 healthy individuals), the remaining samples were used for RT-qPCR to confirm the microarray data. From the microarray results, seven genes were randomly selected for RT-qPCR. RT-qPCR results were analyzed by the 2-ΔΔCt method. Microarray analysis showed that 228 genes were up- regulated and 271 were down-regulated (p ≤ 0.05, |logFC| > 1). Gene ontology showed that these genes belong to 128 cellular components, 521 biological processes, and 151 molecular functions. KEGG pathway analysis showed that these genes are involved in 107 gene pathways. RT-qPCR results for the seven genes showed expression levels consistent with those obtained by microarray. Thus, microarray data could be used to select the pathogenic genes for AMI. Investigating the abnormal expression of these differentially expressed genes might suggest efficient strategies for the prevention, diagnosis, and treatment of AMI.
RESUMO
Abstract This study aimed to use gene chips to investigate differential gene expression profiles in the occurrence and development of acute myocardial infarction (AMI). The study included 12 AMI patients and 12 healthy individuals. Total mRNA of peripheral bloodwas extracted and reversed-transcribed to cDNA for microarray analysis. After establishing two pools with three subjects each (3 AMI patients and 3 healthy individuals), the remaining samples were used for RT-qPCR to confirm the microarray data. From the microarray results, seven genes were randomly selected for RT-qPCR. RT-qPCR results were analyzed by the 2-ΔΔCt method. Microarray analysis showed that 228 genes were up- regulated and 271 were down-regulated (p ≤ 0.05, -logFC- > 1). Gene ontology showed that these genes belong to 128 cellular components, 521 biological processes, and 151 molecular functions. KEGG pathway analysis showed that these genes are involved in 107 gene pathways. RT-qPCR results for the seven genes showed expression levels consistent with those obtained by microarray. Thus, microarray data could be used to select the pathogenic genes for AMI. Investigating the abnormal expression of these differentially expressed genes might suggest efficient strategies for the prevention, diagnosis, and treatment of AMI.
RESUMO
Rhododendron possesses valuable horticultural and medicinal properties. However, the genetic studies have been hindered due to the lack of genetic markers. Based on RNA-seq, large-scale molecular markers were developed from four Rhododendron species endemic to Dabie Mountains (central China): R. fortunei (5.25 Gb; SSRs, 12,756, one/2.37 kb, 147 types; SNPs, 38,313; InDels, 3,174), R. simsii (5.80 Gb; SSRs, 13,294, one/2.58 kb, 167 types; SNPs, 136,590; InDels, 6,258), R. mariesii (6.53 Gb; SSRs, 15,724, one/2.51 kb, 170 types; SNPs, 44,942; InDels, 4,126), and R. molle (4.35 Gb; SSRs, 10,214, one/2.49 kb, 110 types; SNPs, 77,829; InDels, 3,416). Di-nucleotide repeats were the main type (59.126%-64.314%), and AG/CT repeat (55.18%-61.22%) was the most. In particular, 89 species-specific types had been found. Furthermore, C:GâT:A mutation was the main SNP type (30.475%-34.99%). However, C:GâG:C mutation was the least type in R. fortunei, while T:AâG:C mutation was the least in the other three species. InDels with length of 3 nt was most in R. fortunei, but 1 nt InDels were the main type in the other three species. Twelve microsatellite markers developed from R. simsii reveled high genetic diversity in the four populations, and heterozygote excess was observed. This research would benefit the genetic study, molecular marker-assisted selection, and breeding studies in Rhododendron species.