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Träfflista för sökning "WFRF:(Gidlöf Olof) ;conttype:(scientificother)"

Sökning: WFRF:(Gidlöf Olof) > Övrigt vetenskapligt/konstnärligt

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1.
  • Badhai, Jitendra, et al. (författare)
  • Differential expression of RPS19 5’UTR variants implicated in Diamond-Blackfan anemia
  • 2012
  • Annan publikation (övrigt vetenskapligt/konstnärligt)abstract
    • Heterozygous mutations in the ribosomal protein (RP) S19 gene RPS19 are found in about 25% of patients with the congenital erythroblastopenia Diamond-Blackfan anemia (DBA). The RPS19 gene encodes a single RPS19 isoform from three known transcriptional start sites (TSS) with different 5’ untranslated region (UTR). The regulation of RPS19 expression is poorly understood as well as the significance of different 5’UTRs. A few rare sequence variants within the 5’UTR have also been reported in patients with DBA. We determined the transcriptional start sites (TSS) and the tissue distribution of variant 5’UTRs of RPS19. Twenty-nine novel TSS in K562 cells and testis were identified. We then analyzed the relative proportion of three selected 5’UTRs of different length on a panel of primary tissues. The shorter 5’UTR were most abundant in all tissues but with large variations in relative levels of shorter versus longer transcripts. To clarify the effect of different RPS19 5’UTRs on translation we designed and expressed constructs using three 5’UTRs of different length. The short 5’UTR(+35nt.) translate 4-6 folds more efficiently than the two longer variants with 5’UTRs of 382nt. and 467nt., respectively We also introduced DBA associated insertion (c.-149_-148insGCCA, c.-149_-148insAGCC ) and deletion (c.-144_-141delTTTC) variants in the 5’UTR. . Interestingly, the DBA associated 5’UTR sequence variants showed a 20-30% reduction in RPS19 levels when compared to the corresponding w.t. constructs. Our results indicate that the RPS19 gene has a broad range of TSS with tissue specific variations. We also show that sequence variants in the 5’UTR in some DBA patients reduce RPS19 expression with implications for the pathophysiology of the disease.
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2.
  • Gidlöf, Olof (författare)
  • Clinical and Biological Aspects of Cardiovascular microRNA
  • 2013
  • Doktorsavhandling (övrigt vetenskapligt/konstnärligt)abstract
    • Ischemic heart disease is the leading cause of death in high-income parts of the world and is caused mainly by atherosclerosis in the coronary arteries. The rupture of an atherosclerotic plaque with subsequent platelet activation and clot formation can lead to myocardial infarction (MI). Atherosclerosis is a complex process, which involves the accumulation and oxidation of low-density lipoprotein in the vessel wall followed by endothelial inflammation, infiltration of monocytes and proliferation and migration of vascular smooth muscle cells towards the vessel lumen. microRNA (miRNA) is a class of short non-coding RNA which regulate gene expression through part-complimentary binding to target sites preferably within the 3’-UTR of specific mRNAs. miRNAs have pervasive roles in animal biology and aberrant expression of miRNAs have been linked with a wide spectrum of human disease. Additionally, the tissue specific manner of miRNA expression together with remarkable stability in plasma and evidence of release of miRNA from stressed or apoptotic cells have made miRNAs interesting as biomarkers for various diseases. The aim of this thesis was (1) to assess the diagnostic and prognostic value of cardiac-enriched miRNAs in the context of coronary artery disease, (2) to screen for differences in miRNA content in platelets from myocardial infarction patients and elucidate a potential paracrine function for platelet miRNA and (3) to investigate the role of miRNAs in regulating endothelial inflammation in response to extracellular ATP/UTP. In Study I and II, we found that cardiac-enriched miRNAs are increased 100-3000 fold within 12 h following onset of symptoms in patients with myocardial infarction and that the levels of two specific miRNAs, miR-208b and-499-5p, could be used to discriminate MI-patients from non-MI patients and were associated with increased risk of death and development of heart failure. In Study III, we found differentially expressed platelet miRNAs in MI patients compared to healthy controls using RNA-sequencing. Release of miRNAs upon platelet activation, as well as microparticle-dependent transfer of functional platelet-derived miRNA to endothelial cells was also shown in vitro. In Study IV, we showed that the effects of ATP and UTP on cell surface expression of intercellular adhesion molecule 1 (ICAM-1) and leukocyte adhesion is mediated in part by miR-22 in endothelial cells. In conclusion, the levels of circulating cardiac-enriched miRNA have diagnostic and prognostic value in the context of coronary artery disease, platelet-derived miRNA can act as paracrine mediators in endothelial cells and miR-22 plays an anti-inflammatory role in the endothelium.
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Gidlöf, Olof (3)
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