Introduction: Acute coronary syndrome (ACS) is caused by destabilization and rupture of atherosclerotic plaque in the coronary artery via mechanisms affecting leukocyte signaling, rolling, adhesion, extravasation and inflammation-promoting factors. The majority of cellular communication takes place on the membrane surface that is covered with glycoproteins and glycolipids synthesized by glycosyltransferases. The aim of this study was to determine the mRNA expression of leukocyte adhesion-related glycosyltransferases in patients during the onset and the chronic phase of ACS and to compare the expression with matching subjects without coronary disease.
Subjects And Methods: The study included 26 ACS patients and 26 ACS-free matched-pair controls. Blood samples were collected at the time of hospital admittance and 8 days later. Expression analysis of six fucosyltransferases and six sialyltransferases was performed by a real-time polymerase chain reaction.
Results: At the time of admittance ACS subjects had lower expression levels of FUT4, ST6GalNac4, ST6Gal1 and GM3 synthase (p < 0.05) than the control subjects, and moreover, after 8 days down-regulation of FUT7 and ST6GalNac3 was also observed (p < 0.05). When compared to the initial gene expression, after treatment and stabilization of ACS subjects, FUT7, ST6GalNac2 and ST6GalNac3 were down-regulated, whereas ST6GalNac1 was up-regulated. Expression levels of FUT7, ST6GalNac1, ST6GalNac2 and ST6GalNac3 were predicted by several drugs and medical history.
Conclusion: Expression of glycosyltransferase genes differs in ACS and control subjects. During the course of the ACS study we established further changes in gene expression levels. Medical history was predictive of gene expression levels while drugs were shown to modulate expression levels.
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http://dx.doi.org/10.1007/s00011-014-0735-3 | DOI Listing |
J Cell Mol Med
January 2025
Department of Leukemia, The University of Texas MD Anderson Cancer Center, Houston, Texas, USA.
Induced pluripotent stem cell (iPSC)-derived natural killer (NK) cells offer an opportunity for a standardized, off-the-shelf treatment with the potential to treat a wider population of acute myeloid leukaemia (AML) patients than the current standard of care. FT538 iPSC-NKs express a high-affinity, noncleavable CD16 to maximize antibody dependent cellular cytotoxicity, a CD38 knockout to improve metabolic fitness, and an IL-15/IL-15 receptor fusion preventing the need for cytokine administration, the main source of adverse effects in NK cell-based therapies. Here, we sought to evaluate the potential of FT538 iPSC-NKs as a therapy for AML through their effect on AML cell lines and primary AML cells.
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Department of Medical Microbiology and Immunology, Medical School, University of Pecs, 12 Szigeti Street, 7624 Pecs, Hungary.
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Division of Basic Biomedical Sciences, University of South Dakota Sanford School of Medicine, Vermillion, SD 57069, USA.
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Arthritis and Clinical Immunology Research Program, Oklahoma Medical Research Foundation, Oklahoma City, OK 73104, USA.
Systemic lupus erythematosus (SLE) is a complex autoimmune disorder characterized by widespread inflammation and autoantibody production. Its development and progression involve genetic, epigenetic, and environmental factors. Although genome-wide association studies (GWAS) have repeatedly identified a susceptibility signal at 16p13, its fine-scale source and its functional and mechanistic role in SLE remain unclear.
View Article and Find Full Text PDFInt J Mol Sci
December 2024
Department of Internal Medicine, Division of Gastroenterology and Hepatology, Carver College of Medicine, University of Iowa, Iowa City, IA 52242, USA.
Bone marrow transplantation (BMT) is mainly performed to restore an anti-tumor immune response, called the graft-versus-tumor (GVT) effect, against leukemia, myeloma and lymphoma. This GVT reactivity is driven by donor T cells, and it can also cause lethal graft-versus-host disease (GVHD). We previously demonstrated that the colonization of mice with helminths preserves the GVT response while suppressing GVHD.
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