liu.seSearch for publications in DiVA
Change search
Link to record
Permanent link

Direct link
BETA
Magnusson, Karl-Eric
Alternative names
Publications (10 of 155) Show all publications
Aksenova, V., Turoverova, L., Khotin, M., Magnusson, K.-E., Tulchinsky, E., Melino, G., . . . Tentler, D. (2018). Correction: Actin-binding protein alpha-actinin 4 (ACTN4) is a transcriptional co-activator of RelA/p65 sub-unit of NF-kB (vol 4, pg 362, 2013). OncoTarget, 9(76), 34450-34450
Open this publication in new window or tab >>Correction: Actin-binding protein alpha-actinin 4 (ACTN4) is a transcriptional co-activator of RelA/p65 sub-unit of NF-kB (vol 4, pg 362, 2013)
Show others...
2018 (English)In: OncoTarget, ISSN 1949-2553, E-ISSN 1949-2553, Vol. 9, no 76, p. 34450-34450Article in journal (Other academic) Published
Abstract [en]

[This corrects the article DOI: 10.18632/oncotarget.901.].

Place, publisher, year, edition, pages
Impact Journals, 2018
National Category
Clinical Medicine
Identifiers
urn:nbn:se:liu:diva-156018 (URN)10.18632/oncotarget.26206 (DOI)30344954 (PubMedID)
Available from: 2019-04-02 Created: 2019-04-02 Last updated: 2019-04-02
Tjellstrom, B., Högberg, L., Stenhammar, L., Magnusson, K.-E., Midtvedt, T., Norin, E. & Sundqvist, T. (2016). Letter: A Role for Bacteria in Celiac Disease? in DIGESTIVE DISEASES AND SCIENCES, vol 61, issue 7, pp 2140-2140 [Letter to the editor]. Digestive Diseases and Sciences, 61(7), 2140-2140
Open this publication in new window or tab >>Letter: A Role for Bacteria in Celiac Disease? in DIGESTIVE DISEASES AND SCIENCES, vol 61, issue 7, pp 2140-2140
Show others...
2016 (English)In: Digestive Diseases and Sciences, ISSN 0163-2116, E-ISSN 1573-2568, Vol. 61, no 7, p. 2140-2140Article in journal, Letter (Other academic) Published
Abstract [en]

n/a

Place, publisher, year, edition, pages
SPRINGER, 2016
National Category
Clinical Medicine
Identifiers
urn:nbn:se:liu:diva-130728 (URN)10.1007/s10620-016-4131-4 (DOI)000379013300046 ()27017223 (PubMedID)
Available from: 2016-08-22 Created: 2016-08-22 Last updated: 2017-11-28
Molinas, A., Mirazimi, A., Holm, A., Loitto, V. M., Magnusson, K.-E. & Vikström, E. (2016). Protective role of host aquaporin 6 against Hazara virus, a model for Crimean–Congo hemorrhagic fever virus infection. FEMS Microbiology Letters, 363(8), Article ID fnw058.
Open this publication in new window or tab >>Protective role of host aquaporin 6 against Hazara virus, a model for Crimean–Congo hemorrhagic fever virus infection
Show others...
2016 (English)In: FEMS Microbiology Letters, ISSN 0378-1097, E-ISSN 1574-6968, Vol. 363, no 8, article id fnw058Article in journal (Refereed) Published
Abstract [en]

Crimean–Congo hemorrhagic fever virus (CCHFV) is an arthropod-borne pathogen that causes infectious disease with severe hemorrhagic manifestations in vascular system in humans. The proper function of the cells in the vascular system is critically regulated by aquaporins (AQP), water channels that facilitate fluxes of water and small solutes across membranes. With Hazara virus as a model for CCHFV, we investigated the effects of viruses on AQP6 and the impact of AQP6 on virus infectivity in host cells, using transiently expressed GFP-AQP6 cells, immunofluorescent assay for virus detection, epifluorescent imaging of living cells and confocal microscopy. In GFP-AQP6 expressing cells, Hazara virus reduced both the cellular and perinuclear AQP6 distribution and changed the cell area. Infection of human cell with CCHFV strain IbAR 10200 downregulated AQP6 expression at mRNA level. Interestingly, the overexpression of AQP6 in host cells decreased the infectivity of Hazara virus, speaking for a protective role of AQP6. We suggest the possibility for AQP6 being a novel player in the virus–host interactions, which may lead to less severe outcomes of an infection.

Place, publisher, year, edition, pages
Oxford University Press, 2016
Keywords
Host–virus interactions; Nairovirus; Crimean–Congo hemorrhagic fever virus; aquaporin; virus infectivity; water homeostasis
National Category
Cell and Molecular Biology Microbiology in the medical area
Identifiers
urn:nbn:se:liu:diva-127499 (URN)10.1093/femsle/fnw058 (DOI)000377970600013 ()26976854 (PubMedID)
Funder
Swedish Research Council, 2010-3045European Science Foundation (ESF)Magnus Bergvall FoundationSwedish Research Council, 214–7495Linköpings universitet
Note

Funding agencies: Swedish Research Council [2010-3045]; European Science foundation; Magnus Bergvall Foundation; Faculty of Medicine and Health Sciences, Linkoping University; Infect-ERA Second Call (Swedish Research Council) [214-7495]

Available from: 2016-04-28 Created: 2016-04-28 Last updated: 2018-01-10Bibliographically approved
Holm, A., Magnusson, K.-E. & Vikström, E. (2016). Pseudomonas aeruginosa N-3-oxo-dodecanoyl-homoserine Lactone Elicits Changes in Cell Volume, Morphology, and AQP9 Characteristics in Macrophages. Frontiers in Cellular and Infection Microbiology, 6(32)
Open this publication in new window or tab >>Pseudomonas aeruginosa N-3-oxo-dodecanoyl-homoserine Lactone Elicits Changes in Cell Volume, Morphology, and AQP9 Characteristics in Macrophages
2016 (English)In: Frontiers in Cellular and Infection Microbiology, E-ISSN 2235-2988, ISSN 2235-2988, Vol. 6, no 32Article in journal (Refereed) Published
Abstract [en]

Quorum sensing (QS) communication allows Pseudomonas aeruginosa to collectively control its population density and the production of biofilms and virulence factors. QS signal molecules, like N-3-oxo-dodecanoyl-L-homoserine lactone (30-C-12-HSL), can also affect the behavior of host cells, e.g., by modulating the chemotaxis, migration, and phagocytosis of human leukocytes. Moreover, host water homeostasis and water channels aquaporins (AQP) are critical for cell morphology and functions as AQP interact indirectly with the cell cytoskeleton and signaling cascades. Here, we investigated how P aeruginosa 30-C-12-HSL affects cell morphology, area, volume and AQP9 expression and distribution in human primary macrophages, using quantitative PCR, immunoblotting, two- and three-dimensional live imaging, confocal and nanoscale imaging. Thus, 30-C-12-HSL enhanced cell volume and area and induced cell shape and protrusion fluctuations in macrophages, processes tentatively driven by fluxes of water across cell membrane through AQP9, the predominant AQP in macrophages. Moreover, 30-C-12-HSL upregulated the expression of AQP9 at both the protein and mRNA levels. This was accompanied with enhanced whole cell AQP9 fluorescent intensity and redistribution of AQP9 to the leading and trailing regions, in parallel with increased cell area in the macrophages. Finally, nanoscopy imaging provided details on AQP9 dynamics and architecture within the lamellipodial area of 30-C-12-HSL-stimulated cells. We suggest that these novel events in the interaction between P aeruginosa and macrophage may have an impact on the effectiveness of innate immune cells to fight bacteria, and thereby resolve the early stages of infections and inflammations.

Place, publisher, year, edition, pages
FRONTIERS MEDIA SA, 2016
Keywords
host-bacteria interactions; quorum sensing; N-acylhomoserinelactone; innate immunity; macrophage; water homeostasis; aquaporin
National Category
Clinical Medicine
Identifiers
urn:nbn:se:liu:diva-127262 (URN)10.3389/fcimb.2016.00032 (DOI)000372710500001 ()27047801 (PubMedID)
Note

Funding Agencies|Swedish Research Council [2010-3045]; European Science foundation (TraPPs Euromembrane project); Magnus Bergvall Foundation; Faculty of Medicine and Health Sciences, Linkoping University

Available from: 2016-04-20 Created: 2016-04-19 Last updated: 2018-05-14
Vicente Carrillo, A., Edebert, I., Garside, H., Cotgreave, I., Rigler, R., Loitto, V., . . . Rodriguez-Martinez, H. (2015). Boar spermatozoa successfully predict mitochondrial modes of toxicity: Implications for drug toxicity testing and the 3R principles. Toxicology in Vitro, 29(3), 582-591
Open this publication in new window or tab >>Boar spermatozoa successfully predict mitochondrial modes of toxicity: Implications for drug toxicity testing and the 3R principles
Show others...
2015 (English)In: Toxicology in Vitro, ISSN 0887-2333, E-ISSN 1879-3177, Vol. 29, no 3, p. 582-591Article in journal (Refereed) Published
Abstract [en]

Replacement of animal testing by in vitro methods (3-R principles) requires validation of suitable cell models, preferably obtained non-invasively, defying traditional use of explants. Ejaculated spermatozoa are highly dependent on mitochondrial production and consumption of ATP for their metabolism, including motility display, thus becoming a suitable model for capturing multiple modes of action of drugs and other chemicals acting via mitochondrial disturbance. In this study, a hypothesis was tested that the boar spermatozoon is a suitable cell type for toxicity assessment, providing a protocol for 3R-replacement of animals for research and drug-testing. Boar sperm kinetics was challenged with a wide variety of known frank mito-toxic chemicals with previously shown mitochondrial effects, using a semi-automated motility analyser allied with real-time fluorescent probing of mitochondrial potential (MitoTracker and JC-1). Output of this sperm assay (obtained after 30 min) was compared to cell viability (ATP-content, data obtained after 24-48 h) of a hepatome-cell line (HepG2). Results of compound effects significantly correlated (P less than 0.01) for all sperm variables and for most variables in (HepG2). Dose-dependent decreases of relative ATP content in HepG2 cells correlated to sperm speed (r= 0.559) and proportions of motile (r = 0.55) or progressively motile (r = 0.53) spermatozoa. The significance of the study relies on the objectivity of computerized testing of sperm motility inhibition which is comparable albeit of faster output than somatic cell culture models. Sperm suspensions, easily and painlessly obtained from breeding boars, are confirmed as suitable biosensors for preclinical toxicology screening and ranking of lead compounds in the drug development processes.

Place, publisher, year, edition, pages
Elsevier, 2015
Keywords
Sperm; Motility; Mitochondria; Drug; Toxicity; Boar
National Category
Clinical Medicine
Identifiers
urn:nbn:se:liu:diva-117655 (URN)10.1016/j.tiv.2015.01.004 (DOI)000352050100019 ()25624015 (PubMedID)
Note

Funding Agencies|Swedish Research Council (VR); Research Council Formas, Stockholm, Sweden

Available from: 2015-05-12 Created: 2015-05-06 Last updated: 2017-12-04
Bolshakova, A., Magnusson, K.-E., Pinaev, G. & Petukhova, O. (2015). EGF-induced dynamics of NF-kappa B and F-actin in A431 cells spread on fibronectin. Histochemistry and Cell Biology, 144(3), 223-235
Open this publication in new window or tab >>EGF-induced dynamics of NF-kappa B and F-actin in A431 cells spread on fibronectin
2015 (English)In: Histochemistry and Cell Biology, ISSN 0948-6143, E-ISSN 1432-119X, Vol. 144, no 3, p. 223-235Article in journal (Refereed) Published
Abstract [en]

To evaluate the role of actin cytoskeleton in the regulation of NF-kappa B transcription factor, we analyzed its involvement in the intracellular transport and nuclear translocation of the NF-kappa B RelA/p65 subunit in A431 epithelial cells stimulated with fibronectin and EGF. Live cell imaging and confocal microscopy showed that EGF activated the movement of RelA/p65 in the cytoplasm. Upon cell adhesion to fibronectin, RelA/p65 concentrated onto stress fibers, and EGF stimulated its subsequent allocation to membrane ruffles, newly organized stress fibers, and discrete cytoplasmic actin-rich patches. These patches also contained alpha-actinin-1 and alpha-actinin-4, vinculin, paxillin, alpha-tubulin, and PI3-kinase. Cytochalasin D treatment resulted in RelA/p65 redistribution to actin-containing aggregates, with the number of cells with RelA/p65-containing clusters in the cytoplasm increasing under the effect of EGF. Furthermore, EGF proved to induce RelA/p65 accumulation in the nucleus after cell pretreatment with actin-stabilizing and actin-destabilizing agents, which was accompanied by changes in its DNA-binding activity after either EGF stimulation or cytochalasin D treatment. Thus, EGF treatment of A431 cells results in simultaneous nuclear RelA/p65 translocation and cytoplasmic redistribution, with part of RelA/p65 pool forming a very tight association with actin-rich structures. Apparently, nuclear transport is independent on drug stabilization or destabilization of the actin.

Place, publisher, year, edition, pages
Springer Verlag (Germany), 2015
Keywords
RelA/p65; Actin cytoskeleton; Fibronectin; EGF; Cytochalasin D; Jasplakinolide
National Category
Clinical Medicine
Identifiers
urn:nbn:se:liu:diva-121098 (URN)10.1007/s00418-015-1331-5 (DOI)000359650000003 ()25990946 (PubMedID)
Note

Funding Agencies|Swedish Institute [879/2009]; wedish Research Council [2010-3045]; Faculty of Health Science, Linkoping University; European Science Foundation; Molecular and Cellular Biology Program of Russian Academy of Sciences; Russian Foundation for Basic Research [13-04-00497]

Available from: 2015-09-07 Created: 2015-09-07 Last updated: 2017-12-04
Turkina, M., Olofsson, A., Magnusson, K.-E., Arnqvist, A. & Vikström, E. (2015). Helicobacter pylori vesicles carrying CagA localize in the vicinity of cell-cell contacts and induce histone H1 binding to ATP in epithelial cells. FEMS Microbiology Letters, 362(11), fnv076
Open this publication in new window or tab >>Helicobacter pylori vesicles carrying CagA localize in the vicinity of cell-cell contacts and induce histone H1 binding to ATP in epithelial cells
Show others...
2015 (English)In: FEMS Microbiology Letters, ISSN 0378-1097, E-ISSN 1574-6968, Vol. 362, no 11, p. fnv076-Article in journal (Refereed) Published
Abstract [en]

Helicobacter pylori produces outer membrane vesicles (OMV), delivering bacterial substances including the oncogenic cytotoxin-associated CagA protein to their surroundings. We investigated the effects of H. pylori OMV carrying CagA (OMV-CagA) on cell junctions and ATP-binding proteome of epithelial monolayers, using proteomics, mass spectrometry and imaging. OMV-CagA localized in close vicinity of ZO-1 tight junction protein and induced histone H1 binding to ATP. We suggest the expression of novel events in the interactions between H. pylori OMV and epithelia, which may have an influence on host gene transcription and lead to different outcomes of an infection and development of cancer.

Place, publisher, year, edition, pages
Oxford University Press (OUP): Policy B - Oxford Open Option D, 2015
Keywords
Helicobacter pylori; outer membrane vesicles; CagA; ATP-proteome; histone H1; epithelial cell-cell junctions
National Category
Clinical Medicine
Identifiers
urn:nbn:se:liu:diva-120236 (URN)10.1093/femsle/fnv076 (DOI)000356890900007 ()25956174 (PubMedID)
Note

Funding Agencies|Swedish Research Council [2005-4636, 2008-3000, 2014-4361, 2007-3483, 2010-3045]; Euro-BioImaging; Magnus Bergvalls Foundation; Faculty of Health Sciences, Linkoping University; Kempe Memorial Foundation; Cancerfonden [CAN 2012/759]; Cancerforskningsfonden i Norrland; Insamlingstiftelsen for medicinsk forskning vid Umea universitet

Available from: 2015-07-21 Created: 2015-07-20 Last updated: 2017-12-04
Tjellström, B., Stenhammar, L., Magnusson, K.-E., Midtvedt, T., Norin, E., Sundqvist, T. & Högberg, L. (2015). Letter: Exclusive Enteral Nutrition Does Not Normalize Gut Microflora Function in Pediatric Perianal Crohn Disease in JOURNAL OF PEDIATRIC GASTROENTEROLOGY AND NUTRITION, vol 61, issue 1, pp E4-E4 [Letter to the editor]. Journal of Pediatric Gastroenterology and Nutrition - JPGN, 61(1), E4-E4
Open this publication in new window or tab >>Letter: Exclusive Enteral Nutrition Does Not Normalize Gut Microflora Function in Pediatric Perianal Crohn Disease in JOURNAL OF PEDIATRIC GASTROENTEROLOGY AND NUTRITION, vol 61, issue 1, pp E4-E4
Show others...
2015 (English)In: Journal of Pediatric Gastroenterology and Nutrition - JPGN, ISSN 0277-2116, E-ISSN 1536-4801, Vol. 61, no 1, p. E4-E4Article in journal, Letter (Other academic) Published
Abstract [en]

n/a

Place, publisher, year, edition, pages
Lippincott, Williams andamp; Wilkins, 2015
National Category
Clinical Medicine
Identifiers
urn:nbn:se:liu:diva-120654 (URN)10.1097/MPG.0000000000000831 (DOI)000358168800001 ()25905542 (PubMedID)
Available from: 2015-08-20 Created: 2015-08-20 Last updated: 2017-12-04
Navakauskiene, R., Borutinskaite, V. V., Treigyte, G., Savickiene, J., Matuzevicius, D., Navakauskas, D. & Magnusson, K.-E. (2014). Epigenetic changes during hematopoietic cell granulocytic differentiation - comparative analysis of primary CD34+cells, KG1 myeloid cells and mature neutrophils. BMC Cell Biology, 15(4)
Open this publication in new window or tab >>Epigenetic changes during hematopoietic cell granulocytic differentiation - comparative analysis of primary CD34+cells, KG1 myeloid cells and mature neutrophils
Show others...
2014 (English)In: BMC Cell Biology, ISSN 1471-2121, E-ISSN 1471-2121, Vol. 15, no 4Article in journal (Refereed) Published
Abstract [en]

Background: Epigenetic regulation is known to affect gene expression, and recent research shows that aberrant DNA methylation patterning and histone modifications may play a role in leukemogenesis. In order to highlight the co-operation of epigenetic mechanisms acting during the latter process it is important to clarify their potential as biomarkers of granulocytic differentiation. Results: In this study we investigated epigenetic alterations in human hematopoietic cells at a distinct differentiation stages: primary hematopoietic CD34+ cells, KG1 myeloid leukemic cells, whose development is stopped at early stage of differentiation, and mature neutrophils. We focused on the epigenetic status of cell cycle regulating (p15, p16) and differentiation related (E-cadherin and RAR beta) genes. We found that the methylation level in promoter regions of some of these genes was considerably higher in KG1 cells and lower in CD34+ cells and human neutrophils. As examined and evaluated by computer-assisted methods, histone H3 and H4 modifications, i.e. H3K4Me3, H3K9Ac, H3K9Ac/S10Ph and H4 hyperAc, were similar in CD34+ cells and human mature neutrophils. By contrast, in the KG1 cells, histone H3 and H4 modifications were quite high and increased after induction of granulocytic differentiation with the HDAC inhibitor phenyl butyrate. Conclusions: We found the methylation status of the examined gene promoters and histone modifications to be characteristically associated with the hematopoietic cell progenitor state, induced to differentiate myeloid KG1 cells and normal blood neutrophils. This could be achieved through epigenetic regulation of E-cadherin, p15, p16 and RAR beta genes expression caused by DNA methylation/demethylation, core and linker histones distribution in stem hematopoietic cells, induced to differentiation KG1 cells and mature human neutrophils, as well as the histone modifications H3K4Me3, H3K9Ac, H3K9Ac/S10Ph and H4 hyperAc in relation to hematopoietic cell differentiation to granulocyte. These findings also suggest them as potentially important biomarkers of hematopoietic cell granulocytic differentiation and could be valuable for leukemia induced differentiation therapy.

Place, publisher, year, edition, pages
BioMed Central, 2014
Keywords
CD34+cells; Neutrophils; KG1 cells; Histones; Gene methylation/demethylation
National Category
Medical and Health Sciences
Identifiers
urn:nbn:se:liu:diva-104289 (URN)10.1186/1471-2121-15-4 (DOI)000330065200001 ()
Available from: 2014-02-17 Created: 2014-02-14 Last updated: 2017-12-06
Sjöberg, V., Hollén, E., Pietz, G., Magnusson, K.-E., Fälth-Magnusson, K., Sundström, M., . . . Hammarström, M.-L. (2014). Noncontaminated dietary oats may hamper normalization of the intestinal immune status in childhood celiac disease.. Clinical and Translational Gastroenterology, 5(e58)
Open this publication in new window or tab >>Noncontaminated dietary oats may hamper normalization of the intestinal immune status in childhood celiac disease.
Show others...
2014 (English)In: Clinical and Translational Gastroenterology, ISSN 2155-384X, E-ISSN 2155-384X, Vol. 5, no e58Article in journal (Refereed) Published
Abstract [en]

OBJECTIVES: Life-long, strict gluten-free diet (GFD) is the only treatment for celiac disease (CD). Because there is still uncertainty regarding the safety of oats for CD patients, the aim was to investigate whether dietary oats influence the immune status of their intestinal mucosa.

METHODS: Paired small intestinal biopsies, before and after >11 months on a GFD, were collected from children with CD who were enrolled in a randomized, double-blind intervention trial to either of two diets: standard GFD (GFD-std; n=13) and noncontaminated oat-containing GFD (GFD-oats; n=15). Expression levels of mRNAs for 22 different immune effector molecules and tight junction proteins were determined by quantitative reverse transcriptase (RT)-PCR.

RESULTS: The number of mRNAs that remained elevated was higher in the GFD-oats group (P=0.05). In particular, mRNAs for the regulatory T cell (Treg) signature molecules interleukin-10 (IL-10) and transforming growth factor-β1 (TGF-β1), the cytotoxicity-activating natural killer (NK) receptors KLRC2/NKG2C and KLRC3/NKG2E, and the tight junction protein claudin-4 remained elevated. Between the two groups, most significant differences were seen for claudin-4 (P=0.003) and KLRC3/NKG2E (P=0.04).

CONCLUSIONS: A substantial fraction of pediatric CD patients seem to not tolerate oats. In these patients, dietary oats influence the immune status of the intestinal mucosa with an mRNA profile suggesting presence of activated cytotoxic lymphocytes and Tregs and a stressed epithelium with affected tight junctions. Assessment of changes in levels of mRNA for claudin-4 and KLC3/NKG2E from onset to after a year on oats containing GFD shows promise to identify these CD patients.

Place, publisher, year, edition, pages
Nature Publishing Group, 2014
National Category
Pediatrics
Identifiers
urn:nbn:se:liu:diva-115888 (URN)10.1038/ctg.2014.9 (DOI)000355530800002 ()24964993 (PubMedID)2-s2.0-84903278030 (Scopus ID)
Available from: 2015-03-23 Created: 2015-03-23 Last updated: 2017-12-04Bibliographically approved
Organisations

Search in DiVA

Show all publications