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BETA
Sehlin, Janove
Alternative names
Publications (10 of 16) Show all publications
Stenberg, Å., Karlsson, A., Feuk-Lagerstedt, E., Christenson, K., Bylund, J., Oldenborg, A., . . . Oldenborg, P.-A. (2014). Signal regulatory protein alpha is present in several neutrophil granule populations and is rapidly mobilized to the cell surface to negatively fine-tune neutrophil accumulation in inflammation. Journal of Innate Immunity, 6(4), 553-560
Open this publication in new window or tab >>Signal regulatory protein alpha is present in several neutrophil granule populations and is rapidly mobilized to the cell surface to negatively fine-tune neutrophil accumulation in inflammation
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2014 (English)In: Journal of Innate Immunity, ISSN 1662-811X, E-ISSN 1662-8128, Vol. 6, no 4, p. 553-560Article in journal (Refereed) Published
Abstract [en]

Signal regulatory protein alpha (SIRPα) is a cell surface glycoprotein with inhibitory functions, which may regulate neutrophil transmigration. SIRPα is mobilized to the neutrophil surface from specific granules, gelatinase granules, and secretory vesicles following inflammatory activation in vitro and in vivo. The lack of SIRPα signaling and the ability to upregulate SIRPα to the cell surface promote neutrophil accumulation during inflammation in vivo.

Keywords
Neutrophils, Inflammation, Signal regulatory protein alpha, Chemotactic factor, Skin window, Exudate
National Category
Other Basic Medicine
Identifiers
urn:nbn:se:umu:diva-86668 (URN)10.1159/000357820 (DOI)000337655900013 ()24516072 (PubMedID)
Available from: 2014-03-04 Created: 2014-03-04 Last updated: 2018-06-08Bibliographically approved
Stenberg, Å., Sehlin, J. & Oldenborg, P.-A. (2013). Neutrophil apoptosis is associated with loss of signal regulatory protein alpha (SIRP alpha) from the cell surface. Journal of Leukocyte Biology, 93(3), 403-412
Open this publication in new window or tab >>Neutrophil apoptosis is associated with loss of signal regulatory protein alpha (SIRP alpha) from the cell surface
2013 (English)In: Journal of Leukocyte Biology, ISSN 0741-5400, E-ISSN 1938-3673, Vol. 93, no 3, p. 403-412Article in journal (Refereed) Published
Abstract [en]

Cells of the innate immune system, including monocytes, macrophages, and neutrophils, play a major role in the development of inflammatory diseases. During inflammation, large numbers of neutrophils are recruited from the blood and subsequently undergo apoptosis, which involves changes in the cell surface expression of a number of receptors. Neutrophils express the Ig superfamily member, SIRP alpha, which is a receptor involved in regulating cell adhesion and migration. As apoptotic neutrophils down-regulate their capacity for adhesion and migration, we here investigated whether neutrophil expression of SIRP alpha was affected during apoptosis. We found that apoptotic neutrophils lost SIRP alpha from their cell surface with kinetics similar to the loss of CD16. The majority of neutrophils with reduced SIRP alpha also expressed PS on their surface, and the loss of the receptor was reduced proportional to the reduction of apoptosis by caspase inhibitors during Fas-induced apoptosis but less so during spontaneous apoptosis. Neutrophil loss of SIRP alpha or CD16 was inhibited by the protease inhibitor TAPI-2, as well as specific inhibitors of MMP3 or -8, suggesting that proteolytic mechanisms were involved. Finally, SIRP alpha was also found on smaller membrane vesicles released from the cells during apoptosis. Our data suggest that neutrophils reduce their SIRP alpha expression during apoptosis, which may be part of the functional down-regulation seen in apoptotic neutrophils. J. Leukoc. Biol. 93: 403-412; 2013.

Keywords
inflammation, proteolytic shedding, Fas, caspase, CD16
National Category
Cell Biology
Identifiers
urn:nbn:se:umu:diva-67799 (URN)10.1189/jlb.1110637 (DOI)000315579700010 ()
Available from: 2013-04-05 Created: 2013-04-03 Last updated: 2018-06-08Bibliographically approved
Zashikhin, A. L., Sehlin, J. & Barmina, A. (2010). Mechanisms of the contractile activity control in smooth muscle cells. Morfologiia, 138(6), 56-59
Open this publication in new window or tab >>Mechanisms of the contractile activity control in smooth muscle cells
2010 (Russian)In: Morfologiia, ISSN 1026-3543, Vol. 138, no 6, p. 56-59Article in journal (Refereed) Published
National Category
Basic Medicine
Identifiers
urn:nbn:se:umu:diva-42835 (URN)
Available from: 2011-04-14 Created: 2011-04-14 Last updated: 2018-06-08Bibliographically approved
Zashikhin, A. L., Sehlin, J. & Barmina, A. O. (2010). [Reactive changes in the smooth muscle tissue of the rat small intestine during experimental intestinal obstruction].. Morfologiia (Saint Petersburg, Russia), 137(2), 48-53
Open this publication in new window or tab >>[Reactive changes in the smooth muscle tissue of the rat small intestine during experimental intestinal obstruction].
2010 (Russian)In: Morfologiia (Saint Petersburg, Russia), ISSN 1026-3543, Vol. 137, no 2, p. 48-53Article in journal (Refereed) Published
Abstract [ru]

Using light, electron microscopy and immunohistochemical methods, the reactive transformation of smooth muscle tissue (SMT) was studied in the intestinal wall during the development of acute partial high intestinal obstruction. The material of small intestine was taken from 10 male rats in both the zone of ligature application, and proximal and distal zones, 3 cm distant from the ligation zone. The results of the study demonstrate that in partial intestinal obstruction, the nature of structural and functional SMT transformation was variable depending upon differences in functional and destructive loads. During these changes, the remodeling of smooth myocyte population was shown to be one of the mechanisms of SMT adaptation to the changing conditions of functioning. Immunohistochemical analysis found no changes in the pattern of expression of marker and phenotypic proteins in the intestinal zones studied during the dynamics of an experiment.

National Category
Medical and Health Sciences
Identifiers
urn:nbn:se:umu:diva-41360 (URN)20572395 (PubMedID)
Available from: 2011-03-23 Created: 2011-03-23 Last updated: 2018-06-08Bibliographically approved
Saiepour, D., Sehlin, J. & Oldenborg, P.-A. (2006). Insulin inhibits phagocytosis in normal human neutrophils via PKCalpha/beta-dependent priming of F-actin assembly.. Inflammation Research, 55(3), 85-91
Open this publication in new window or tab >>Insulin inhibits phagocytosis in normal human neutrophils via PKCalpha/beta-dependent priming of F-actin assembly.
2006 (English)In: Inflammation Research, ISSN 1023-3830, E-ISSN 1420-908X, Vol. 55, no 3, p. 85-91Article in journal (Refereed) Published
Abstract [en]

OBJECTIVE: This study investigated the effects of insulin on the phagocytosis of C3bi - and IgG-opsonized yeast particles in normal human neutrophils. METHODS: Neutrophils were incubated in different insulin concentrations for 30 minutes and stimulated by C3bi - or IgG-opsonized yeast particles. Phagocytosis was quantified by both light microscopy and FACscan flow cytometry. Laser confocal microscopy was used for quantification of F-actin levels. RESULTS: Elevated insulin concentrations decreased neutrophil phagocytosis of both types of targets. This defect was shown to be in part due to a delayed phagocytosis in the presence of insulin. Following a 30 minute incubation, insulin was found to increase the accumulation of cortical F-actin, without affecting the total cellular F-actin content. The specific PKCalpha/beta inhibitor, Go6976, abolished the insulin-mediated increase in cortical F-actin content and both Go6976 and the PKCalpha/beta/delta/epsilon-specific inhibitor GF109203X reversed the inhibitory effects of insulin on phagocytosis. CONCLUSION: Hyperinsulinemia in vitro can inhibit phagocytosis of opsonized targets in normal human neutrophils. This effect of insulin is dependent on activation of PKCalpha and/or PKCbeta, and these insulin signals may interfere with the dynamic assembly/disassembly and/or distribution of F-actin, which is required for the phagocytosis process.

Identifiers
urn:nbn:se:umu:diva-12283 (URN)doi:10.1007/s00011-005-0009-1 (DOI)16673150 (PubMedID)
Available from: 2008-01-11 Created: 2008-01-11 Last updated: 2018-06-09Bibliographically approved
Zashikhin, A. L., Sehlin, J., Bolduev, V. A. & Agafonov, I. V. (2005). Organization of the muscular component of the lymphangion wall in different parts of the lymphatic bed. Morfologiia, 127(1), 29-32
Open this publication in new window or tab >>Organization of the muscular component of the lymphangion wall in different parts of the lymphatic bed
2005 (English)In: Morfologiia, ISSN 1026-3543, Vol. 127, no 1, p. 29-32Article in journal (Other academic) Published
Abstract [en]

Complex comparative analysis of the organization of smooth muscle (SM) forming the wall of lymphatic vessels in bovine small intestinal mesenterium was performed using the methods of morphometry, quantitative histochemistry (including the analysis of nuclear DNA content, and cytoplasmic protein content) and electron microscopy. SM cells (SMC) isolated by dissociation were studied and were found to possess various levels of differentiation, associated with specific morphometric and metabolic characteristics. The structure of SMC population was shown to vary in both different parts of lymphatic bed and within the wall of an individual lymphangion. The results obtained indicate the cellular heteromorphism of lymphatic bed SM. The peculiarities of SM organization in lymphatic vessels are functionally dependent and are determined not only by the level of SM representation in their wall but also by the proportions of different SMC types.

Keywords
Animals, Cattle, DNA/analysis, Intestine; Small/ultrastructure, Lymphatic Vessels/*cytology/ultrastructure, Male, Mesentery/ultrastructure, Myocytes; Smooth Muscle/*cytology/ultrastructure
Identifiers
urn:nbn:se:umu:diva-12226 (URN)16080344 (PubMedID)
Available from: 2007-04-20 Created: 2007-04-20 Last updated: 2018-06-09Bibliographically approved
Saiepour, D., Sehlin, J. & Oldenborg, P.-A. (2003). Hyperglycemia-induced protein kinase C (PKC) activation inhibits phagocytosis of C3b- and IgG-opsonized yeast particles in normal human neutrophils. Experimental Diabesity Research, 4(2), 125-132
Open this publication in new window or tab >>Hyperglycemia-induced protein kinase C (PKC) activation inhibits phagocytosis of C3b- and IgG-opsonized yeast particles in normal human neutrophils
2003 (English)In: Experimental Diabesity Research, ISSN 1543-8600, E-ISSN 1543-8619, Vol. 4, no 2, p. 125-132Article in journal (Refereed) Published
Abstract [en]

The aim of this study was to investigate the effects of elevated glucose concentrations on complement receptor- and Fcgamma receptor-mediated phagocytosis in normal human neutrophils. D-Glucose at 15 or 25 mM dose-dependently inhibited both complement receptor- and Fcgamma receptor-mediated phagocytosis, as compared to that at a normal physiological glucose concentration. The protein kinase C (PKC) inhibitors GF109203X and Go6976 both dose-dependently and completely reversed the inhibitory effect of 25 mM D-glucose on phagocytosis. Complement receptor-mediated phagocytosis was dose-dependently inhibited by the cell permeable diacylglycerol analogue 1,2-dioctanoyl-sn-glycerol (DAG), an effect that was abolished by PKC inhibitors. Furthermore, suboptimal inhibitory concentrations of DAG and glucose showed an additive inhibitory effect on complement receptor-mediated phagocytosis. The authors conclude that elevated glucose concentrations can inhibit complement receptor and Fcgamma receptor-mediated phagocytosis in normal human neutrophils by activating PKCalpha and/or PKCbeta, an effect possibly mediated by DAG.

Identifiers
urn:nbn:se:umu:diva-4928 (URN)10.1155/EDR.2003.125 (DOI)14630574 (PubMedID)
Available from: 2006-02-01 Created: 2006-02-01 Last updated: 2018-06-09Bibliographically approved
Larsson-Nyrén, G. & Sehlin, J. (2002). Anion-selective amplification of glucose-induced insulin secretion.. Acta Diabetologica, 39(1), 41-7
Open this publication in new window or tab >>Anion-selective amplification of glucose-induced insulin secretion.
2002 (English)In: Acta Diabetologica, ISSN 0940-5429, E-ISSN 1432-5233, Vol. 39, no 1, p. 41-7Article in journal (Refereed) Published
Abstract [en]

The functional roles of anions on glucose-induced insulin secretion are poorly understood. We investigated the effects of the monovalent anions thiocyanate, iodide, bromide, nitrate and chloride on the dynamics of insulin secretion in isolated pancreatic islets from non-inbred Umeå ob/ob mice. All anion species (12 mM), except Cl-, significantly amplified glucose-induced (20 mM) first- and second-phase insulin secretion (selectivity sequence: SCN->NO3->I->Br->Cl-). Simultaneously, the anions reduced the lag-time prior to the initiation of the secretion (SCN-=I-=NO3->Br->Cl-). The results indicate that pancreatic beta-cell activation can be initiated and amplified by an anion-selective mechanism showing increasing degrees of activation in the order of the anion series of Hofmeister. On the basis of the strikingly similar anion selectivity of amplified secretion and shortened lag-phase, we suggest that both types of anion effects are caused by action at a single site on the beta-cell.

National Category
Basic Medicine
Identifiers
urn:nbn:se:umu:diva-82534 (URN)12043938 (PubMedID)
Available from: 2013-11-05 Created: 2013-11-05 Last updated: 2018-06-08
Ravier, M. A., Sehlin, J. & Henquin, J. C. (2002). Disorganization of cytoplasmic Ca(2+) oscillations and pulsatile insulin secretion in islets from ob/ obmice. Diabetologia, 45(8), 1154-1163
Open this publication in new window or tab >>Disorganization of cytoplasmic Ca(2+) oscillations and pulsatile insulin secretion in islets from ob/ obmice
2002 (English)In: Diabetologia, ISSN 0012-186X, E-ISSN 1432-0428, Vol. 45, no 8, p. 1154-1163Article in journal (Refereed) Published
Abstract [en]

AIMS/HYPOTHESIS: In normal mouse islets, glucose induces synchronous cytoplasmic [Ca(2+)](i) oscillations in beta cells and pulses of insulin secretion. We investigated whether this fine regulation of islet function is preserved in hyperglycaemic and hyperinsulinaemic ob/ obmice.

METHODS: Intact islets from ob/ ob mice and their lean littermates were used after overnight culture for measurement of [Ca(2+)](i) and insulin secretion.

RESULTS: We observed three types of [Ca(2+)](i) responses during stimulation by 9 to 12 mmol/l of glucose: sustained increase, rapid oscillations and slow (or mixed) oscillations. They occurred in 8, 18 and 74% of lean islets and 9, 0 and 91% of ob/ ob islets, respectively. Subtle desynchronisation of [Ca(2+)](i) oscillations between regions occurred in 11% of lean islets. In ob/ ob islets, desynchronisation was frequent (66-82% depending on conditions) and prominent: oscillations were out of phase in different regions because of distinct periods and shapes. Only small ob/ ob islets were well synchronised, but sizes of synchronised lean and desynchronised ob/ ob islets were markedly overlapped. The occurrence of desynchronisation in clusters of 5 to 50 islet cells from ob/ obmice and not from lean mice further indicates that islet hypertrophy is not the only causal factor. In both types of islets, synchronous [Ca(2+)](i) oscillations were accompanied by oscillations of insulin secretion. In poorly synchronised ob/ ob islets, secretion was irregular but followed the pattern of the global [Ca(2+)](i) changes.

CONCLUSIONS/INTERPRETATION: The regularity of glucose-induced [Ca(2+)](i) oscillations is disrupted in islets from ob/ ob mice and this desynchronisation perturbs the pulsatility of insulin secretion. A similar mechanism could contribute to the irregularity of insulin oscillations in Type II (non-insulin-dependent) diabetes mellitus.

Place, publisher, year, edition, pages
Springer-Verlag New York, 2002
Keywords
insulin secretion, pancreatic islet, beta cell, cytosolic Ca2+, pulsatility, ob/ob mouse
National Category
Endocrinology and Diabetes
Identifiers
urn:nbn:se:umu:diva-82647 (URN)10.1007/s00125-002-0883-9 (DOI)000177865900010 ()12189446 (PubMedID)
Available from: 2013-11-06 Created: 2013-11-06 Last updated: 2018-06-08Bibliographically approved
Larsson-Nyrén, G., Pakhtusova, N. & Sehlin, J. (2002). Isolated mouse pancreatic β-cells show cell-specific temporal response pattern. American Journal of Physiology - Cell Physiology, 282(6), C1199-C1204
Open this publication in new window or tab >>Isolated mouse pancreatic β-cells show cell-specific temporal response pattern
2002 (English)In: American Journal of Physiology - Cell Physiology, ISSN 0363-6143, E-ISSN 1522-1563, Vol. 282, no 6, p. C1199-C1204Article in journal (Refereed) Published
Abstract [en]

The length of the silent lag time before elevation of the cytosolic free Ca2+ concentration ([Ca2+]i) differs between individual pancreatic beta-cells. One important question is whether these differences reflect a random phenomenon or whether the length of lag time is inherent in the individual beta-cell. We compared the lag times, initial dips, and initial peak heights for [Ca2+]i from two consecutive glucose stimulations (with either 10 or 20 mM glucose) in individual ob/ob mouse beta-cells with the fura 2 technique in a microfluorimetric system. There was a strong correlation between the lengths of the lag times in each beta-cell (10 mM glucose: r = 0.94, P < 0.001; 20 mM glucose: r = 0.96, P < 0.001) as well as between the initial dips in [Ca2+]i (10 mM glucose: r = 0.93, P < 0.001; 20 mM glucose: r = 0.79, P < 0.001) and between the initial peak heights (10 mM glucose: r = 0.51, P < 0.01; 20 mM glucose: r = 0.77, P < 0.001). These data provide evidence that the response pattern, including both the length of the lag time and the dynamics of the subsequent [Ca2+]i, is specific for the individual beta-cell.

Place, publisher, year, edition, pages
?, 2002
Identifiers
urn:nbn:se:umu:diva-4883 (URN)10.1152/ajpcell.00009.2001 (DOI)11997233 (PubMedID)
Available from: 2005-12-21 Created: 2005-12-21 Last updated: 2018-06-09Bibliographically approved
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