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Serglycin is part of the secretory repertoire of LPS-activated monocytes

Permanent lenke
https://hdl.handle.net/10037/8854
DOI
https://doi.org/10.1002/iid3.47
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article.pdf (976.4Kb)
(PDF)
Dato
2015-02-11
Type
Journal article
Tidsskriftartikkel
Peer reviewed

Forfatter
Kolseth, Ingrid Moss; Reine, Trine M.; Vuong, Tram Thu; Meen, Astri Jeanette; Fan, Qiong; Jenssen, Trond Geir; Grønning-Wang, Line Mariann; Kolset, Svein Olav
Sammendrag
Monocytes play multiple roles in the immune system, and are active in both acute and chronic diseases. Patients exposed to bacterial infections depend on monocytes in defense reactions, but excessive immune reactions may also cause morbidity through systemic inflammatory responses. Few studies have addressed the importance of proteoglycans, and in particular, the hematopoietic serglycin, in such monocyte immune reactions. Adherent primary monocytes were cultured in absence and presence of LPS. Media were analyzed by ELISA for detection of serglycin. Lysed cell fractions were used to determine the mRNA level of serglycin. Monocytes were also cultured on chamber slides to investigate if serglycin could be detected intracellularly by immunocytochemistry. Monocytes secreted serglycin, and LPS-stimulation increased the secretion. Secretion of inflammatory cytokines increased to a larger extent than serglycin. mRNA levels of serglycin were also increased, suggesting both increased expression and secretion. Immunocytochemistry revealed the presence of serglycin in intracellular vesicles, many destined for secretion. Serglycin containing vesicles increased in number and size when the cells were exposed to LPS. Intracellular vesicle localization and secretion of the proteoglycan serglycin is shown for the first time in primary human monocytes. Monocyte activation by LPS increased the expression and secretion of serglycin, suggesting roles for serglycin in inflammatory processes.
Beskrivelse
Published version. Also available at http://dx.doi.org/10.1002/iid3.47
Forlag
Wiley Open Access
Sitering
Immunity, Inflammation and Disease 2015, 3(1):23-31
Metadata
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  • Artikler, rapporter og annet (klinisk medisin) [1974]

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