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Nuclear expression of mu-opioid receptors in a human mesothelial cell line
Karlstads universitet, Fakulteten för teknik- och naturvetenskap, Avdelningen för kemi och biomedicinsk vetenskap.
Vise andre og tillknytning
2009 (engelsk)Inngår i: Autonomic & Autacoid Pharmacology, ISSN 1474-8665, E-ISSN 1474-8673, Vol. 29, nr 4, s. 165-170Artikkel i tidsskrift (Fagfellevurdert)
Abstract

1 Possibly acting via mu-opioid receptors (MORs), morphine inhibits the formation of

experimentally induced postoperative abdominal adhesions in rats. Mesothelial cells may

participate in adhesion formation by secreting mediators that interfere negatively with

fibrinolysis. Morphine may prevent adhesions by inhibiting the release of pro-adhesion

mediators from mesothelial cells. This study aimed to investigate whether human mesothelial

cells express MOR-1; if so, such could constitute a site of action for morphine in adhesion

prevention.

2 Cells from Met-5A, a human mesothelial cell line were seeded and prepared for

immunocytochemistry and Western blotting.

3 Immunocytochemistry showed MOR-1 expression in mesothelial cells, predominantly in the

nuclei. Western blotting showed two bands (c. 35 and 50 kDa) which correspond to those

obtained with a control lysate from cells known to express MORs. In addition, we found

MOR-1 expression with nuclear and cytoplasmatic localization in biopsies from human

abdominal adhesions.

4 The current findings may suggest that morphine could interact directly with mesothelial cells

via MOR-1 receptors, and thereby modulate adhesion formation, possibly by interfering with

the release of pro-adhesion factors from these cells

sted, utgiver, år, opplag, sider
2009. Vol. 29, nr 4, s. 165-170
Emneord [en]
adhesion, G-protein coupled receptor, intracrine, morphine, mu-opioid receptor, nuclear exression
HSV kategori
Forskningsprogram
Biomedicin
Identifikatorer
URN: urn:nbn:se:kau:diva-9982OAI: oai:DiVA.org:kau-9982DiVA, id: diva2:493496
Tilgjengelig fra: 2012-02-08 Laget: 2012-02-08 Sist oppdatert: 2017-12-07bibliografisk kontrollert

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