A. Khorram-Manesh, S. Nordlander, A. Novotny, C. Bengtsson, G. Nylund, M. Levin, S. Nordgren, D. S. Delbro
{"title":"μ-阿片受体在人间皮细胞系中的核表达","authors":"A. Khorram-Manesh, S. Nordlander, A. Novotny, C. Bengtsson, G. Nylund, M. Levin, S. Nordgren, D. S. Delbro","doi":"10.1111/j.1474-8665.2009.00444.x","DOIUrl":null,"url":null,"abstract":"<div>\n \n <p> <b>1</b> Possibly acting via μ-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 ΜΟR-1; if so, such could constitute a site of action for morphine in adhesion prevention.</p>\n <p> <b>2</b> Cells from Met-5A, a human mesothelial cell line were seeded and prepared for immunocytochemistry and Western blotting.</p>\n <p> <b>3</b> Immunocytochemistry showed MOR-1 expression in mesothelial cells, predominantly in the <i>nuclei</i>. Western blotting showed two bands (<i>c</i>. 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.</p>\n <p> <b>4</b> 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.</p>\n </div>","PeriodicalId":100151,"journal":{"name":"Autonomic and Autacoid Pharmacology","volume":"29 4","pages":"165-170"},"PeriodicalIF":0.0000,"publicationDate":"2009-09-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1111/j.1474-8665.2009.00444.x","citationCount":"7","resultStr":"{\"title\":\"Nuclear expression of μ-opioid receptors in a human mesothelial cell line\",\"authors\":\"A. Khorram-Manesh, S. Nordlander, A. Novotny, C. Bengtsson, G. Nylund, M. Levin, S. Nordgren, D. S. Delbro\",\"doi\":\"10.1111/j.1474-8665.2009.00444.x\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<div>\\n \\n <p> <b>1</b> Possibly acting via μ-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 ΜΟR-1; if so, such could constitute a site of action for morphine in adhesion prevention.</p>\\n <p> <b>2</b> Cells from Met-5A, a human mesothelial cell line were seeded and prepared for immunocytochemistry and Western blotting.</p>\\n <p> <b>3</b> Immunocytochemistry showed MOR-1 expression in mesothelial cells, predominantly in the <i>nuclei</i>. Western blotting showed two bands (<i>c</i>. 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.</p>\\n <p> <b>4</b> 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.</p>\\n </div>\",\"PeriodicalId\":100151,\"journal\":{\"name\":\"Autonomic and Autacoid Pharmacology\",\"volume\":\"29 4\",\"pages\":\"165-170\"},\"PeriodicalIF\":0.0000,\"publicationDate\":\"2009-09-09\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"https://sci-hub-pdf.com/10.1111/j.1474-8665.2009.00444.x\",\"citationCount\":\"7\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Autonomic and Autacoid Pharmacology\",\"FirstCategoryId\":\"1085\",\"ListUrlMain\":\"https://onlinelibrary.wiley.com/doi/10.1111/j.1474-8665.2009.00444.x\",\"RegionNum\":0,\"RegionCategory\":null,\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"\",\"PubModel\":\"\",\"JCR\":\"\",\"JCRName\":\"\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"Autonomic and Autacoid Pharmacology","FirstCategoryId":"1085","ListUrlMain":"https://onlinelibrary.wiley.com/doi/10.1111/j.1474-8665.2009.00444.x","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"","JCRName":"","Score":null,"Total":0}
Nuclear expression of μ-opioid receptors in a human mesothelial cell line
1 Possibly acting via μ-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 ΜΟR-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.