Estrogen regulation of JE/MCP-1 mRNA expression in fibroblasts
We have recently demonstrated that 17β‐estradiol (E2) inhibits peritoneal adhesion formation. Because macrophages play a central role in inflammation and wound healing, we chose to investigate whether the E2 could inhibit the expression of JE, the murine monocyte chemoattractant protein‐1 (MCP‐1). T...
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| Veröffentlicht in: | Journal of leukocyte biology 1996-04, Vol.59 (4), p.562-568 |
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| container_issue | 4 |
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| container_title | Journal of leukocyte biology |
| container_volume | 59 |
| creator | Kovacs, E. J. Faunce, D. E. Ramer‐Quinn, D. S. Mott, F. J. Dy, P. ‐W. W. Frazier‐Jessen, M. R. |
| description | We have recently demonstrated that 17β‐estradiol (E2) inhibits peritoneal adhesion formation. Because macrophages play a central role in inflammation and wound healing, we chose to investigate whether the E2 could inhibit the expression of JE, the murine monocyte chemoattractant protein‐1 (MCP‐1). To accomplish this, murine fibroblasts were cultured with physiological concentrations of E2 (3–300 pg/ml) with or without inducers of JE/MCP‐1 mRNA expression. Untreated cells failed to express the message, but, following stimulation, a marked increase in JE/MCP‐1 mRNA expression was observed. At 10–30 pg/ml, E2 had no effect on JE/MCP‐1 mRNA expression in stimulated fibroblasts. In contrast, lower and higher doses of E2 inhibited the expression of JE/MCP‐1 mRNA in stimulated fibroblasts. Treatment with tamoxifen reversed the E2‐inhibition of expression of the message. These data demonstrate that JE/MCP‐1 mRNA expression is controlled, in part, by estrogen and suggest that macrophage recruitment may be affected by circulating levels of E2. |
| doi_str_mv | 10.1002/jlb.59.4.562 |
| format | Article |
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J. ; Faunce, D. E. ; Ramer‐Quinn, D. S. ; Mott, F. J. ; Dy, P. ‐W. W. ; Frazier‐Jessen, M. R.</creator><creatorcontrib>Kovacs, E. J. ; Faunce, D. E. ; Ramer‐Quinn, D. S. ; Mott, F. J. ; Dy, P. ‐W. W. ; Frazier‐Jessen, M. R.</creatorcontrib><description>We have recently demonstrated that 17β‐estradiol (E2) inhibits peritoneal adhesion formation. Because macrophages play a central role in inflammation and wound healing, we chose to investigate whether the E2 could inhibit the expression of JE, the murine monocyte chemoattractant protein‐1 (MCP‐1). To accomplish this, murine fibroblasts were cultured with physiological concentrations of E2 (3–300 pg/ml) with or without inducers of JE/MCP‐1 mRNA expression. Untreated cells failed to express the message, but, following stimulation, a marked increase in JE/MCP‐1 mRNA expression was observed. At 10–30 pg/ml, E2 had no effect on JE/MCP‐1 mRNA expression in stimulated fibroblasts. In contrast, lower and higher doses of E2 inhibited the expression of JE/MCP‐1 mRNA in stimulated fibroblasts. Treatment with tamoxifen reversed the E2‐inhibition of expression of the message. These data demonstrate that JE/MCP‐1 mRNA expression is controlled, in part, by estrogen and suggest that macrophage recruitment may be affected by circulating levels of E2.</description><identifier>ISSN: 0741-5400</identifier><identifier>EISSN: 1938-3673</identifier><identifier>DOI: 10.1002/jlb.59.4.562</identifier><identifier>PMID: 8613705</identifier><language>eng</language><publisher>United States: Society for Leukocyte Biology</publisher><subject>3T3 Cells - drug effects ; 3T3 Cells - metabolism ; 3T3 Cells - physiology ; Animals ; Cells, Cultured ; Chemokine CCL2 - biosynthesis ; Chemokine CCL2 - genetics ; chemotactic cytokines ; Dexamethasone - pharmacology ; Estradiol - pharmacology ; estrogen ; Estrogen Antagonists - pharmacology ; Fibroblasts - drug effects ; Fibroblasts - metabolism ; Fibroblasts - physiology ; Gene Expression Regulation - drug effects ; Humans ; inflammation ; Mice ; Platelet-Derived Growth Factor - antagonists & inhibitors ; Platelet-Derived Growth Factor - pharmacology ; RNA, Messenger - genetics ; RNA, Messenger - metabolism ; Sensitivity and Specificity ; steroid hormones ; Tamoxifen - pharmacology</subject><ispartof>Journal of leukocyte biology, 1996-04, Vol.59 (4), p.562-568</ispartof><rights>1996 Society for Leukocyte Biology</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c3892-51b3acc52fcc599b12f9615bceeff7128ea4f416b2949457ab6e19999ce47493</citedby></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,780,784,27924,27925</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/8613705$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Kovacs, E. J.</creatorcontrib><creatorcontrib>Faunce, D. E.</creatorcontrib><creatorcontrib>Ramer‐Quinn, D. S.</creatorcontrib><creatorcontrib>Mott, F. J.</creatorcontrib><creatorcontrib>Dy, P. ‐W. W.</creatorcontrib><creatorcontrib>Frazier‐Jessen, M. R.</creatorcontrib><title>Estrogen regulation of JE/MCP-1 mRNA expression in fibroblasts</title><title>Journal of leukocyte biology</title><addtitle>J Leukoc Biol</addtitle><description>We have recently demonstrated that 17β‐estradiol (E2) inhibits peritoneal adhesion formation. Because macrophages play a central role in inflammation and wound healing, we chose to investigate whether the E2 could inhibit the expression of JE, the murine monocyte chemoattractant protein‐1 (MCP‐1). To accomplish this, murine fibroblasts were cultured with physiological concentrations of E2 (3–300 pg/ml) with or without inducers of JE/MCP‐1 mRNA expression. Untreated cells failed to express the message, but, following stimulation, a marked increase in JE/MCP‐1 mRNA expression was observed. At 10–30 pg/ml, E2 had no effect on JE/MCP‐1 mRNA expression in stimulated fibroblasts. In contrast, lower and higher doses of E2 inhibited the expression of JE/MCP‐1 mRNA in stimulated fibroblasts. Treatment with tamoxifen reversed the E2‐inhibition of expression of the message. These data demonstrate that JE/MCP‐1 mRNA expression is controlled, in part, by estrogen and suggest that macrophage recruitment may be affected by circulating levels of E2.</description><subject>3T3 Cells - drug effects</subject><subject>3T3 Cells - metabolism</subject><subject>3T3 Cells - physiology</subject><subject>Animals</subject><subject>Cells, Cultured</subject><subject>Chemokine CCL2 - biosynthesis</subject><subject>Chemokine CCL2 - genetics</subject><subject>chemotactic cytokines</subject><subject>Dexamethasone - pharmacology</subject><subject>Estradiol - pharmacology</subject><subject>estrogen</subject><subject>Estrogen Antagonists - pharmacology</subject><subject>Fibroblasts - drug effects</subject><subject>Fibroblasts - metabolism</subject><subject>Fibroblasts - physiology</subject><subject>Gene Expression Regulation - drug effects</subject><subject>Humans</subject><subject>inflammation</subject><subject>Mice</subject><subject>Platelet-Derived Growth Factor - antagonists & inhibitors</subject><subject>Platelet-Derived Growth Factor - pharmacology</subject><subject>RNA, Messenger - genetics</subject><subject>RNA, Messenger - metabolism</subject><subject>Sensitivity and Specificity</subject><subject>steroid hormones</subject><subject>Tamoxifen - pharmacology</subject><issn>0741-5400</issn><issn>1938-3673</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>1996</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqFkL1PwzAQxS0EKqWwsSJlgYm0tmMn8YJUqvJRlQ-h7pYdzm2Q0xQ7Ueh_T6pUHeGGu-H97j3pIXRJ8JBgTEdfVg-5GLIhj-kR6hMRpWEUJ9Ex6uOEkZAzjE_RmfdfGOOIxriHemlMogTzPrqb-sqVS1gHDpa1VVVeroPSBLPp6GXyHpKg-HgdB_CzceD9TsvXgcm1K7VVvvLn6MQo6-Fifwdo8TBdTJ7C-dvj82Q8D7MoFTTkREcqyzg17RJCE2pETLjOAIxJCE1BMcNIrKlggvFE6RiIaCcDljARDdBNZ7tx5XcNvpJF7jOwVq2hrL1MUowTnPJ_QcJjxqkgLXjbgZkrvXdg5MblhXJbSbDc1SrbWiUXksm21ha_2vvWuoDPA7zvsdVJpze5he2fXnI2v8ed53X3s8qXqyZ3IH2hrG0TqGya5pD9C6xtjbs</recordid><startdate>199604</startdate><enddate>199604</enddate><creator>Kovacs, E. 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J.</creatorcontrib><creatorcontrib>Faunce, D. E.</creatorcontrib><creatorcontrib>Ramer‐Quinn, D. S.</creatorcontrib><creatorcontrib>Mott, F. J.</creatorcontrib><creatorcontrib>Dy, P. ‐W. W.</creatorcontrib><creatorcontrib>Frazier‐Jessen, M. R.</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Immunology Abstracts</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>MEDLINE - Academic</collection><jtitle>Journal of leukocyte biology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Kovacs, E. J.</au><au>Faunce, D. E.</au><au>Ramer‐Quinn, D. S.</au><au>Mott, F. J.</au><au>Dy, P. ‐W. W.</au><au>Frazier‐Jessen, M. R.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Estrogen regulation of JE/MCP-1 mRNA expression in fibroblasts</atitle><jtitle>Journal of leukocyte biology</jtitle><addtitle>J Leukoc Biol</addtitle><date>1996-04</date><risdate>1996</risdate><volume>59</volume><issue>4</issue><spage>562</spage><epage>568</epage><pages>562-568</pages><issn>0741-5400</issn><eissn>1938-3673</eissn><abstract>We have recently demonstrated that 17β‐estradiol (E2) inhibits peritoneal adhesion formation. Because macrophages play a central role in inflammation and wound healing, we chose to investigate whether the E2 could inhibit the expression of JE, the murine monocyte chemoattractant protein‐1 (MCP‐1). To accomplish this, murine fibroblasts were cultured with physiological concentrations of E2 (3–300 pg/ml) with or without inducers of JE/MCP‐1 mRNA expression. Untreated cells failed to express the message, but, following stimulation, a marked increase in JE/MCP‐1 mRNA expression was observed. At 10–30 pg/ml, E2 had no effect on JE/MCP‐1 mRNA expression in stimulated fibroblasts. In contrast, lower and higher doses of E2 inhibited the expression of JE/MCP‐1 mRNA in stimulated fibroblasts. Treatment with tamoxifen reversed the E2‐inhibition of expression of the message. These data demonstrate that JE/MCP‐1 mRNA expression is controlled, in part, by estrogen and suggest that macrophage recruitment may be affected by circulating levels of E2.</abstract><cop>United States</cop><pub>Society for Leukocyte Biology</pub><pmid>8613705</pmid><doi>10.1002/jlb.59.4.562</doi><tpages>7</tpages></addata></record> |
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| ispartof | Journal of leukocyte biology, 1996-04, Vol.59 (4), p.562-568 |
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| language | eng |
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| source | MEDLINE; Oxford University Press Journals All Titles (1996-Current) |
| subjects | 3T3 Cells - drug effects 3T3 Cells - metabolism 3T3 Cells - physiology Animals Cells, Cultured Chemokine CCL2 - biosynthesis Chemokine CCL2 - genetics chemotactic cytokines Dexamethasone - pharmacology Estradiol - pharmacology estrogen Estrogen Antagonists - pharmacology Fibroblasts - drug effects Fibroblasts - metabolism Fibroblasts - physiology Gene Expression Regulation - drug effects Humans inflammation Mice Platelet-Derived Growth Factor - antagonists & inhibitors Platelet-Derived Growth Factor - pharmacology RNA, Messenger - genetics RNA, Messenger - metabolism Sensitivity and Specificity steroid hormones Tamoxifen - pharmacology |
| title | Estrogen regulation of JE/MCP-1 mRNA expression in fibroblasts |
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