Vitamin A is a key regulator for cell growth, cytokine production, and differentiation in normal B cells
In the present paper we demonstrate that retinol-retinol-binding protein and chylomicron remnant retinyl esters in concentrations normally found in human plasma inhibit growth of normal human B lymphocytes. Physiological concentrations of retinoic acid (about 30 nM) were less active than physiologic...
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Veröffentlicht in: | The Journal of biological chemistry 1992-11, Vol.267 (33), p.23988-23992 |
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container_title | The Journal of biological chemistry |
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creator | Blomhoff, H K Smeland, E B Erikstein, B Rasmussen, A M Skrede, B Skjønsberg, C Blomhoff, R |
description | In the present paper we demonstrate that retinol-retinol-binding protein and chylomicron remnant retinyl esters in concentrations
normally found in human plasma inhibit growth of normal human B lymphocytes. Physiological concentrations of retinoic acid
(about 30 nM) were less active than physiological concentrations of retinol (about 3 microM). Pharmacological concentrations
of retinol and retinoic acid were more active than the concentrations normally found in plasma. Retinol (3 microM) inhibited
anti-IgM-mediated DNA synthesis as measured by [3H]thymidine uptake at 72 h by 78%. Furthermore, we found that the cells were
blocked in the mid-G1 phase of the cell cycle. Thus, neither MYC up-regulation measured at 3 h nor the expression of the early
activation antigen 4F2 was reduced by retinol, whereas the late activation markers (transferrin receptor expression and actinomycin
D staining at 48 h of stimulation) were markedly inhibited. Retinol reduced the interleukin 6 production induced by anti-IgM
and interleukin 4 after 48 h, whereas the induction of interleukin 6 and tumor necrosis factor by O-tetradecanoylphorbol-13-acetate
and ionomycin was less affected. We also noted that the retinoids reduced the formation of plaque-forming cells (i.e. Ig synthesis).
These data imply that vitamin A present in human plasma is a normal modulator of B cell function. |
doi_str_mv | 10.1016/S0021-9258(18)35934-9 |
format | Article |
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normally found in human plasma inhibit growth of normal human B lymphocytes. Physiological concentrations of retinoic acid
(about 30 nM) were less active than physiological concentrations of retinol (about 3 microM). Pharmacological concentrations
of retinol and retinoic acid were more active than the concentrations normally found in plasma. Retinol (3 microM) inhibited
anti-IgM-mediated DNA synthesis as measured by [3H]thymidine uptake at 72 h by 78%. Furthermore, we found that the cells were
blocked in the mid-G1 phase of the cell cycle. Thus, neither MYC up-regulation measured at 3 h nor the expression of the early
activation antigen 4F2 was reduced by retinol, whereas the late activation markers (transferrin receptor expression and actinomycin
D staining at 48 h of stimulation) were markedly inhibited. Retinol reduced the interleukin 6 production induced by anti-IgM
and interleukin 4 after 48 h, whereas the induction of interleukin 6 and tumor necrosis factor by O-tetradecanoylphorbol-13-acetate
and ionomycin was less affected. We also noted that the retinoids reduced the formation of plaque-forming cells (i.e. Ig synthesis).
These data imply that vitamin A present in human plasma is a normal modulator of B cell function.</description><identifier>ISSN: 0021-9258</identifier><identifier>EISSN: 1083-351X</identifier><identifier>DOI: 10.1016/S0021-9258(18)35934-9</identifier><identifier>PMID: 1429735</identifier><language>eng</language><publisher>United States: American Society for Biochemistry and Molecular Biology</publisher><subject>B-Lymphocytes - cytology ; B-Lymphocytes - drug effects ; B-Lymphocytes - physiology ; Cell Cycle - drug effects ; Cell Differentiation - drug effects ; Cell Division - drug effects ; Cells, Cultured ; Chylomicrons - pharmacology ; Cytokines - biosynthesis ; DNA - biosynthesis ; Dose-Response Relationship, Drug ; Humans ; Interleukin-6 - biosynthesis ; Kinetics ; Thymidine - metabolism ; Tretinoin - pharmacology ; Tritium ; Tumor Necrosis Factor-alpha - biosynthesis ; Vitamin A - pharmacology</subject><ispartof>The Journal of biological chemistry, 1992-11, Vol.267 (33), p.23988-23992</ispartof><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c380t-b38dae70dc19740daf078b2a0c44b6f6c193f5257834699e69deb04e9832c0ae3</citedby><cites>FETCH-LOGICAL-c380t-b38dae70dc19740daf078b2a0c44b6f6c193f5257834699e69deb04e9832c0ae3</cites></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/1429735$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Blomhoff, H K</creatorcontrib><creatorcontrib>Smeland, E B</creatorcontrib><creatorcontrib>Erikstein, B</creatorcontrib><creatorcontrib>Rasmussen, A M</creatorcontrib><creatorcontrib>Skrede, B</creatorcontrib><creatorcontrib>Skjønsberg, C</creatorcontrib><creatorcontrib>Blomhoff, R</creatorcontrib><title>Vitamin A is a key regulator for cell growth, cytokine production, and differentiation in normal B cells</title><title>The Journal of biological chemistry</title><addtitle>J Biol Chem</addtitle><description>In the present paper we demonstrate that retinol-retinol-binding protein and chylomicron remnant retinyl esters in concentrations
normally found in human plasma inhibit growth of normal human B lymphocytes. Physiological concentrations of retinoic acid
(about 30 nM) were less active than physiological concentrations of retinol (about 3 microM). Pharmacological concentrations
of retinol and retinoic acid were more active than the concentrations normally found in plasma. Retinol (3 microM) inhibited
anti-IgM-mediated DNA synthesis as measured by [3H]thymidine uptake at 72 h by 78%. Furthermore, we found that the cells were
blocked in the mid-G1 phase of the cell cycle. Thus, neither MYC up-regulation measured at 3 h nor the expression of the early
activation antigen 4F2 was reduced by retinol, whereas the late activation markers (transferrin receptor expression and actinomycin
D staining at 48 h of stimulation) were markedly inhibited. Retinol reduced the interleukin 6 production induced by anti-IgM
and interleukin 4 after 48 h, whereas the induction of interleukin 6 and tumor necrosis factor by O-tetradecanoylphorbol-13-acetate
and ionomycin was less affected. We also noted that the retinoids reduced the formation of plaque-forming cells (i.e. Ig synthesis).
These data imply that vitamin A present in human plasma is a normal modulator of B cell function.</description><subject>B-Lymphocytes - cytology</subject><subject>B-Lymphocytes - drug effects</subject><subject>B-Lymphocytes - physiology</subject><subject>Cell Cycle - drug effects</subject><subject>Cell Differentiation - drug effects</subject><subject>Cell Division - drug effects</subject><subject>Cells, Cultured</subject><subject>Chylomicrons - pharmacology</subject><subject>Cytokines - biosynthesis</subject><subject>DNA - biosynthesis</subject><subject>Dose-Response Relationship, Drug</subject><subject>Humans</subject><subject>Interleukin-6 - biosynthesis</subject><subject>Kinetics</subject><subject>Thymidine - metabolism</subject><subject>Tretinoin - pharmacology</subject><subject>Tritium</subject><subject>Tumor Necrosis Factor-alpha - biosynthesis</subject><subject>Vitamin A - pharmacology</subject><issn>0021-9258</issn><issn>1083-351X</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>1992</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNpFkNtKxDAQhoMouq4-gpALEYWt5tC0yeUqnkDwwgPehTSdbqNto0mL7Nvb3RUdGAZm_vln-BA6ouScEppdPBHCaKKYkKdUnnGheJqoLTShRPKEC_q2jSZ_kj20H-M7GSNVdBft0pSpnIsJql9db1rX4Tl2ERv8AUscYDE0pvcBV2NaaBq8CP67r2fYLnv_4TrAn8GXg-2d72bYdCUuXVVBgK53ZtXEo2PnQ2safLl2iAdopzJNhMPfOkUvN9fPV3fJw-Pt_dX8IbFckj4puCwN5KS0VOUpKU1FclkwQ2yaFlmVjW1eCSZyydNMKchUCQVJQUnOLDHAp-hk4zt--DVA7HXr4uoD04EfoqaZYJwJMgrFRmiDjzFApT-Da01Yakr0irBeE9YrfJpKvSas1bh39HtgKFoo_7c2SMf58WZeu0X97QLownlbQ6tZlmvONeNKSv4DhySDAg</recordid><startdate>19921125</startdate><enddate>19921125</enddate><creator>Blomhoff, H K</creator><creator>Smeland, E B</creator><creator>Erikstein, B</creator><creator>Rasmussen, A M</creator><creator>Skrede, B</creator><creator>Skjønsberg, C</creator><creator>Blomhoff, R</creator><general>American Society for Biochemistry and Molecular Biology</general><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7T5</scope><scope>H94</scope></search><sort><creationdate>19921125</creationdate><title>Vitamin A is a key regulator for cell growth, cytokine production, and differentiation in normal B cells</title><author>Blomhoff, H K ; Smeland, E B ; Erikstein, B ; Rasmussen, A M ; Skrede, B ; Skjønsberg, C ; Blomhoff, R</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c380t-b38dae70dc19740daf078b2a0c44b6f6c193f5257834699e69deb04e9832c0ae3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>1992</creationdate><topic>B-Lymphocytes - cytology</topic><topic>B-Lymphocytes - drug effects</topic><topic>B-Lymphocytes - physiology</topic><topic>Cell Cycle - drug effects</topic><topic>Cell Differentiation - drug effects</topic><topic>Cell Division - drug effects</topic><topic>Cells, Cultured</topic><topic>Chylomicrons - pharmacology</topic><topic>Cytokines - biosynthesis</topic><topic>DNA - biosynthesis</topic><topic>Dose-Response Relationship, Drug</topic><topic>Humans</topic><topic>Interleukin-6 - biosynthesis</topic><topic>Kinetics</topic><topic>Thymidine - metabolism</topic><topic>Tretinoin - pharmacology</topic><topic>Tritium</topic><topic>Tumor Necrosis Factor-alpha - biosynthesis</topic><topic>Vitamin A - pharmacology</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Blomhoff, H K</creatorcontrib><creatorcontrib>Smeland, E B</creatorcontrib><creatorcontrib>Erikstein, B</creatorcontrib><creatorcontrib>Rasmussen, A M</creatorcontrib><creatorcontrib>Skrede, B</creatorcontrib><creatorcontrib>Skjønsberg, C</creatorcontrib><creatorcontrib>Blomhoff, 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><jtitle>The Journal of biological chemistry</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Blomhoff, H K</au><au>Smeland, E B</au><au>Erikstein, B</au><au>Rasmussen, A M</au><au>Skrede, B</au><au>Skjønsberg, C</au><au>Blomhoff, R</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Vitamin A is a key regulator for cell growth, cytokine production, and differentiation in normal B cells</atitle><jtitle>The Journal of biological chemistry</jtitle><addtitle>J Biol Chem</addtitle><date>1992-11-25</date><risdate>1992</risdate><volume>267</volume><issue>33</issue><spage>23988</spage><epage>23992</epage><pages>23988-23992</pages><issn>0021-9258</issn><eissn>1083-351X</eissn><abstract>In the present paper we demonstrate that retinol-retinol-binding protein and chylomicron remnant retinyl esters in concentrations
normally found in human plasma inhibit growth of normal human B lymphocytes. Physiological concentrations of retinoic acid
(about 30 nM) were less active than physiological concentrations of retinol (about 3 microM). Pharmacological concentrations
of retinol and retinoic acid were more active than the concentrations normally found in plasma. Retinol (3 microM) inhibited
anti-IgM-mediated DNA synthesis as measured by [3H]thymidine uptake at 72 h by 78%. Furthermore, we found that the cells were
blocked in the mid-G1 phase of the cell cycle. Thus, neither MYC up-regulation measured at 3 h nor the expression of the early
activation antigen 4F2 was reduced by retinol, whereas the late activation markers (transferrin receptor expression and actinomycin
D staining at 48 h of stimulation) were markedly inhibited. Retinol reduced the interleukin 6 production induced by anti-IgM
and interleukin 4 after 48 h, whereas the induction of interleukin 6 and tumor necrosis factor by O-tetradecanoylphorbol-13-acetate
and ionomycin was less affected. We also noted that the retinoids reduced the formation of plaque-forming cells (i.e. Ig synthesis).
These data imply that vitamin A present in human plasma is a normal modulator of B cell function.</abstract><cop>United States</cop><pub>American Society for Biochemistry and Molecular Biology</pub><pmid>1429735</pmid><doi>10.1016/S0021-9258(18)35934-9</doi><tpages>5</tpages><oa>free_for_read</oa></addata></record> |
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source | MEDLINE; EZB-FREE-00999 freely available EZB journals; Alma/SFX Local Collection |
subjects | B-Lymphocytes - cytology B-Lymphocytes - drug effects B-Lymphocytes - physiology Cell Cycle - drug effects Cell Differentiation - drug effects Cell Division - drug effects Cells, Cultured Chylomicrons - pharmacology Cytokines - biosynthesis DNA - biosynthesis Dose-Response Relationship, Drug Humans Interleukin-6 - biosynthesis Kinetics Thymidine - metabolism Tretinoin - pharmacology Tritium Tumor Necrosis Factor-alpha - biosynthesis Vitamin A - pharmacology |
title | Vitamin A is a key regulator for cell growth, cytokine production, and differentiation in normal B cells |
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