1α,25‐dihydroxyvitamin D3‐mediated stimulation of steroid sulphatase activity in myeloid leukaemic cell lines requires VDRnuc‐mediated activation of the RAS/RAF/ERK‐MAP kinase signalling pathway
Identifieur interne : 001D90 ( Main/Exploration ); précédent : 001D89; suivant : 001D911α,25‐dihydroxyvitamin D3‐mediated stimulation of steroid sulphatase activity in myeloid leukaemic cell lines requires VDRnuc‐mediated activation of the RAS/RAF/ERK‐MAP kinase signalling pathway
Auteurs : Philip J. Hughes [Royaume-Uni] ; Geoffrey Brown [Royaume-Uni]Source :
- Journal of Cellular Biochemistry [ 0730-2312 ] ; 2006-06-01.
Abstract
1α,25‐dihydroxyvitamin D3 (1α,25(OH)2D3) stimulates the activity of steroid sulphatase (STS) in myeloid cells [Hughes et al., 2001, 2005]. This was attenuated by inhibitors of phospholipase D (PLD) (n‐butanol, 2,3‐diphosphoglyceric acid, C2‐ceramide) and phosphatidate phosphohydrolase (PAP) (propranolol and chlorpromazine), but was unaffected by inhibitors of phospholipase C. The 1α,25(OH)2D3‐induced STS activity was also attenuated by inhibitors of protein kinase Cα and protein kinase Cδ (Go 6976, HBDDE and rottlerin), but not by an inhibitor of protein kinase Cβ (LY379196). Additionally, 1α,25(OH)2D3‐induced STS activity was attenuated by inhibitors of RAS (manumycin A), RAF (GW5074), MEK (PD098059 and U1026) and JNK (SP600125), but not p38 (PD169316). 1α,25(OH)2D3 produced a rapid and long lasting stimulation of the ERK‐MAP kinase signalling cascade in HL60 myeloid leukaemic cells. This ‘non‐genomic’ effect of 1α,25(OH)2D3 blocked by pharmacological antagonists of nuclear vitamin D receptors (VDRnuc) and does not appear to require hetero‐dimerisation with the retinoid‐X receptor (RXR). Inhibitors of the Src tyrosine kinase (PP1), RAS (manumycin A), RAS–RAF interactions (sulindac sulphide and RAS inhibitory peptide), RAF (GW5074 or chloroquine), and protein kinase Cα (HBDDE) abrogated the 1α,25(OH)2D3‐stimulated increase in ERK‐MAP kinase activity. Taken together, these results show that 1α,25(OH)2D3/VDRnuc activation of the RAS/RAF/ERK‐MAP kinase signalling pathway plays an important role in augmenting STS activity in human myeloid leukaemic cell lines. J. Cell. Biochem. 98: 590–617, 2006. � 2006 Wiley‐Liss, Inc.
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DOI: 10.1002/jcb.20787
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Hughes</name></author><author><name sortKey="Brown, Geoffrey" sort="Brown, Geoffrey" uniqKey="Brown G" first="Geoffrey" last="Brown">Geoffrey Brown</name></author></titleStmt><publicationStmt><idno type="wicri:source">ISTEX</idno><idno type="RBID">ISTEX:AFE96A095B0EE94E7B4301B79732016C288FE47B</idno><date when="2006" year="2006">2006</date><idno type="doi">10.1002/jcb.20787</idno><idno type="url">https://api.istex.fr/ark:/67375/WNG-2VHW1L2F-V/fulltext.pdf</idno><idno type="wicri:Area/Istex/Corpus">001713</idno><idno type="wicri:explorRef" wicri:stream="Istex" wicri:step="Corpus" wicri:corpus="ISTEX">001713</idno><idno type="wicri:Area/Istex/Curation">001713</idno><idno type="wicri:Area/Istex/Checkpoint">000C58</idno><idno type="wicri:explorRef" wicri:stream="Istex" wicri:step="Checkpoint">000C58</idno><idno type="wicri:doubleKey">0730-2312:2006:Hughes P:dihydroxyvitamin:d:mediated</idno><idno type="wicri:Area/Main/Merge">001E02</idno><idno type="wicri:Area/Main/Curation">001D90</idno><idno type="wicri:Area/Main/Exploration">001D90</idno></publicationStmt><sourceDesc><biblStruct><analytic><title level="a" type="main">1α,25‐dihydroxyvitamin D3‐mediated stimulation of steroid sulphatase activity in myeloid leukaemic cell lines requires VDRnuc‐mediated activation of the RAS/RAF/ERK‐MAP kinase signalling pathway</title><author><name sortKey="Hughes, Philip J" sort="Hughes, Philip J" uniqKey="Hughes P" first="Philip J." last="Hughes">Philip J. Hughes</name><affiliation wicri:level="4"><country xml:lang="fr">Royaume-Uni</country><wicri:regionArea>Division of Immunity and Infection, The Medical School, University of Birmingham, Edgbaston, Birmingham B15 2TT</wicri:regionArea><orgName type="university">Université de Birmingham</orgName><placeName><settlement type="city">Birmingham</settlement><region type="country">Angleterre</region><region type="région" nuts="1">Midlands de l'Ouest</region></placeName></affiliation><affiliation wicri:level="1"><country wicri:rule="url">Royaume-Uni</country></affiliation><affiliation wicri:level="4"><country xml:lang="fr">Royaume-Uni</country><wicri:regionArea>Correspondence address: Division of Immunity and Infection, The Medical School, University of Birmingham, Edgbaston, Birmingham B15 2TT</wicri:regionArea><orgName type="university">Université de Birmingham</orgName><placeName><settlement type="city">Birmingham</settlement><region type="country">Angleterre</region><region type="région" nuts="1">Midlands de l'Ouest</region></placeName></affiliation></author><author><name sortKey="Brown, Geoffrey" sort="Brown, Geoffrey" uniqKey="Brown G" first="Geoffrey" last="Brown">Geoffrey Brown</name><affiliation wicri:level="4"><country xml:lang="fr">Royaume-Uni</country><wicri:regionArea>Division of Immunity and Infection, The Medical School, University of Birmingham, Edgbaston, Birmingham B15 2TT</wicri:regionArea><orgName type="university">Université de Birmingham</orgName><placeName><settlement type="city">Birmingham</settlement><region type="country">Angleterre</region><region type="région" nuts="1">Midlands de l'Ouest</region></placeName></affiliation></author></analytic><monogr></monogr><series><title level="j" type="main">Journal of Cellular Biochemistry</title><title level="j" type="alt">JOURNAL OF CELLULAR BIOCHEMISTRY</title><idno type="ISSN">0730-2312</idno><idno type="eISSN">1097-4644</idno><imprint><biblScope unit="vol">98</biblScope><biblScope unit="issue">3</biblScope><biblScope unit="page" from="590">590</biblScope><biblScope unit="page" to="617">617</biblScope><biblScope unit="page-count">28</biblScope><publisher>Wiley Subscription Services, Inc., A Wiley Company</publisher><pubPlace>Hoboken</pubPlace><date type="published" when="2006-06-01">2006-06-01</date></imprint><idno type="ISSN">0730-2312</idno></series></biblStruct></sourceDesc><seriesStmt><idno type="ISSN">0730-2312</idno></seriesStmt></fileDesc><profileDesc><textClass></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="fr">1α,25‐dihydroxyvitamin D3 (1α,25(OH)2D3) stimulates the activity of steroid sulphatase (STS) in myeloid cells [Hughes et al., 2001, 2005]. This was attenuated by inhibitors of phospholipase D (PLD) (n‐butanol, 2,3‐diphosphoglyceric acid, C2‐ceramide) and phosphatidate phosphohydrolase (PAP) (propranolol and chlorpromazine), but was unaffected by inhibitors of phospholipase C. The 1α,25(OH)2D3‐induced STS activity was also attenuated by inhibitors of protein kinase Cα and protein kinase Cδ (Go 6976, HBDDE and rottlerin), but not by an inhibitor of protein kinase Cβ (LY379196). Additionally, 1α,25(OH)2D3‐induced STS activity was attenuated by inhibitors of RAS (manumycin A), RAF (GW5074), MEK (PD098059 and U1026) and JNK (SP600125), but not p38 (PD169316). 1α,25(OH)2D3 produced a rapid and long lasting stimulation of the ERK‐MAP kinase signalling cascade in HL60 myeloid leukaemic cells. This ‘non‐genomic’ effect of 1α,25(OH)2D3 blocked by pharmacological antagonists of nuclear vitamin D receptors (VDRnuc) and does not appear to require hetero‐dimerisation with the retinoid‐X receptor (RXR). Inhibitors of the Src tyrosine kinase (PP1), RAS (manumycin A), RAS–RAF interactions (sulindac sulphide and RAS inhibitory peptide), RAF (GW5074 or chloroquine), and protein kinase Cα (HBDDE) abrogated the 1α,25(OH)2D3‐stimulated increase in ERK‐MAP kinase activity. Taken together, these results show that 1α,25(OH)2D3/VDRnuc activation of the RAS/RAF/ERK‐MAP kinase signalling pathway plays an important role in augmenting STS activity in human myeloid leukaemic cell lines. J. Cell. Biochem. 98: 590–617, 2006. � 2006 Wiley‐Liss, Inc.</div></front></TEI><affiliations><list><country><li>Royaume-Uni</li></country><region><li>Angleterre</li><li>Midlands de l'Ouest</li></region><settlement><li>Birmingham</li></settlement><orgName><li>Université de Birmingham</li></orgName></list><tree><country name="Royaume-Uni"><region name="Angleterre"><name sortKey="Hughes, Philip J" sort="Hughes, Philip J" uniqKey="Hughes P" first="Philip J." last="Hughes">Philip J. Hughes</name></region><name sortKey="Brown, Geoffrey" sort="Brown, Geoffrey" uniqKey="Brown G" first="Geoffrey" last="Brown">Geoffrey Brown</name><name sortKey="Hughes, Philip J" sort="Hughes, Philip J" uniqKey="Hughes P" first="Philip J." last="Hughes">Philip J. Hughes</name><name sortKey="Hughes, Philip J" sort="Hughes, Philip J" uniqKey="Hughes P" first="Philip J." last="Hughes">Philip J. Hughes</name></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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