Disassociation of the macrophage-maturational effects of vitamin D from respiratory burst priming
During the process of enhancing monocytic differentiation of the human leukemia line HL-60, 1,25-dihydroxyvitamin D3 (1,25(OH)2D3) also "primes" the cell for respiratory burst by increasing the uptake of Ca2+ across the plasma membrane (Hruska, K.A., Bar-Shavit, Z., Malone, J.D., and Teite...
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Published in | The Journal of biological chemistry Vol. 266; no. 17; pp. 10888 - 10892 |
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Main Authors | , , , , , |
Format | Journal Article |
Language | English |
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Bethesda, MD
American Society for Biochemistry and Molecular Biology
15.06.1991
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Abstract | During the process of enhancing monocytic differentiation of the human leukemia line HL-60, 1,25-dihydroxyvitamin D3 (1,25(OH)2D3)
also "primes" the cell for respiratory burst by increasing the uptake of Ca2+ across the plasma membrane (Hruska, K.A., Bar-Shavit,
Z., Malone, J.D., and Teitelbaum, S.L. (1988) J. Biol. Chem. 263, 16039-16044). The present study asked if the maturational
effect of vitamin D is dependent upon this "priming" phenomenon. To this end, we exposed HL-60 to either 1,25(OH)2D3 or its
synthetic analogue (1 alpha, 3 beta, 5Z, 7E)-9-10-Secocholesta-5,7,10(19)-triene-1, 3, 25-triol (22-oxa). We found that 22-oxa
induced HL-60 maturation as effectively as does the natural steroid. As expected, 48 h of 1,25(OH)2D3 exposure more than doubles
(p less than 0.005) HL-60 basal cytosolic Ca2+ and increases inositol triphosphate-sensitive Ca2+ stores approximately 4-fold
(p less than 0.01). 22-oxa in contrast alters neither Ca(2+)- nor inositol triphosphate-mobilizable deposits. Moreover, 1,25(OH)2D3
treatment prompts a transient Ca2+ "spike" in response to formyl-methionyl-leucyl-phenylalanine (fMLP) and a marked increase
in superoxide (O-2) generation when exposed to the chemotactic peptide (p less than 0.01) or phorbol ester (p less than 0.02).
Treatment with 22-oxa does not enable HL-60 to respond to fMLP with a Ca2+ spike or prime the cell for respiratory burst unless
it is co-incubated with the Ca2+ ionophore, ionomycin. Similarly, phorbol ester impacts more profoundly on O-2 generation
by 1,25(OH)2D3 than 22-oxa preincubated cells (p less than 0.02), unless the latter is added with ionomycin. Our findings
indicate that the maturational effects of vitamin D sterols are independent of their capacity to prime cells for respiratory
burst and that the Ca2+ ionophoretic effects of 1,25(OH)2D3 play a major role in such priming. |
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AbstractList | During the process of enhancing monocytic differentiation of the human leukemia line HL-60, 1,25-dihydroxyvitamin D3 (1,25(OH)2D3) also "primes" the cell for respiratory burst by increasing the uptake of Ca2+ across the plasma membrane (Hruska, K.A., Bar-Shavit, Z., Malone, J.D., and Teitelbaum, S.L. (1988) J. Biol. Chem. 263, 16039-16044). The present study asked if the maturational effect of vitamin D is dependent upon this "priming" phenomenon. To this end, we exposed HL-60 to either 1,25(OH)2D3 or its synthetic analogue (1 alpha, 3 beta, 5Z, 7E)-9-10-Secocholesta-5,7,10(19)-triene-1, 3, 25-triol (22-oxa). We found that 22-oxa induced HL-60 maturation as effectively as does the natural steroid. As expected, 48 h of 1,25(OH)2D3 exposure more than doubles (p less than 0.005) HL-60 basal cytosolic Ca2+ and increases inositol triphosphate-sensitive Ca2+ stores approximately 4-fold (p less than 0.01). 22-oxa in contrast alters neither Ca(2+)- nor inositol triphosphate-mobilizable deposits. Moreover, 1,25(OH)2D3 treatment prompts a transient Ca2+ "spike" in response to formyl-methionyl-leucyl-phenylalanine (fMLP) and a marked increase in superoxide (O-2) generation when exposed to the chemotactic peptide (p less than 0.01) or phorbol ester (p less than 0.02). Treatment with 22-oxa does not enable HL-60 to respond to fMLP with a Ca2+ spike or prime the cell for respiratory burst unless it is co-incubated with the Ca2+ ionophore, ionomycin. Similarly, phorbol ester impacts more profoundly on O-2 generation by 1,25(OH)2D3 than 22-oxa preincubated cells (p less than 0.02), unless the latter is added with ionomycin. Our findings indicate that the maturational effects of vitamin D sterols are independent of their capacity to prime cells for respiratory burst and that the Ca2+ ionophoretic effects of 1,25(OH)2D3 play a major role in such priming. During the process of enhancing monocytic differentiation of the human leukemia line HL-60, 1,25-dihydroxyvitamin D3 (1,25(OH)2D3) also "primes" the cell for respiratory burst by increasing the uptake of Ca2+ across the plasma membrane (Hruska, K.A., Bar-Shavit, Z., Malone, J.D., and Teitelbaum, S.L. (1988) J. Biol. Chem. 263, 16039-16044). The present study asked if the maturational effect of vitamin D is dependent upon this "priming" phenomenon. To this end, we exposed HL-60 to either 1,25(OH)2D3 or its synthetic analogue (1 alpha, 3 beta, 5Z, 7E)-9-10-Secocholesta-5,7,10(19)-triene-1, 3, 25-triol (22-oxa). We found that 22-oxa induced HL-60 maturation as effectively as does the natural steroid. As expected, 48 h of 1,25(OH)2D3 exposure more than doubles (p less than 0.005) HL-60 basal cytosolic Ca2+ and increases inositol triphosphate-sensitive Ca2+ stores approximately 4-fold (p less than 0.01). 22-oxa in contrast alters neither Ca(2+)- nor inositol triphosphate-mobilizable deposits. Moreover, 1,25(OH)2D3 treatment prompts a transient Ca2+ "spike" in response to formyl-methionyl-leucyl-phenylalanine (fMLP) and a marked increase in superoxide (O-2) generation when exposed to the chemotactic peptide (p less than 0.01) or phorbol ester (p less than 0.02). Treatment with 22-oxa does not enable HL-60 to respond to fMLP with a Ca2+ spike or prime the cell for respiratory burst unless it is co-incubated with the Ca2+ ionophore, ionomycin. Similarly, phorbol ester impacts more profoundly on O-2 generation by 1,25(OH)2D3 than 22-oxa preincubated cells (p less than 0.02), unless the latter is added with ionomycin. Our findings indicate that the maturational effects of vitamin D sterols are independent of their capacity to prime cells for respiratory burst and that the Ca2+ ionophoretic effects of 1,25(OH)2D3 play a major role in such priming. |
Author | Y Nishii K A Hruska H Tanaka S L Teitelbaum J D Malone Y Seino |
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Cites_doi | 10.1016/0014-5793(87)80550-1 10.1042/bj2040713 10.1073/pnas.74.3.1204 10.1038/312315a0 10.1126/science.3014651 10.1248/cpb.34.2286 10.1016/0145-2126(83)90057-7 10.1016/0076-6879(87)41075-6 10.1073/pnas.80.19.5907 10.1248/cpb.34.4410 10.1016/0006-291X(81)91628-4 10.1083/jcb.98.2.391 10.1016/0003-2697(84)90457-3 10.1016/S0021-9258(18)37553-7 10.1016/0003-2697(87)90284-3 10.1016/S0190-9622(88)70207-8 10.1172/JCI111249 10.4049/jimmunol.138.6.1680 10.1042/bj2320323 10.1016/S0021-9258(19)86577-8 10.1016/S0021-9258(18)47677-6 10.1007/BF02409507 10.1210/endo-118-2-679 |
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Keywords | Human Signal transduction Calcium Vitamin D Reaction mechanism Respiratory burst Cell differentiation Macrophage |
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References | Jaken (10.1016/S0021-9258(18)99102-7_bib18) 1987; 141 Babior (10.1016/S0021-9258(18)99102-7_bib23) 1984; 73 Lacey (10.1016/S0021-9258(18)99102-7_bib13) 1987; 138 Miyaura (10.1016/S0021-9258(18)99102-7_bib1) 1981; 102 Tanaka (10.1016/S0021-9258(18)99102-7_bib2) 1982; 204 McWilliams (10.1016/S0021-9258(18)99102-7_bib16) 1977; 74 Niedel (10.1016/S0021-9258(18)99102-7_bib17) 1979; 254 Hruska (10.1016/S0021-9258(18)99102-7_bib8) 1988; 263 Berridge (10.1016/S0021-9258(18)99102-7_bib25) 1984; 312 Johnson (10.1016/S0021-9258(18)99102-7_bib19) 1985; 44 Bar-Shavit (10.1016/S0021-9258(18)99102-7_bib7) 1981; 33 Kubodera (10.1016/S0021-9258(18)99102-7_bib10) 1986; 34 Smith (10.1016/S0021-9258(18)99102-7_bib21) 1988; 19 Cooke (10.1016/S0021-9258(18)99102-7_bib20) 1985; 232 Kahn (10.1016/S0021-9258(18)99102-7_bib22) 1981; 94 Abe (10.1016/S0021-9258(18)99102-7_bib9) 1987; 226 Bar-Shavit (10.1016/S0021-9258(18)99102-7_bib12) 1986; 118 Clohisy (10.1016/S0021-9258(18)99102-7_bib6) 1987; 262 Hyslop (10.1016/S0021-9258(18)99102-7_bib14) 1984; 141 Murayama (10.1016/S0021-9258(18)99102-7_bib11) 1986; 34 Wymann (10.1016/S0021-9258(18)99102-7_bib15) 1987; 165 Mangelsdorf (10.1016/S0021-9258(18)99102-7_bib5) 1984; 98 Nishizuka (10.1016/S0021-9258(18)99102-7_bib26) 1986; 233 Snyderman (10.1016/S0021-9258(18)99102-7_bib24) 1986; 40 Bar-Shavit (10.1016/S0021-9258(18)99102-7_bib3) 1983; 80 McCarthy (10.1016/S0021-9258(18)99102-7_bib4) 1983; 7 |
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Snippet | During the process of enhancing monocytic differentiation of the human leukemia line HL-60, 1,25-dihydroxyvitamin D3 (1,25(OH)2D3)
also "primes" the cell for... During the process of enhancing monocytic differentiation of the human leukemia line HL-60, 1,25-dihydroxyvitamin D3 (1,25(OH)2D3) also "primes" the cell for... |
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SubjectTerms | Antineoplastic Agents - pharmacology Biological and medical sciences Calcitriol - analogs & derivatives Calcitriol - metabolism Calcitriol - pharmacology Calcium - metabolism Cell Differentiation - drug effects Cell differentiation, maturation, development, hematopoiesis Cell Line Cell physiology Cytoplasm - metabolism Fundamental and applied biological sciences. Psychology Humans Leukemia, Promyelocytic, Acute Macrophages - cytology Macrophages - drug effects Molecular and cellular biology N-Formylmethionine Leucyl-Phenylalanine - pharmacology Receptors, Calcitriol Receptors, Formyl Peptide Receptors, Immunologic - drug effects Receptors, Immunologic - metabolism Receptors, Steroid - drug effects Receptors, Steroid - metabolism Superoxides - metabolism Tetradecanoylphorbol Acetate - pharmacology |
Title | Disassociation of the macrophage-maturational effects of vitamin D from respiratory burst priming |
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