LTD4 increases cytosolic free calcium and inositol phosphates in human neutrophils: inhibition by the novel LTD4 receptor antagonist, SR2640, and possible relation to modulation of chemotaxis
Abstract LTD4 increased the level of free intracellular calcium ([Ca++]i) and stimulated the production of inositol phosphates (IP) in human polymorphonuclear neutrophils (PMN). Calcium was predominantly mobilized from intracellular pools. After a single stimulus, the cells were refractory to a seco...
Ausführliche Beschreibung
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| Autor*in: |
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| Format: |
E-Artikel |
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| Sprache: |
Englisch |
| Erschienen: |
1990 |
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| Umfang: |
9 |
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| Reproduktion: |
Springer Online Journal Archives 1860-2002 |
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| Übergeordnetes Werk: |
in: Inflammation research - 1969, 29(1990) vom: März/Apr., Seite 299-307 |
| Übergeordnetes Werk: |
volume:29 ; year:1990 ; month:03/04 ; pages:299-307 ; extent:9 |
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NLEJ18910547X |
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| 245 | 1 | 0 | |a LTD4 increases cytosolic free calcium and inositol phosphates in human neutrophils: inhibition by the novel LTD4 receptor antagonist, SR2640, and possible relation to modulation of chemotaxis |
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| 520 | |a Abstract LTD4 increased the level of free intracellular calcium ([Ca++]i) and stimulated the production of inositol phosphates (IP) in human polymorphonuclear neutrophils (PMN). Calcium was predominantly mobilized from intracellular pools. After a single stimulus, the cells were refractory to a second challenge with the same concentration of LTD4, but the calcium response to LTB4 was normal. The rise in [Ca++]i as well as the stimulated production of IP was inhibited by the novel LTD4 antagonist, SR2640. SR2640 also abolished the attenuation by LTD4 of LTB4-directed PMN chemotaxis. The results suggest that human PMN contain specific LTD4 receptor that trigger phosphatidyl inositol hydrolysis by activation of phospholipase C, leading to intracellular calcium mobilization, which may be involved in modulation of chemotaxis. | ||
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(DE-627)NLEJ18910547X DE-627 ger DE-627 rakwb eng LTD4 increases cytosolic free calcium and inositol phosphates in human neutrophils: inhibition by the novel LTD4 receptor antagonist, SR2640, and possible relation to modulation of chemotaxis 1990 9 nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier Abstract LTD4 increased the level of free intracellular calcium ([Ca++]i) and stimulated the production of inositol phosphates (IP) in human polymorphonuclear neutrophils (PMN). Calcium was predominantly mobilized from intracellular pools. After a single stimulus, the cells were refractory to a second challenge with the same concentration of LTD4, but the calcium response to LTB4 was normal. The rise in [Ca++]i as well as the stimulated production of IP was inhibited by the novel LTD4 antagonist, SR2640. SR2640 also abolished the attenuation by LTD4 of LTB4-directed PMN chemotaxis. The results suggest that human PMN contain specific LTD4 receptor that trigger phosphatidyl inositol hydrolysis by activation of phospholipase C, leading to intracellular calcium mobilization, which may be involved in modulation of chemotaxis. Springer Online Journal Archives 1860-2002 Bouchelouche, P. N. oth Ahnfelt-Rønne, I. oth Thomsen, M. K. oth in Inflammation research 1969 29(1990) vom: März/Apr., Seite 299-307 (DE-627)NLEJ188993533 (DE-600)1459194-7 1420-908X nnns volume:29 year:1990 month:03/04 pages:299-307 extent:9 http://dx.doi.org/10.1007/BF01966461 GBV_USEFLAG_U ZDB-1-SOJ GBV_NL_ARTICLE AR 29 1990 3/4 299-307 9 |
| spelling |
(DE-627)NLEJ18910547X DE-627 ger DE-627 rakwb eng LTD4 increases cytosolic free calcium and inositol phosphates in human neutrophils: inhibition by the novel LTD4 receptor antagonist, SR2640, and possible relation to modulation of chemotaxis 1990 9 nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier Abstract LTD4 increased the level of free intracellular calcium ([Ca++]i) and stimulated the production of inositol phosphates (IP) in human polymorphonuclear neutrophils (PMN). Calcium was predominantly mobilized from intracellular pools. After a single stimulus, the cells were refractory to a second challenge with the same concentration of LTD4, but the calcium response to LTB4 was normal. The rise in [Ca++]i as well as the stimulated production of IP was inhibited by the novel LTD4 antagonist, SR2640. SR2640 also abolished the attenuation by LTD4 of LTB4-directed PMN chemotaxis. The results suggest that human PMN contain specific LTD4 receptor that trigger phosphatidyl inositol hydrolysis by activation of phospholipase C, leading to intracellular calcium mobilization, which may be involved in modulation of chemotaxis. Springer Online Journal Archives 1860-2002 Bouchelouche, P. N. oth Ahnfelt-Rønne, I. oth Thomsen, M. K. oth in Inflammation research 1969 29(1990) vom: März/Apr., Seite 299-307 (DE-627)NLEJ188993533 (DE-600)1459194-7 1420-908X nnns volume:29 year:1990 month:03/04 pages:299-307 extent:9 http://dx.doi.org/10.1007/BF01966461 GBV_USEFLAG_U ZDB-1-SOJ GBV_NL_ARTICLE AR 29 1990 3/4 299-307 9 |
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(DE-627)NLEJ18910547X DE-627 ger DE-627 rakwb eng LTD4 increases cytosolic free calcium and inositol phosphates in human neutrophils: inhibition by the novel LTD4 receptor antagonist, SR2640, and possible relation to modulation of chemotaxis 1990 9 nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier Abstract LTD4 increased the level of free intracellular calcium ([Ca++]i) and stimulated the production of inositol phosphates (IP) in human polymorphonuclear neutrophils (PMN). Calcium was predominantly mobilized from intracellular pools. After a single stimulus, the cells were refractory to a second challenge with the same concentration of LTD4, but the calcium response to LTB4 was normal. The rise in [Ca++]i as well as the stimulated production of IP was inhibited by the novel LTD4 antagonist, SR2640. SR2640 also abolished the attenuation by LTD4 of LTB4-directed PMN chemotaxis. The results suggest that human PMN contain specific LTD4 receptor that trigger phosphatidyl inositol hydrolysis by activation of phospholipase C, leading to intracellular calcium mobilization, which may be involved in modulation of chemotaxis. Springer Online Journal Archives 1860-2002 Bouchelouche, P. N. oth Ahnfelt-Rønne, I. oth Thomsen, M. K. oth in Inflammation research 1969 29(1990) vom: März/Apr., Seite 299-307 (DE-627)NLEJ188993533 (DE-600)1459194-7 1420-908X nnns volume:29 year:1990 month:03/04 pages:299-307 extent:9 http://dx.doi.org/10.1007/BF01966461 GBV_USEFLAG_U ZDB-1-SOJ GBV_NL_ARTICLE AR 29 1990 3/4 299-307 9 |
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(DE-627)NLEJ18910547X DE-627 ger DE-627 rakwb eng LTD4 increases cytosolic free calcium and inositol phosphates in human neutrophils: inhibition by the novel LTD4 receptor antagonist, SR2640, and possible relation to modulation of chemotaxis 1990 9 nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier Abstract LTD4 increased the level of free intracellular calcium ([Ca++]i) and stimulated the production of inositol phosphates (IP) in human polymorphonuclear neutrophils (PMN). Calcium was predominantly mobilized from intracellular pools. After a single stimulus, the cells were refractory to a second challenge with the same concentration of LTD4, but the calcium response to LTB4 was normal. The rise in [Ca++]i as well as the stimulated production of IP was inhibited by the novel LTD4 antagonist, SR2640. SR2640 also abolished the attenuation by LTD4 of LTB4-directed PMN chemotaxis. The results suggest that human PMN contain specific LTD4 receptor that trigger phosphatidyl inositol hydrolysis by activation of phospholipase C, leading to intracellular calcium mobilization, which may be involved in modulation of chemotaxis. Springer Online Journal Archives 1860-2002 Bouchelouche, P. N. oth Ahnfelt-Rønne, I. oth Thomsen, M. K. oth in Inflammation research 1969 29(1990) vom: März/Apr., Seite 299-307 (DE-627)NLEJ188993533 (DE-600)1459194-7 1420-908X nnns volume:29 year:1990 month:03/04 pages:299-307 extent:9 http://dx.doi.org/10.1007/BF01966461 GBV_USEFLAG_U ZDB-1-SOJ GBV_NL_ARTICLE AR 29 1990 3/4 299-307 9 |
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(DE-627)NLEJ18910547X DE-627 ger DE-627 rakwb eng LTD4 increases cytosolic free calcium and inositol phosphates in human neutrophils: inhibition by the novel LTD4 receptor antagonist, SR2640, and possible relation to modulation of chemotaxis 1990 9 nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier Abstract LTD4 increased the level of free intracellular calcium ([Ca++]i) and stimulated the production of inositol phosphates (IP) in human polymorphonuclear neutrophils (PMN). Calcium was predominantly mobilized from intracellular pools. After a single stimulus, the cells were refractory to a second challenge with the same concentration of LTD4, but the calcium response to LTB4 was normal. The rise in [Ca++]i as well as the stimulated production of IP was inhibited by the novel LTD4 antagonist, SR2640. SR2640 also abolished the attenuation by LTD4 of LTB4-directed PMN chemotaxis. The results suggest that human PMN contain specific LTD4 receptor that trigger phosphatidyl inositol hydrolysis by activation of phospholipase C, leading to intracellular calcium mobilization, which may be involved in modulation of chemotaxis. Springer Online Journal Archives 1860-2002 Bouchelouche, P. N. oth Ahnfelt-Rønne, I. oth Thomsen, M. K. oth in Inflammation research 1969 29(1990) vom: März/Apr., Seite 299-307 (DE-627)NLEJ188993533 (DE-600)1459194-7 1420-908X nnns volume:29 year:1990 month:03/04 pages:299-307 extent:9 http://dx.doi.org/10.1007/BF01966461 GBV_USEFLAG_U ZDB-1-SOJ GBV_NL_ARTICLE AR 29 1990 3/4 299-307 9 |
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ltd4 increases cytosolic free calcium and inositol phosphates in human neutrophils: inhibition by the novel ltd4 receptor antagonist, sr2640, and possible relation to modulation of chemotaxis |
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LTD4 increases cytosolic free calcium and inositol phosphates in human neutrophils: inhibition by the novel LTD4 receptor antagonist, SR2640, and possible relation to modulation of chemotaxis |
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Abstract LTD4 increased the level of free intracellular calcium ([Ca++]i) and stimulated the production of inositol phosphates (IP) in human polymorphonuclear neutrophils (PMN). Calcium was predominantly mobilized from intracellular pools. After a single stimulus, the cells were refractory to a second challenge with the same concentration of LTD4, but the calcium response to LTB4 was normal. The rise in [Ca++]i as well as the stimulated production of IP was inhibited by the novel LTD4 antagonist, SR2640. SR2640 also abolished the attenuation by LTD4 of LTB4-directed PMN chemotaxis. The results suggest that human PMN contain specific LTD4 receptor that trigger phosphatidyl inositol hydrolysis by activation of phospholipase C, leading to intracellular calcium mobilization, which may be involved in modulation of chemotaxis. |
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Abstract LTD4 increased the level of free intracellular calcium ([Ca++]i) and stimulated the production of inositol phosphates (IP) in human polymorphonuclear neutrophils (PMN). Calcium was predominantly mobilized from intracellular pools. After a single stimulus, the cells were refractory to a second challenge with the same concentration of LTD4, but the calcium response to LTB4 was normal. The rise in [Ca++]i as well as the stimulated production of IP was inhibited by the novel LTD4 antagonist, SR2640. SR2640 also abolished the attenuation by LTD4 of LTB4-directed PMN chemotaxis. The results suggest that human PMN contain specific LTD4 receptor that trigger phosphatidyl inositol hydrolysis by activation of phospholipase C, leading to intracellular calcium mobilization, which may be involved in modulation of chemotaxis. |
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Abstract LTD4 increased the level of free intracellular calcium ([Ca++]i) and stimulated the production of inositol phosphates (IP) in human polymorphonuclear neutrophils (PMN). Calcium was predominantly mobilized from intracellular pools. After a single stimulus, the cells were refractory to a second challenge with the same concentration of LTD4, but the calcium response to LTB4 was normal. The rise in [Ca++]i as well as the stimulated production of IP was inhibited by the novel LTD4 antagonist, SR2640. SR2640 also abolished the attenuation by LTD4 of LTB4-directed PMN chemotaxis. The results suggest that human PMN contain specific LTD4 receptor that trigger phosphatidyl inositol hydrolysis by activation of phospholipase C, leading to intracellular calcium mobilization, which may be involved in modulation of chemotaxis. |
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LTD4 increases cytosolic free calcium and inositol phosphates in human neutrophils: inhibition by the novel LTD4 receptor antagonist, SR2640, and possible relation to modulation of chemotaxis |
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<?xml version="1.0" encoding="UTF-8"?><collection xmlns="http://www.loc.gov/MARC21/slim"><record><leader>01000caa a22002652 4500</leader><controlfield tag="001">NLEJ18910547X</controlfield><controlfield tag="003">DE-627</controlfield><controlfield tag="005">20210707114845.0</controlfield><controlfield tag="007">cr uuu---uuuuu</controlfield><controlfield tag="008">070525s1990 xx |||||o 00| ||eng c</controlfield><datafield tag="035" ind1=" " ind2=" "><subfield code="a">(DE-627)NLEJ18910547X</subfield></datafield><datafield tag="040" ind1=" " ind2=" "><subfield code="a">DE-627</subfield><subfield code="b">ger</subfield><subfield code="c">DE-627</subfield><subfield code="e">rakwb</subfield></datafield><datafield tag="041" ind1=" " ind2=" "><subfield code="a">eng</subfield></datafield><datafield tag="245" ind1="1" ind2="0"><subfield code="a">LTD4 increases cytosolic free calcium and inositol phosphates in human neutrophils: inhibition by the novel LTD4 receptor antagonist, SR2640, and possible relation to modulation of chemotaxis</subfield></datafield><datafield tag="264" ind1=" " ind2="1"><subfield code="c">1990</subfield></datafield><datafield tag="300" ind1=" " ind2=" "><subfield code="a">9</subfield></datafield><datafield tag="336" ind1=" " ind2=" "><subfield code="a">nicht spezifiziert</subfield><subfield code="b">zzz</subfield><subfield code="2">rdacontent</subfield></datafield><datafield tag="337" ind1=" " ind2=" "><subfield code="a">nicht spezifiziert</subfield><subfield code="b">z</subfield><subfield code="2">rdamedia</subfield></datafield><datafield tag="338" ind1=" " ind2=" "><subfield code="a">nicht spezifiziert</subfield><subfield code="b">zu</subfield><subfield code="2">rdacarrier</subfield></datafield><datafield tag="520" ind1=" " ind2=" "><subfield code="a">Abstract LTD4 increased the level of free intracellular calcium ([Ca++]i) and stimulated the production of inositol phosphates (IP) in human polymorphonuclear neutrophils (PMN). Calcium was predominantly mobilized from intracellular pools. After a single stimulus, the cells were refractory to a second challenge with the same concentration of LTD4, but the calcium response to LTB4 was normal. The rise in [Ca++]i as well as the stimulated production of IP was inhibited by the novel LTD4 antagonist, SR2640. SR2640 also abolished the attenuation by LTD4 of LTB4-directed PMN chemotaxis. The results suggest that human PMN contain specific LTD4 receptor that trigger phosphatidyl inositol hydrolysis by activation of phospholipase C, leading to intracellular calcium mobilization, which may be involved in modulation of chemotaxis.</subfield></datafield><datafield tag="533" ind1=" " ind2=" "><subfield code="f">Springer Online Journal Archives 1860-2002</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Bouchelouche, P. N.</subfield><subfield code="4">oth</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Ahnfelt-Rønne, I.</subfield><subfield code="4">oth</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Thomsen, M. K.</subfield><subfield code="4">oth</subfield></datafield><datafield tag="773" ind1="0" ind2="8"><subfield code="i">in</subfield><subfield code="t">Inflammation research</subfield><subfield code="d">1969</subfield><subfield code="g">29(1990) vom: März/Apr., Seite 299-307</subfield><subfield code="w">(DE-627)NLEJ188993533</subfield><subfield code="w">(DE-600)1459194-7</subfield><subfield code="x">1420-908X</subfield><subfield code="7">nnns</subfield></datafield><datafield tag="773" ind1="1" ind2="8"><subfield code="g">volume:29</subfield><subfield code="g">year:1990</subfield><subfield code="g">month:03/04</subfield><subfield code="g">pages:299-307</subfield><subfield code="g">extent:9</subfield></datafield><datafield tag="856" ind1="4" ind2="0"><subfield code="u">http://dx.doi.org/10.1007/BF01966461</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_USEFLAG_U</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">ZDB-1-SOJ</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_NL_ARTICLE</subfield></datafield><datafield tag="951" ind1=" " ind2=" "><subfield code="a">AR</subfield></datafield><datafield tag="952" ind1=" " ind2=" "><subfield code="d">29</subfield><subfield code="j">1990</subfield><subfield code="c">3/4</subfield><subfield code="h">299-307</subfield><subfield code="g">9</subfield></datafield></record></collection>
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