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血清、缓激肽和血管加压素可刺激人成纤维细胞释放肌醇磷酸。

Serum, bradykinin and vasopressin stimulate release of inositol phosphates from human fibroblasts.

作者信息

Vicentini L M, Villereal M L

出版信息

Biochem Biophys Res Commun. 1984 Sep 17;123(2):663-70. doi: 10.1016/0006-291x(84)90280-8.

DOI:10.1016/0006-291x(84)90280-8
PMID:6435618
Abstract

The mitogens serum, vasopressin and bradykinin stimulate a significant rise in the inositol phosphate content of cultured human fibroblasts within 10 seconds, while serum- and bradykinin-stimulated arachidonic acid release does not occur until after 30 seconds. The release of inositol phosphates is not secondary to a rise in Ca activity since the Ca ionophore ionomycin does not stimulate release of inositol phosphates. Moreover, we show that phospholipase C in human fibroblasts is activated by these mitogens at resting Ca levels since TMB-8, which blocks the mitogen-induced rise in Ca activity, does not affect the serum-stimulated accumulation of inositol phosphates.

摘要

促细胞分裂剂血清、血管加压素和缓激肽可在10秒内刺激培养的人成纤维细胞中的肌醇磷酸含量显著升高,而血清和缓激肽刺激的花生四烯酸释放直到30秒后才会发生。肌醇磷酸的释放并非继发于Ca活性的升高,因为钙离子载体离子霉素不会刺激肌醇磷酸的释放。此外,我们发现,在静息Ca水平下,人成纤维细胞中的磷脂酶C可被这些促细胞分裂剂激活,因为可阻断促细胞分裂剂诱导的Ca活性升高的TMB-8并不影响血清刺激的肌醇磷酸积累。

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1
Serum, bradykinin and vasopressin stimulate release of inositol phosphates from human fibroblasts.血清、缓激肽和血管加压素可刺激人成纤维细胞释放肌醇磷酸。
Biochem Biophys Res Commun. 1984 Sep 17;123(2):663-70. doi: 10.1016/0006-291x(84)90280-8.
2
Mitogen-stimulated release of inositol phosphates in human fibroblasts.丝裂原刺激的人成纤维细胞中肌醇磷酸的释放
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Epidermal-growth-factor-induced formation of inositol phosphates in human A431 cells. Differences from the effect of bradykinin.表皮生长因子诱导人A431细胞中肌醇磷酸的形成。与缓激肽作用的差异。
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Mediation of growth factor induced DNA synthesis and calcium mobilization by Gq and Gi2.生长因子诱导的DNA合成和钙动员由Gq和Gi2介导。
J Cell Biol. 1993 Apr;121(1):91-9. doi: 10.1083/jcb.121.1.91.
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Control of Ca2+ entry into HL60 and U937 human leukaemia cells by the filling state of the intracellular Ca2+ stores.
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Biochem J. 1993 Feb 1;289 ( Pt 3)(Pt 3):761-6. doi: 10.1042/bj2890761.
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Decreased bradykinin binding sites in fibroblasts from progressive systemic scleroderma.进行性系统性硬化症患者成纤维细胞中缓激肽结合位点减少。
Arch Dermatol Res. 1994;286(3-4):133-6. doi: 10.1007/BF00374207.
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