Platelet‐derived growth factor and angiotensin II cause increases in cytosolic free calcium by different mechanisms in vascular smooth muscle cells

Journal of Cellular Physiology - Tập 139 Số 1 - Trang 100-108 - 1989
Michael W. Roe1,2, John R. Hepler3, T. Kendall Harden4, Brian Herman2,5
1Department of Cell Biology and Anatomy, The University of North Carolina School of Medicine, Chapel Hill, North Carolina 27599
2Laboratories for Cell Biology, The University of North Carolina School of Medicine, Chapel Hill, North Carolina 27599
3Program in Neurobiology, The University of North Carolina School of Medicine, Chapel Hill, North Carolina 27599
4Department of Pharmacology, The University of North Carolina School of Medicine, Chapel Hill, North Carolina 27599
5Lineberger Cancer Research Center, The University of North Carolina School of Medicine, Chapel Hill, North Carolina 27599

Tóm tắt

AbstractPlatelet‐derived growth factor (PDGF) and angiotensin II (All) are thought to mediate their biological effects in vascular smooth muscle cells (VSMCs) by causing alterations in cytosolic free calcium ([Ca2+]i). In this study we examine the pathways by which PDGF and All alter [Ca2 +]i in VSMCs. Addition of PDGF resulted in a rapid, transient, concentration‐dependent increase in [Ca2+]i; this rise in [Ca2 +]i was blocked completely by preincubation of cells with ethylene glycol‐bis (β‐aminoethyl ether) N,N,N′,N′‐tetraacetic acid (EGTA) or CoCl2, by the voltage‐sensitive Ca2 +‐channel antagonists verapamil or nifedipine, by 12‐O‐tetradecanoylphorbol‐13‐acetate (TPA), or by pertussis toxin. All also caused an increase in [Ca2 +]i; however, All‐stimulated alterations in [Ca2+]i displayed different kinetics compared with those caused by PDGF. Pretreatment of cells with 8‐(diethylamine)‐octyl‐3,4,5‐trimethyoxybenzoate hydrochloride (TMB‐8), almost totally inhibited All‐induced increases in [Ca2+]i. EGTA or CoCl2 only slightly diminished All‐stimulated increases in [Ca2+]i. Nifedipine, verapamil, TPA, and pertussis toxin pretreatment were without effect on All‐induced increases in [Ca2+]i. PDGF and All both stimulated increases in total inositol phosphate accumulation, although the one‐half maximal concentration (ED50) for alterations in [Ca2+]i and phosphoinisitide hydrolysis differed by a factor of 10 for PDGF (3 × 10−10 M for Ca2+ vs. 2.5 × 10−9 M for phosphoinositide hydrolysis), but they were essentially identical for All (7.5 × 10−9 M for Ca2+ vs. 5.0 × 10−9 M for phosphoinositide hydrolysis). PDGF stimulated mitogenesis (as measured by [3H]‐thymidine incorporation into DNA) in VSMCs with an ED50 similar to that for PDGF‐induced alterations in phosphoinositide hydrolysis. PDGF‐stimulated mitogenesis was blocked by pretreatment of cells with voltage‐sensitive Ca2 + channel blockers, TPA, or pertussis toxin. These results suggest that PDGF and All cause alterations in [Ca2+]i in VSMCs by at least quantitatively distinct mechanisms. PDGF binding activates a pertussis‐toxin‐sensitive Ca2+ influx into cells via voltage‐sensitive Ca2+ channels (blocked by EGTA, verapamil, and nifedipine), as well as stimulating phosphoinositide hydrolysis leading to release of Ca2+ from intracellular stores. All‐induced alterations in [Ca2+]i are mainly the result of phosphoinositide hydrolysis and consequent entry of Ca2+ into the cytoplasm from intracellular stores. Our data also suggest that changes in [Ca2 +]i caused by PDGF are required for PDGF‐stimulated mitogenesis.

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Tài liệu tham khảo

Abdel‐Latif A. A., 1986, Calcium‐mobilizing receptors, polyphosphoinositides, and the generation of second messengers, Pharmacol., Rev., 38, 227

10.1042/bj1920783

10.1042/bj2240291

10.1016/S0021-9258(18)48280-4

Ambler S. K., 1984, The relationship between phosphatadylinositol metabolisms and mobilization of intracellular calcium elicited by alpha1‐adrenergic receptor stimulation in BC3H1 cells, Mol. Pharmacol., 26, 405

Ambler S. K., 1986, Mobilization of intracellular calcium by a1‐adrenergic receptor activation in muscle cell monolayers, J. Biol. Chem., 261, 5866, 10.1016/S0021-9258(17)38463-6

10.1126/science.3485309

Berk B. C., 1987, Early agonist mediated ionic events in cultured vascular smooth muscle cells: Calcium mobilization is associated with intracellular acidification, J. Biol. Chem., 262, 5065, 10.1016/S0021-9258(18)61154-8

10.1146/annurev.bi.56.070187.001111

10.1042/bj2220195

10.1111/j.1749-6632.1988.tb33381.x

Capponi A. M., 1985, Cytosolic free calcium levels in monolayers of cultured rat aortic smooth muscle cells: Effects of angiotensin II and vasopressin, J. Biol. Chem., 260, 7836, 10.1016/S0021-9258(17)39528-5

10.1146/annurev.bi.56.070187.002143

10.1002/jcp.1041240306

10.1038/313313a0

10.1016/0014-5793(86)80288-5

Doyle V. M., 1985, Vasopressin induced production of inositol trisphosphate and calcium efflux in a smooth muscle cell line, Biochem. Biophys. Res. Commun., 131, 469, 10.1016/0006-291X(85)91826-1

Drummond A. H., 1977, Beta adrenergic regulation of glycogen phosphorylase activity and adenosine 3′,5′‐monophosphate accumulation in control and desensitized C‐6 astrocytoma cells, Mol. Pharmacol., 13, 1159

10.1073/pnas.85.10.3633

10.1016/0014-4827(85)90454-9

Gores G. J. Nieminen A.‐L. Wray B. Herman B. andLemasters J. J.(1988) Intracellular pH during “chemical hypoxia” in cultured rat hepatocytes: Protection by intracellular acidosis against the onset of cell death.J. Clin. Invest. (in press).

Griendling K. K., 1986, Sustained diacylglycerol formation from inositol phospholipids in angiotensin II‐stimulated vascular smooth muscle cells, J. Biol. Chem., 261, 5901, 10.1016/S0021-9258(17)38468-5

10.1042/bj1760541

10.1002/jcp.1041130213

10.1016/S0021-9258(19)83641-4

Habenicht A. J. R., 1981, Early changes in phophatidylinositol and arachidonic acid metabolism in quiescent Swiss 3T3 cells stimulated to divide by platelet‐derived growth factor, J. Biol. Chem., 256, 12329, 10.1016/S0021-9258(18)43275-9

10.1126/science.2836952

10.1042/bj2320099

10.1111/j.1749-6632.1988.tb33382.x

Hepler J. R., 1987, Epidermal growth factor stimulates the formation of inositol (1,4,5)‐trisphosphate and a rise in cytosolic calcium from mobilization of intracellular stores, J. Biol. Chem., 262, 2951, 10.1016/S0021-9258(18)61452-8

10.1016/S0022-2828(87)80642-9

10.1002/cm.970080202

10.1038/325445a0

10.1146/annurev.pa.26.040186.001301

10.1016/0021-9150(88)90004-4

Johnson R. M., 1987, Epidermal growth factor and angiotensin II stimulate the formation of inositol 1,4,5‐ and inositol 1,3,4‐phosphate in hepatocytes: Differential inhibition by pertussis toxin and phorbol 12‐myristate‐13‐acetate, J. Biol Chem., 262, 17285, 10.1016/S0021-9258(18)45375-6

10.1016/0014-4827(87)90290-4

10.1016/0006-291X(88)90485-8

10.1038/325078a0

10.1016/0014-4827(87)90161-3

10.1016/0014-5793(76)80640-0

Moolenaar W. H., 1984, Growth factors immediately raise intracellular free Ca2 + in human fibroblasts, J. Biol. Chem., 259, 8066, 10.1016/S0021-9258(17)39690-4

10.1007/BF00591101

Nabika T., 1985, Increase in cytosolic free calcium and phosphoinositide metabolism induced by angiotensin II and [Arg] vasopressin in vascular smooth muscle cells, J. Biol. Chem., 260, 4661, 10.1016/S0021-9258(18)89121-9

Nishimoto I., 1987, Insulin‐like growth factor II stimulates calcium influx in competent BALB/c‐3T3 cells primed with epidermal growth factor, J. Biol. Chem., 262, 12120, 10.1016/S0021-9258(18)45324-0

Ohta H., 1985, Inhibition by islet activating protein of a chemotactic peptide‐induced early breakdown of inositol phospholipids and Ca2 + mobilization in guinea pig neutrophils, J. Biol. Chem., 260, 15771, 10.1016/S0021-9258(17)36325-1

Pace C. S., 1984, Influence of a tumor prompting phorbol ester on the electrical response of B‐cells to glucose and glyburide, Mol. Pharmacol., 26, 267

Putney J. W., 1987, Formation and actions of calcium‐mobilizing messenger, inositol 1,4,5‐trisphosphate, Am. J. Physiol., 252, G149

10.1016/0006-291X(85)90463-2

10.1073/pnas.71.4.1207

10.1016/0092-8674(86)90733-6

10.1016/0006-291X(86)90935-6

Smith J. B., 1986, Angiotensin‐receptor signalling in cultured vascular smooth muscle cells, Am. J. Physiol., 250, F759

10.1073/pnas.81.24.7812

10.1111/j.1476-5381.1987.tb10292.x

Sperti G., 1987, Ca2+ channel antagonists inhibit DNA synthesis and proliferation of A7r5 vascular smooth muscle cells, Fed. Proc., 46, 974

10.1507/endocrj1954.34.313

10.1016/0014-5793(85)80009-0

10.1016/0006-291X(85)91846-7

10.1126/science.2446390

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Journal of Cellular Physiology

Tập 139 Số 1

100-108

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