Interconversion of inositol (1,4,5)-trisphosphate to inositol (1,3,4,5)-tetrakisphosphate and (1,3,4)-trisphosphate in permeabilized adrenal glomerulosa cells is calcium-sensitive and ATP-dependent

Mf, Rossier; Ia, Dentand; Pd, Lew; Am, Capponi; Mb, Vallotton

doi:10.1016/s0006-291x(86)80107-3

Cited by 44 publications

(13 citation statements)

References 9 publications

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“…3). In addition, it is known that removal of ATP from the medium prevents the appearance of Ins(1,3,4)P3 in permeabilized adrenal glomerulosa cells (Rossier et al, 1986). Finally, incubation of parotid homogenates with Ins(1,3,4,5)P4 leads to the formation of Ins(1,3,4)P3 .…”

Section: Discussionmentioning

confidence: 99%

“…The cells were resuspended in the above non-ionic buffer at a concentration of 3 x 106 cells (1.5 mg of protein)/50 gl and then permeabilized by exposure to a high-voltage electric field (2 kV/cm), by the method of Knight & Baker (1982), and as previously described for adrenal glomerulosa cells (Rossier et al, 1986). Incubation of the cells A portion (50 ,1) of this cell preparation was mixed with 350 ,ul of various buffers containing an 'intracellular cationic background' (5 mM-NaCl, 115 mM-KCl, 5 mm-NaHCO3, 1 mM-KH2PO4, 1 mM-MgCl2), an ATPregenerating system (2 mM-MgATP, 10 mM-phosphocreatine and 8 units of creatine kinase/ml), 0.05% albumin and 20 mM-Hepes, pH 7.2.…”

Section: Permeabilization Of the Cellsmentioning

confidence: 99%

“…Incubation of the cells A portion (50 ,1) of this cell preparation was mixed with 350 ,ul of various buffers containing an 'intracellular cationic background' (5 mM-NaCl, 115 mM-KCl, 5 mm-NaHCO3, 1 mM-KH2PO4, 1 mM-MgCl2), an ATPregenerating system (2 mM-MgATP, 10 mM-phosphocreatine and 8 units of creatine kinase/ml), 0.05% albumin and 20 mM-Hepes, pH 7.2. The free Ca2+ concentration was buffered in these media with 1 mM-EGTA and various amounts of CaCl2, and was measured with a Ca2+-selective mini-electrode as previously described (Rossier et al, 1986).…”

Section: Permeabilization Of the Cellsmentioning

confidence: 99%

“…after muscarinic stimulation of brain slices (Batty et al, 1985). An Ins(1,4,5)P3 3-kinase activity has been observed and characterized after addition of [3H]Ins(1,4,5)P3 to various cell homogenates Hansen et al, 1986;Hawkins et al, 1986), and has been shown to be Ca2+-sensitive in intact HL-60 cells , in permeabilized adrenal glomerulosa cells (Rossier et al, 1986) and in subcellular fractions from insulin-secreting RINm5F cells (Biden & Wollheim, 1986). In the present work, the existence of this metabolic pathway and its Ca2+-sensitivity were tested in vascular smooth-muscle cells.…”

Section: Introductionmentioning

confidence: 99%

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Metabolism of inositol 1,4,5-trisphosphate in permeabilized rat aortic smooth-muscle cells. Dependence on calcium concentration

Rossier

Capponi

Vallotton

1987

Biochemical Journal

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The metabolism of [3H]inositol 1,4,5-trisphosphate ([3H]Ins(1,4,5)P3) was studied in permeabilized rat aortic smooth-muscle cells. Addition of [3H]Ins(1,4,5)P3 to the leaky cells led to formation of several labelled metabolites. Amounts of [3H]inositol bisphosphate and [3H]inositol 1,3,4,5-tetrakisphosphate ([3H]InsP4) reached a maximum within 2 min of incubation, whereas production of [3H]inositol monophosphate and [3H]inositol 1,3,4-trisphosphate ([3H]Ins(1,3,4)P3) was delayed. Formation of InsP4 and Ins(1,3,4)P3 was Ca2+-sensitive in the physiological intracellular range (0.06-5 microM), showing a maximum at 1 microM-Ca2+. A correlation between the formation of InsP4 and that of Ins(1,3,4)P3 was observed, suggesting that the former is the precursor of the latter. These results suggest that, in vascular smooth-muscle cells, Ins(1,4,5)P3 is metabolized via two distinct pathways: (1) a dephosphorylation pathway, leading to formation of inositol bis- and mono-phosphate; and (2) a Ca2+-sensitive phosphorylation/dephosphorylation pathway, involving formation of InsP4 and leading to formation of Ins(1,3,4)P3.

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Section: Discussionmentioning

confidence: 99%

Section: Permeabilization Of the Cellsmentioning

confidence: 99%

Section: Permeabilization Of the Cellsmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

See 2 more Smart Citations

Metabolism of inositol 1,4,5-trisphosphate in permeabilized rat aortic smooth-muscle cells. Dependence on calcium concentration

Rossier

Capponi

Vallotton

1987

Biochemical Journal

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“…Dephosphorylation by 5-phosphomonoesterase is the prevailing metabolic route in the resting cell. After stimulation with angiotensin II elevated cytoplasmic Ca2" activates InsP3 3-kinase (Biden & Wollheim, 1986;Rossier, Dentand & Lew, 1986;Balla, Baukal, Guillemette & Catt, 1988) and more InsP3 is converted into higher inositol phosphates. Due to the efforts of Catt's group, the complex metabolism of the so-called higher inositol phosphates has been revealed in bovine glomerulosa cells Balla et al 1988;Hunyady, Baukal, Guillemette, Balla & Catt, 1988 a;Balla, Baukal, Hunyady & Catt, 1989 a;Balla, Hunyady, Baukal & Catt, 1989 b).…”

Section: Metabolism Of Higher Inositol Phosphatesmentioning

confidence: 99%

Generation and role of calcium signal in adrenal glomerulosa cells

Spät¹,

Enyedi²,

Hajnóczky³

et al. 1991

Experimental Physiology

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Regulation of inositol phospholipid and inositol phosphate metabolism in chemoattractant‐activated human polymorphonuclear leukocytes

Dillon

Murray

Uhing

et al. 1987

J of Cellular Biochemistry

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Binding of chemoattractants to specific cell surface receptors on polymorphonuclear leukocytes (PMNs) initiates a series of biochemical responses leading to cellular activation. A critical early biochemical event in chemoattractant (CTX) receptor-mediated signal transduction is the phosphodiesteric cleavage of plasma membrane phosphatidylinositol 4,5-bisphosphate (PIP2), with concomitant production of the calcium mobilizing inositol-1,4,5-trisphosphate (IP3) isomer, and the protein kinase C activator, 1,2-diacylglycerol (DAG). The following lines of experimental evidence collectively suggest that CTX receptors are coupled to phospholipase C via a guanine nucleotide binding (G) protein. Receptor-mediated hydrolysis of PIP2 in PMN plasma membrane preparations requires both fMet-Leu-Phe and GTP, and incubation of intact PMNs with pertussis toxin (which ADP ribosylates and inactivates some G proteins) eliminates the ability of fMet-Leu-Phe plus GTP to promote PIP2 breakdown in isolated plasma membranes. Studies with both PMN particulate fractions and with partially purified fMet-Leu-Phe receptor preparations indicate that guanine nucleotides regulate CTX receptor affinity. Finally, fMet-Leu-Phe stimulates high-affinity binding of GTP gamma S to PMN membranes as well as GTPase activity. A G alpha subunit has been identified in phagocyte membranes which is different from other G alpha subunits on the basis of molecular weight and differential sensitivity to ribosylation by bacterial toxins. Thus, a novel G protein may be involved in coupling CTX receptors to phospholipase C. Studies in intact and sonicated PMNs demonstrate that metabolism of 1,4,5-IP3 proceeds via two distinct pathways: 1) sequential dephosphorylation to 1,4-IP2, 4-IP1 and inositol, or 2) ATP-dependent conversion to inositol 1,3,4,5-tetrakisphosphate (IP4) followed by sequential dephosphorylation to 1,3,4-IP3, 3,4-IP2, 3-IP1 and inositol. Receptor-mediated hydrolysis of PIP2 occurs at ambient intracellular Ca2+ levels; but metabolism of 1,4,5-IP3 via the IP4 pathway requires elevated cytosolic Ca2+ levels associated with cellular activation. Thus, the two pathways for 1,4,5-IP3 metabolism may serve different metabolic functions. Additionally, inositol phosphate production appears to be controlled by protein kinase C, as phorbol myristate acetate (PMA) abrogates PIP2 hydrolysis by interfering with the ability of the activated G protein to stimulate phospholipase C. This implies a physiologic mechanism for terminating biologic responses via protein kinase C mediated feedback inhibition of PIP2 hydrolysis.

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Interconversion of inositol (1,4,5)-trisphosphate to inositol (1,3,4,5)-tetrakisphosphate and (1,3,4)-trisphosphate in permeabilized adrenal glomerulosa cells is calcium-sensitive and ATP-dependent

Cited by 44 publications

References 9 publications

Metabolism of inositol 1,4,5-trisphosphate in permeabilized rat aortic smooth-muscle cells. Dependence on calcium concentration

Metabolism of inositol 1,4,5-trisphosphate in permeabilized rat aortic smooth-muscle cells. Dependence on calcium concentration

Generation and role of calcium signal in adrenal glomerulosa cells

Regulation of inositol phospholipid and inositol phosphate metabolism in chemoattractant‐activated human polymorphonuclear leukocytes

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