Protein phosphorylation events and changes in inositol metabolism during HL60 cell differentiation

Lord, Janet M.; Bunce, Christopher M.; French, Philip J.; Jones, Nick D.; Baxter, Michael A.; Grafton, Gillian; Michell, Robert H.; Brown, Geoffrey

doi:10.1042/bst0190315

Cited by 3 publications

(2 citation statements)

References 3 publications

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“…: DMSO, retinoic acid, histamine and dbcAMP [19,[21][22][23]. We have chosen for differentiation with dbcAMP as it is reported that in a rather short period the cell line HL60 can be induced to differentiate into morphologically and functionally mature myelocytes.…”

Section: Discussionmentioning

confidence: 99%

The effect of histamine on the oxidative burst of HL60 cells before and after exposure to reactive oxygen species

1995

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During an inflammation neutrophils are stimulated to produce reactive oxygen species (ROS). These ROS induce the release of histamine from mast cells, which are also present at the inflammation site. In this study dibutyryl cAMP differentiated HL60 cells are used as a model for human neutrophils. The effect of histamine on formyl-methionyl-leucyl-phenylalanine (fmlp) stimulated cells is examined. Except for histamine also an accumulation of ROS takes place at the inflammation site and we investigated if ROS can influence the response of the stimulated HL60 cells. It is found that 10(-3) M histamine can inhibit the fmlp induced superoxide anion radical production. This occurs partly via an H2 receptor because H2 antagonists like famotidine, mifentidine and ranitidine could partially antagonize this effect of histamine. When HL60 cells are exposed to hydrogen peroxide or hypochlorous acid (20 min), an increased fmlp response is found while the inhibiting effect of histamine remains unchanged.

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Section: Discussionmentioning

confidence: 99%

The effect of histamine on the oxidative burst of HL60 cells before and after exposure to reactive oxygen species

1995

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“…This is of some concern, as we report in this paper that HL60 cells only survive for four days when transferred from the usual high-inositol RPM I 1640 medium to inositol-free medium. Some of the studies discussed below have been reported in brief form elsewhere (French et al 1988;Michell et al 1988Lord et al 1991.…”

Section: Introductionmentioning

confidence: 99%

Changes in the levels of inositol lipids and phosphates during the differentiation of HL60 promyelocytic cells towards neutrophils or monocytes

French

Bunce

Stephens

et al. 1991

Proc. R. Soc. Lond. B

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HL60 cells were adapted to grow in a serum-free medium containing 1 mg l-1 inositol, in which they differentiated normally towards neutrophils (in 0.9% by volume dimethylsulphoxide) and towards monocytes (in 10 nM phorbol myristate acetate). Cells that had been equilibrium-labelled with [2-3H]myo-inositol contained a complex pattern of inositol metabolites, several of which were at relatively high concentrations. These included InsP5 and InsP6, which were present at concentrations of about 25 microM and 60 microM, respectively. Striking and different changes occurred in the levels of some of the inositol polyphosphates as the cells differentiated towards either neutrophils or monocytes. Most notable were a large but gradual accumulation of Ins(1,3,4,5,6)P5 as HL60 cells decreased in size and acquired neutrophil characteristics, and much more rapid and sequential declines in InsP4, InsP5 and InsP6 as the cells started to take on monocyte character. There was a marked accumulation of free inositol and of phosphatidylinositol in the cells during neutrophil differentiation, probably caused at least in part by an increased rate of inositol uptake providing an increased intracellular inositol supply. The same accumulation of Ins(1,3,4,5,6)P5 occurred during neutrophil differentiation, whether it was induced by dimethylsulphoxide or by a combination of retinoic acid and a T-lymphocyte cell line-derived differentiation factor. Ins(1,4,5)P3, a physiological intracellular mediator of Ca2+ release from membrane stores, did not change in concentration during these differentiation processes. These observations suggest that some of the more abundant cellular inositol polyphosphates play some important, but not yet understood, role either in the processes of haemopoietic differentiation or in the expression of differentiated cell character in myeloid cells.

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Inositol and inositol 1,4,5‐trisphosphate content of Down syndrome fibroblasts exhibiting enhanced inositol uptake

Fruen¹,

Lester²

1991

FEBS Letters

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Fibroblasts from individuals with Down syndrome (DS; trisomy 21) exhibit increased inositol uptake. Here we examine the relationship between this increase in uptake and mass levels of free inositol and inositol 1,4,5-trisphosphate (IP3) in DS fibroblasts. We report that human fibroblasts contain high levels of free inositol which are not significantly affected by the increase in inositol uptake associated with DS. In addition, increased uptake is accompanied by increased efflux of radiolabelled inositol from DS cells. Neither basal nor bradykinin-stimulated IP3 levels in DS cells differ significantly from normal values. This work highlights the usefulness of the DS cells in uncovering the role of transport across the plasma membrane in cellular inositol homeostasis.

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Protein phosphorylation events and changes in inositol metabolism during HL60 cell differentiation

Cited by 3 publications

References 3 publications

The effect of histamine on the oxidative burst of HL60 cells before and after exposure to reactive oxygen species

The effect of histamine on the oxidative burst of HL60 cells before and after exposure to reactive oxygen species

Changes in the levels of inositol lipids and phosphates during the differentiation of HL60 promyelocytic cells towards neutrophils or monocytes

Inositol and inositol 1,4,5‐trisphosphate content of Down syndrome fibroblasts exhibiting enhanced inositol uptake

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