G-Protein-coupled receptors in HL-60 human leukemia cells

Klinker, Jan F.; Wenzel-Seifert, Katharina; Seifert, Roland

doi:10.1016/0306-3623(95)00107-7

Cited by 89 publications

(81 citation statements)

References 172 publications

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“…This transient increase in intracellular free calcium correlates with acidification and stimulation of superoxide (O 2− ) release. The level of free fMLF required for half-maximal effect on Ca 2+ release has been reported to be 2-4 nM (Wenzel-Seifert and Seifert, 1990), in approximate agreement with our determination of 5 nM, while the EC 50 for superoxide production has been reported to be 15-30 nM fMLF (Klinker et al, 1996). In this study all conjugates with four or more copies of fMLF and free fMLF displayed an EC 50 value of about 5 nM for calcium release (Table 1 and Figure 4).…”

Section: Discussionsupporting

confidence: 89%

Conjugates Bearing Multiple Formyl-Methionyl Peptides Display Enhanced Binding to but Not Activation of Phagocytic Cells

et al. 2002

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N -Formyl-methionyl peptides can specifically bind to surface receptors on phagocytic cells. A single copy of N-formyl-methionine-leucine-phenylalanine (fMLF) covalently linked to a poly(ethylene glycol)-based polymer displayed reduced binding avidity (K d = 190 nM) for differentiated HL-60 cells relative to free fMLF (K d = 28 nM). Increasing the number of fMLF residues (up to eight) attached to a single polymer results in enhanced avidity for these cells (K d = 0.18 nM), which appears to be independent of whether the polymer backbone is linear or branched. However, no conjugate showed enhanced ability to activate phagocytic cells, relative to the free peptide (EC 50 = 5 nM), as measured by transient stimulation of release of calcium ions from intracellular stores into the cytoplasm. A polymer bearing four fMLF and four digoxigenin residues showed specific enhancement in binding to differentiated HL-60 cells and mouse peritoneal macrophages in situ relative to a polymer lacking fMLF; no such enhancement was seen in binding to receptor-negative lymphocytic Jurkat cells. These results suggest that multiple fMLF residues linked to a drug-delivery polymer can be used to target appended drugs to phagocytic cells with relatively little toxicity due to cellular activation.

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Section: Discussionsupporting

confidence: 89%

Conjugates Bearing Multiple Formyl-Methionyl Peptides Display Enhanced Binding to but Not Activation of Phagocytic Cells

et al. 2002

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“…6). This is in agreement with the well known fact that FPR is a G-proteinlinked receptor (35). Downstream of the G-protein, activation of the phosphoinositide-specific phospholipase C (PLC) leads to an increase in inositol 1,4,5-trisphosphate and diacylglycerol, two second messengers that induce release of Ca 2ϩ from intracellular stores and translocate/activate PKC, respectively.…”

Section: Deactivation Of the Formyl Peptidesupporting

confidence: 87%

Reactivation of Formyl Peptide Receptors Triggers the Neutrophil NADPH-oxidase but Not a Transient Rise in Intracellular Calcium

Bylund

Björstad

Granfeldt

et al. 2003

Journal of Biological Chemistry

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In neutrophils, coupling of chemoattractants to their cell surface receptor at low temperature (<15°C) leads to receptor deactivation/desensitization without any triggering of the superoxide anion-generating NADPHoxidase. We show that the deactivated formyl peptide receptors (FPRs) can be reactivated/resensitized by the cytoskeleton-disrupting drug cytochalasin B. Such cytoskeleton-dependent receptor reactivation occurs also with the closely related receptors FPR-like-1 and C5aR but not with the receptors for interleukin-8 and plateletactivating factor. The reactivation state was further characterized with FPR as a model. The signals generated by receptor reactivation induced superoxide production that was terminated in 5-8 min, after which the neutrophils entered a new state of homologous deactivation. FPR antagonists were potent inhibitors of the superoxide production induced by the reactivated receptors, suggesting that the occupied receptors turn into an actively signaling state when the cytoskeleton is disrupted. The signals generated by the reactivated receptor were pertussis toxin-sensitive, indicating involvement of a G-protein. However, no transient elevation of intracellular Ca 2؉ accompanies the NADPH-oxidase activation. This was not due to a general down-regulation of phospholipase C/Ca 2؉ signaling, and despite the fact that no intracellular Ca 2؉ transient was generated, protein kinase C still appeared to be involved in the response. Further, phosphatidylinositol 3-kinase, mitogen-activated protein kinase, and MEK all participated in the generation of second messengers from the reactivated receptors.

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“…HL-60 cells have served as a good model in which to study signal transduction of various pharmacological receptors before and after di erentiation of the hemopoietic cells (Klinker et al, 1996). HL-60 cells can be forced to terminally di erentiate into neutrophil-like cells by dibutyryl cyclic AMP, DMSO, or retinoic acid treatment and into adherent macrophage-like cells by 1, 25-dihydroxy vitamin D 3 and phorbol esters (Klinker et al, 1996;Collins et al, 1978).…”

Section: Introductionmentioning

confidence: 99%

“…HL-60 cells can be forced to terminally di erentiate into neutrophil-like cells by dibutyryl cyclic AMP, DMSO, or retinoic acid treatment and into adherent macrophage-like cells by 1, 25-dihydroxy vitamin D 3 and phorbol esters (Klinker et al, 1996;Collins et al, 1978).…”

Section: Introductionmentioning

confidence: 99%

Characterization of high affinity neurotensin receptor NTR1 in HL‐60 cells and its down regulation during granulocytic differentiation

Choi

Chae

Park

et al. 1999

British J Pharmacology

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1 We investigated responses to neurotensin in human promyelocytic leukaemia HL-60 cells. 2 Neurotensin increased the cytosolic calcium concentration ([Ca 2+ ] i ) in a concentration-dependent manner and also produced inositol 1,4,5-trisphosphate (InsP 3 ). 3 Among the tested neurotensin analogues, neurotensin 8-13, neuromedin-N, and xenopsin also increased [Ca 2+ ] i , whereas neurotensin 1 ± 11 and neurotensin 1 ± 8 did not elicit detectable responses. 4 SR48692, an antagonist of NTR1 neurotensin receptors, blocked the neurotensin-induced [Ca 2+ ] i increase, whereas levocabastine, which is known as an NTR2 neurotensin receptor antagonist, did not attenuate the neurotensin-evoked e ect. 5 The expression of NTR1 neurotensin receptors was con®rmed by Northern blot analysis and reverse transcriptase-polymerase chain reaction (RT ± PCR). 6 During 1.25% dimethylsulfoxide (DMSO)-triggered granulocytic di erentiation of HL-60 cells, the neurotensin-induced [Ca 2+ ] i rise became gradually smaller and completely disappeared 4 days after treatment with DMSO. The mRNA level for neurotensin receptors was also decreased after di erentiation. 7 The results show that HL-60 cells express NTR1 neurotensin receptors and suggest that granulocytic di erentiation involves transcriptional regulation of the receptors resulting in downregulation of the neurotensin-induced signalling.

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G-Protein-coupled receptors in HL-60 human leukemia cells

Cited by 89 publications

References 172 publications

Conjugates Bearing Multiple Formyl-Methionyl Peptides Display Enhanced Binding to but Not Activation of Phagocytic Cells

Conjugates Bearing Multiple Formyl-Methionyl Peptides Display Enhanced Binding to but Not Activation of Phagocytic Cells

Reactivation of Formyl Peptide Receptors Triggers the Neutrophil NADPH-oxidase but Not a Transient Rise in Intracellular Calcium

Characterization of high affinity neurotensin receptor NTR1 in HL‐60 cells and its down regulation during granulocytic differentiation

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