Nitric Oxide Inhibits Capping in HL-60 Cells

Lee, Jung‐Hee; Ryu, Hoon; Han, Myung‐Kwan; Kim, Uh-Hyun; Chung, Hun‐Taeg

doi:10.1006/bbrc.1997.6380

Cited by 9 publications

(6 citation statements)

References 22 publications

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“…Densitometry analysis of four experiments revealed that [ 32 P]adenylate NAD phosphorylation in vitro was 3.1 Ϯ 0.3-and 8.5 Ϯ 0.5-fold greater in lysates of cells treated with 0.5 and 1 mM SNP, respectively, than in lysates not treated with SNP (P Ͻ 0.01). The results in CaSki cells are similar to studies in other cell types (5,6,8,34,38,44) and indicate that the assay can yield semiquantitative data.…”

Section: Resultssupporting

confidence: 81%

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cGMP-dependent ADP depolymerization of actin mediates estrogen increase in cervical epithelial permeability

Gorodeski

2000

American Journal of Physiology-Cell Physiology

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Estrogen increases secretion of cervical mucus in women, and the effect depends on fragmentation of the cytoskeleton. The objective of the present study was to understand the molecular mechanism of estrogen action. Treatment of human cervical epithelial cells with 17beta-estradiol, sodium nitroprusside (SNP), or 8-bromoguanosine 3', 5'-cyclic monophosphate (8-Br-cGMP) increased cellular monomeric G-actin and decreased polymerized F-actin. The effects of estradiol were blocked by tamoxifen, by the guanylate cyclase inhibitor LY-83583, and by the cGMP-dependent protein kinase inhibitor KT-5823. The effects of SNP were blocked by LY-83583 and KT-5823, while the effects of 8-Br-cGMP were blocked only by KT-5823. Treatment with phalloidin decreased paracellular permeability and G-actin. Treatment with 17beta-estradiol, SNP, or 8-Br-cGMP attenuated SNP-induced phosphorylation of [(32)P]adenylate NAD in vitro: tamoxifen blocked the effect of estrogen; LY-83583 blocked the effect of SNP but not that of 8-Br-cGMP, while KT-5823 blocked effects of both SNP and 8-Br-cGMP. These results indicate that estrogen, nitric oxide (NO), and cGMP stimulate actin depolymerization. A possible mechanism is NO-induced, cGMP-dependent protein kinase augmentation of ADP-ribosylation of monomeric actin.

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Section: Resultssupporting

confidence: 81%

“…The assay used in these experiments was NO-induced ADP-ribosylation in vitro, in broken cell preparations (5,6,38,44). The reaction was initiated by adding the NO donor SNP and monitored by preincubation of cell lysates with [ 32 P]adenylate NAD, which is a substrate for ADPribosylation (8,34).…”

Section: Resultsmentioning

confidence: 99%

cGMP-dependent ADP depolymerization of actin mediates estrogen increase in cervical epithelial permeability

Gorodeski

2000

American Journal of Physiology-Cell Physiology

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“…Along this same line of reasoning, agents that inhibit actin polymerization may also have profound effects on receptor patching and clapping [50]. While syndecan cytoplasmic domains are commonly encountered in cytoskeletal regulation, lateral associations with other cell surface molecules seem more likely.…”

Section: Discussionmentioning

confidence: 99%

Syndecan-2 expression increases serum-withdrawal-induced apoptosis, mediated by re-distribution of Fas into lipid rafts, in stably transfected Swiss 3T3 cells

et al. 2006

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To examine the function of syndecan-2, one of the most abundant heparan sulfate proteoglycans in fibroblasts, we obtained stably transfected Swiss 3T3 clones. We examined the effects of stable syndecan-2 overexpression on programmed cell death, finding that syndecan-2 transfected cells were more sensitive to apoptosis induced by serum-withdrawal than control cells. In addition, overexpression of syndecan-2 correlates with increased membrane levels of the Fas/CD95 receptor, suggesting that the increased serum-withdrawal apoptosis observed in Swiss 3T3 cells might be Fas receptor-dependent. Differences in Fas membrane levels between both control and syndecan-2 transfected cells result from a redistribution of the Fas receptor. Our data clearly demonstrate that increased Fas levels are primarily related to lipid rafts and that this increase is a key factor in Fas/CD95-mediated apoptosis. Moreover, disruption of lipid rafts with methyl-beta-cyclodextrin or filipin significantly reduced apoptosis in response to serum withdrawal. The differences in Fas/CD95 membrane distribution could explain why syndecan-2 transfected cells have a higher susceptibility to serum-withdrawal-induced apoptosis.

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“…Stretch‐activated channels are tightly associated with the cytoskeleton (Sackin, 1995). Depolymerization of actin filaments by NO (Lee et al . 1997) could potentially increase their stretch sensitivity (Guharay & Sachs, 1984) producing a hyperexcitability state.…”

Section: Discussionmentioning

confidence: 99%

Transient action of the endothelial constitutive nitric oxide synthase (ecNOS) mediates the development of thermal hypersensitivity following peripheral nerve injury

Levy

Tal

Höke

et al. 2000

Eur J of Neuroscience

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Neuropathic pain is a disabling feature of peripheral nerve injury. Following injury, local inflammation and the release of mediators may contribute to ectopic mechanosensitivity of the nerve-trunk and pain hypersensitivity. In the present study we investigated whether nitric oxide (NO) action and local nitric oxide synthase (NOS) expression play a role in pain hypersensitivity and A fibre-mediated ectopic hyperexcitability following a chronic constriction injury to a rat sciatic nerve. Using immunohistochemical methods we provide evidence for a unique endothelial constitutive nitric oxide synthase (ecNOS) immunoreactivity localized in early axonal endbulb-like structures of injured peripheral nerve axons. Moreover, we show that following nerve injury there is increased ecNOS-mRNA expression within the lumbar sympathetic ganglia, and that axoplasmic transport in sympathetic and other axons rather than local non-neural synthesis accounts for its accumulation in nerve fibres. We also demonstrate here that local inhibition of NOS action with the broad-spectrum inhibitor NG-nitro-L-arginine-methyl ester (L-NAME), but not more specific inhibitors of other NOS isoforms, has stereospecific, dose- and time-dependent analgesic effects that were reversed by local administration of L-arginine, the natural precursor of NO. In further work, using a teased fibre preparation, we show that administration of L-NAME, but not D-NAME, to the injury site also blocks ectopic mechanosensitivity of injured A-fibres. Our results indicate that an early and transient local ecNOS expression within early axonal endbulb-like structures, some arising from sympathetic axons, plays a critical role in the development of neuropathic pain.

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Nitric Oxide Inhibits Capping in HL-60 Cells

Cited by 9 publications

References 22 publications

cGMP-dependent ADP depolymerization of actin mediates estrogen increase in cervical epithelial permeability

cGMP-dependent ADP depolymerization of actin mediates estrogen increase in cervical epithelial permeability

Syndecan-2 expression increases serum-withdrawal-induced apoptosis, mediated by re-distribution of Fas into lipid rafts, in stably transfected Swiss 3T3 cells

Transient action of the endothelial constitutive nitric oxide synthase (ecNOS) mediates the development of thermal hypersensitivity following peripheral nerve injury

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