Cytochalasins distinguish by their action resting human T lymphocytes from activated T-cell blasts*1

Otteskog, Per; Wanger, L; Sundqvist, Kristina

doi:10.1016/0014-4827(83)90423-8

Cited by 8 publications

(2 citation statements)

References 16 publications

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“…6A and B, bottom panels) consistent with a disruption of microvilli. Treatment of human peripheral T lymphocytes with cytochalasins B and D has also been shown elsewhere to cause a reduction in the number of microvilli (50). Since cytochalasin B has been shown elsewhere to inhibit HIV-1 Env-mediated fusion with the lymphocyte cell line SupT1 (22, 23), we examined whether the effects of cytochalasin were similar to those of M␤CD.…”

Section: Resultsmentioning

confidence: 96%

Role of Cholesterol in Human Immunodeficiency Virus Type 1 Envelope Protein-Mediated Fusion with Host Cells

Viard¹,

Parolini

Sargiacomo

et al. 2002

J Virol

155

142

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In this study we examined the effects of target membrane cholesterol depletion and cytoskeletal changes on human immunodeficiency virus type 1 (HIV-1) Env-mediated membrane fusion by dye redistribution assays. We found that treatment of peripheral blood lymphocytes (PBL) with methyl-␤-cyclodextrin (M␤CD) or cytochalasin reduced their susceptibility to membrane fusion with cells expressing HIV-1 Env that utilize CXCR4 or CCR5. However, treatment of human osteosarcoma (HOS) cells expressing high levels of CD4 and coreceptors with these agents did not affect their susceptibility to HIV-1 Env-mediated membrane fusion. Removal of cholesterol inhibited stromal cell-derived factor-1␣-and macrophage inflammatory protein 1␤-induced chemotaxis of both PBL and HOS cells expressing CD4 and coreceptors. The fusion activity as well as the chemotactic activity of PBL was recovered by adding back cholesterol to these cells. Confocal laser scanning microscopy analysis indicated that treatment of lymphocytes with M␤CD reduced the colocalization of CD4 or of CXCR4 with actin presumably in microvilli. These findings indicate that, although cholesterol is not required for HIV-1 Env-mediated membrane fusion per se, its depletion from cells with relatively low coreceptor densities reduces the capacity of HIV-1 Env to engage coreceptor clusters required to trigger fusion. Furthermore, our results suggest that coreceptor clustering may occur in microvilli that are supported by actin polymerization.

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Section: Resultsmentioning

confidence: 96%

Role of Cholesterol in Human Immunodeficiency Virus Type 1 Envelope Protein-Mediated Fusion with Host Cells

Viard¹,

Parolini

Sargiacomo

et al. 2002

J Virol

155

142

View full text Add to dashboard Cite

show abstract

“…The amount of actin per lane was normalized to milligrams of total protein. Preparation of DNase I beads (36): DNase I beads [5-ml latex beads (polystyrene beads, 2 m, 2.5% (wt/vol); Polysciences, Warrington, PA)] were washed three times in 100% ethanol and three times in PBS and mixed with DNase I (10 mg dissolved in 0.2 M sodium phosphate, pH 7.5) and tresyl chloride-activated agarose (1 g, washed with 0.2 M sodium phosphate). The mixture was incubated at 4°C overnight with gentle mixing.…”

Section: Cell Culturesmentioning

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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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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Nitric Oxide Inhibits Capping in HL-60 Cells

Lee

Ryu

Han

et al. 1997

Biochemical and Biophysical Research Communications

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Cytochalasins distinguish by their action resting human T lymphocytes from activated T-cell blasts*1

Cited by 8 publications

References 16 publications

Role of Cholesterol in Human Immunodeficiency Virus Type 1 Envelope Protein-Mediated Fusion with Host Cells

Role of Cholesterol in Human Immunodeficiency Virus Type 1 Envelope Protein-Mediated Fusion with Host Cells

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

Nitric Oxide Inhibits Capping in HL-60 Cells

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