Phospholipids and protein kinase C in acetylcholine-dependent signal transduction in Ascaris suum

1991 ◽  
Vol 48 (2) ◽  
pp. 151-161 ◽  
Author(s):  
Javier Arevalo ◽  
Howard J. Saz
Keyword(s):  
Signal Transduction ◽  
Protein Kinase C ◽  
Protein Kinase ◽  
Ascaris Suum ◽  
Kinase C ◽  
Dependent Signal

scholarly journals A Novel Interaction Between Inhibitory Melatonin Receptors and Protein Kinase C-Dependent Signal Transduction in Ovine Pars Tuberalis Cells*

Endocrinology ◽  
1998 ◽  
Vol 139 (4) ◽  
pp. 1723-1730 ◽  
Author(s):  
Alexander W. Ross ◽  
Catriona A. Webster ◽  
Michael Thompson ◽  
Perry Barrett ◽  
Peter J. Morgan
Keyword(s):  
Signal Transduction ◽  
Protein Kinase C ◽  
Protein Kinase ◽  
Melatonin Receptors ◽  
Pars Tuberalis ◽  
Kinase C ◽  
Dependent Signal

scholarly journals Difference in response to colony-stimulating factors and involvement of protein kinase C signal transduction system in three subclones from the ME-1 cell line and two sublines

Blood ◽  
1994 ◽  
Vol 84 (1) ◽  
pp. 84-93
Author(s):  
K Yanagisawa ◽  
M Sato ◽  
T Horiuchi ◽  
H Hasegawa ◽  
S Fujita
Keyword(s):  
Signal Transduction ◽  
Protein Kinase C ◽  
Protein Kinase ◽  
Cell Line ◽  
Colony Stimulating Factors ◽  
Gm Csf ◽  
Lineage Differentiation ◽  
Kinase C ◽  
Proliferation And Differentiation ◽  
Dependent Signal

We previously established a cell line from a patient with acute myelomonocytic leukemia with eosinophilia (M4E0), ME-1. ME-1 cells are responsive to colony-stimulating factors (CSFs) such as interleukin-3 (IL-3), IL-4, and granulocyte-macrophage CSF (GM-CSF), and exhibit monocyte-macrophage differentiation. We isolated three subclones, ME-F1 from ME-1, and ME-F2 and ME-F3 from two sublines of ME-1. These subclones had different morphologic, cytochemical, phenotypic, and cytogenetic features. They represented different monocytic-lineage differentiation stages and exhibited different responses to IL-3, GM- CSF, and especially IL-4. IL-3, GM-CSF, and IL-4 enhanced proliferation and differentiation to macrophage-like cells in the ME-F1 subclone. However, they enhanced only proliferation of ME-F2 cells and only differentiation to macrophage-like cells in the ME-F3 subclone. To elucidate possible differences in signal transduction mechanisms in ME- F1, ME-F2, and ME-F3 cells following stimulation by CSFs, we studied the effects of IL-3 and IL-4 on protein kinase C (PKC) activity. Both IL-3 and IL-4 induced a rapid, transient decrease of cytosolic PKC in ME-F1 cells, but did not affect PKC activity in ME-F2 and ME-F3 cells. The PKC inhibitors, 1-(5-isoquinolinyl-sulfonyl)-2-methylpiperazine (H- 7) and calphostin C inhibited IL-3-induced enhancement of proliferation and differentiation of ME-F1 cells, but did not inhibit enhancement of proliferation of ME-F2 cells and differentiation of ME-F3 cells. Our data suggest that PKC-dependent signal transduction is considerably related to IL-3-induced proliferation and differentiation of ME-F1 cells. In addition, it was demonstrated that the two subclones, ME-F2 and ME-F3, lost one of the two responses of ME-F1 cells to CSFs, either proliferation or differentiation, and simultaneously lost PKC-dependent response to CSFs.

scholarly journals Difference in response to colony-stimulating factors and involvement of protein kinase C signal transduction system in three subclones from the ME-1 cell line and two sublines

Blood ◽  
1994 ◽  
Vol 84 (1) ◽  
pp. 84-93 ◽  
Author(s):  
K Yanagisawa ◽  
M Sato ◽  
T Horiuchi ◽  
H Hasegawa ◽  
S Fujita
Keyword(s):  
Signal Transduction ◽  
Protein Kinase C ◽  
Protein Kinase ◽  
Cell Line ◽  
Colony Stimulating Factors ◽  
Gm Csf ◽  
Lineage Differentiation ◽  
Kinase C ◽  
Proliferation And Differentiation ◽  
Dependent Signal

Abstract We previously established a cell line from a patient with acute myelomonocytic leukemia with eosinophilia (M4E0), ME-1. ME-1 cells are responsive to colony-stimulating factors (CSFs) such as interleukin-3 (IL-3), IL-4, and granulocyte-macrophage CSF (GM-CSF), and exhibit monocyte-macrophage differentiation. We isolated three subclones, ME-F1 from ME-1, and ME-F2 and ME-F3 from two sublines of ME-1. These subclones had different morphologic, cytochemical, phenotypic, and cytogenetic features. They represented different monocytic-lineage differentiation stages and exhibited different responses to IL-3, GM- CSF, and especially IL-4. IL-3, GM-CSF, and IL-4 enhanced proliferation and differentiation to macrophage-like cells in the ME-F1 subclone. However, they enhanced only proliferation of ME-F2 cells and only differentiation to macrophage-like cells in the ME-F3 subclone. To elucidate possible differences in signal transduction mechanisms in ME- F1, ME-F2, and ME-F3 cells following stimulation by CSFs, we studied the effects of IL-3 and IL-4 on protein kinase C (PKC) activity. Both IL-3 and IL-4 induced a rapid, transient decrease of cytosolic PKC in ME-F1 cells, but did not affect PKC activity in ME-F2 and ME-F3 cells. The PKC inhibitors, 1-(5-isoquinolinyl-sulfonyl)-2-methylpiperazine (H- 7) and calphostin C inhibited IL-3-induced enhancement of proliferation and differentiation of ME-F1 cells, but did not inhibit enhancement of proliferation of ME-F2 cells and differentiation of ME-F3 cells. Our data suggest that PKC-dependent signal transduction is considerably related to IL-3-induced proliferation and differentiation of ME-F1 cells. In addition, it was demonstrated that the two subclones, ME-F2 and ME-F3, lost one of the two responses of ME-F1 cells to CSFs, either proliferation or differentiation, and simultaneously lost PKC-dependent response to CSFs.

scholarly journals Direct evidence for a key role of protein kinase C in the development of vasospasm after subarachnoid hemorrhage

1992 ◽  
Vol 76 (4) ◽  
pp. 635-639 ◽  
Author(s):  
Shigeru Nishizawa ◽  
Nobukazu Nezu ◽  
Kenichi Uemura
Keyword(s):  
Signal Transduction ◽  
Protein Kinase C ◽  
Protein Kinase ◽  
Direct Evidence ◽  
Control Group ◽  
Content Type ◽  
Kinase C ◽  
Protein Kinase C Activity ◽  
Fine Print

✓ Vascular contraction is induced by the activation of intracellular contractile proteins mediated through signal transduction from the outside to the inside of cells. Protein kinase C plays a crucial role in this signal transduction. It is hypothesized that protein kinase C plays a causative part in the development of vasospasm after subarachnoid hemorrhage (SAH). To verify this directly, the authors measured protein kinase C activity in canine basilar arteries in an SAH model with (γ-32P)adenosine triphosphate and the data were compared to those in a control group. Protein kinase C is translocated to the membrane from the cytosol when it is activated, and the translocation is an index of the activation; thus, protein kinase C activity was measured both in the cytosol and in the membrane fractions. Protein kinase C activity in the membrane in the SAH model was remarkably enhanced compared to that in the control group. The percentage of membrane activity to the total was also significantly greater in the SAH vessels than in the control group, and the percentage of cytosol activity in the SAH group was decreased compared to that in the control arteries. The results indicate that protein kinase C in the vascular smooth muscle was translocated to the membrane from the cytosol and was activated when SAH occurred. It is concluded that this is direct evidence for a key role of protein kinase C in the development of vasospasm.

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