Effects of the phorbolester TPA and of the ionophore A 23187 on phospholipase A2 and C activities in the mouse epidermal cell line HEL-30

1987 ◽  
Vol 113 (4) ◽  
pp. 310-318 ◽  
Author(s):  
G. F�rstenberger ◽  
M. Rogers ◽  
J. Faberman ◽  
M. Ganss ◽  
H. Richter ◽  
...  
Keyword(s):  
Phospholipase A2 ◽  
Cell Line ◽  
Epidermal Cell ◽  
A 23187 ◽  
Mouse Epidermal Cell

Analysis of v-Ha-ras and v-fos oncogene transduction into a mouse epidermal cell line with “initiated” phenotype in culture but normal skin phenotype in vivo

1995 ◽  
Vol 13 (2) ◽  
pp. 96-103 ◽  
Author(s):  
Masato Ueda ◽  
Hideki Kawamura ◽  
Christian Sutter ◽  
Adam Glick ◽  
Stuart H. Yuspa ◽  
...  
Keyword(s):  
Cell Line ◽  
Epidermal Cell ◽  
Normal Skin ◽  
Mouse Epidermal Cell

Properties of a SENCAR mouse epidermal cell line and effects of oncogene introduction

1990 ◽  
Vol 1 (5) ◽  
pp. 381
Author(s):  
Masato Ueda ◽  
Stuart H. Yuspa ◽  
James E. Strickland
Keyword(s):  
Cell Line ◽  
Epidermal Cell ◽  
Mouse Epidermal Cell

Glycosaminoglycan synthesis by Pam cells (mouse epidermal cell line)

1987 ◽  
Vol 279 (4) ◽  
pp. 276-277 ◽  
Author(s):  
A. Konohana ◽  
S. Tajima ◽  
T. Nishikawa
Keyword(s):  
Cell Line ◽  
Epidermal Cell ◽  
Glycosaminoglycan Synthesis ◽  
Mouse Epidermal Cell

Phospholipase A2 activation in human neutrophils requires influx of extracellular Ca2+ and leukotriene B4

1995 ◽  
Vol 268 (1) ◽  
pp. C138-C146 ◽  
Author(s):  
S. Reddy ◽  
R. Bose ◽  
G. H. Rao ◽  
M. Murthy
Keyword(s):  
Ethylene Glycol ◽  
Phospholipase A2 ◽  
Platelet Activating Factor ◽  
Leukotriene B4 ◽  
Lipid Mediators ◽  
Oxidation Products ◽  
Human Neutrophils ◽  
Tetraacetic Acid ◽  
A 23187 ◽  
Transient Elevation

We have demonstrated that phospolipase A2 (PLA2) activation in human neutrophils requires both the influx of extracellular Ca2+ and leukotriene B4 (LTB4). Surprisingly, the eicosanoids (LTB4 and its omega-oxidation products) formed were quantitatively very similar in both thapsigargin (Thap)- and A-23187-stimulated neutrophils. In contrast, Thap had very little effect on the activation of PLA2 when 5-lipoxygenase (5-LO) was blocked by BW755C or MK-886, whereas A-23187 caused a substantial activation. The lack of PLA2 activation in Thap-stimulated neutrophils results from the inhibition of LTB4 formation in the presence of 5-LO inhibitors. It appears that A-23187 activates both LTB4-dependent and -independent PLA2, whereas Thap activates LTB4-dependent PLA2. Experiments with ethylene glycol-bis(beta-aminoethyl ether)-N,N,N',N'-tetraacetic acid demonstrated that activation of Thap-sensitive PLA2 and 5-LO requires the influx of Ca2+. Neither the transient elevation of cytosolic Ca2+ from intracellular stores nor the sustained Ca2+ influx alone without LTB4 appears sufficient to cause the activation of LTB4-dependent PLA2. We suggest that the activation of LTB4-dependent PLA2 involves 1) a sustained elevation of cytosolic Ca2+ coupled to the influx of extracellular Ca2+ and 2) a coupling between LTB4 and its receptor. We conclude that LTB4-dependent PLA2 plays an important role in the poststimulatory formation of lipid mediators such as prostaglandins, leukotrienes, and platelet-activating factor.

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