Role of Ca2+/ calmodulin in receptor-mediated phosphoinositide hydrolysis in human astrocytoma cells

1990 ◽  
Vol 183 (4) ◽  
pp. 1607 ◽  
Author(s):  
N. Nakahata ◽  
M.T. Abe ◽  
I. Matsuoka ◽  
H. Nakanishi
Keyword(s):  
Phosphoinositide Hydrolysis ◽  
Astrocytoma Cells ◽  
Human Astrocytoma ◽  
Human Astrocytoma Cells

Mechanisms of regulatory volume decrease in UC-11MG human astrocytoma cells

1993 ◽  
Vol 264 (5) ◽  
pp. C1201-C1209 ◽  
Author(s):  
S. Medrano ◽  
E. Gruenstein
Keyword(s):  
Brain Injuries ◽  
Regulatory Volume Decrease ◽  
Transport Pathways ◽  
Astrocytoma Cells ◽  
Hypotonic Treatment ◽  
Human Astrocytoma ◽  
Stretch Activated Channels ◽  
Human Astrocytoma Cells ◽  
Volume Decrease

Swelling of astrocytes commonly occurs after cerebral ischemia and other brain injuries. Because these cells constitute 20-25% of human brain volume, their swelling is a major factor in the morbidity and mortality associated with cerebral edema. Many cells, including astrocytes, resist or reverse the tendency to swell by activating transport pathways that lead to a regulatory volume decrease. Here we report the results of studies designed to elucidate the mechanisms of the regulatory volume decrease that occurs after astrocytes are swollen by exposure to hypotonic medium. Using UC-11MG cells, a well-characterized, human, astrocytoma-derived line, we observed an increase in membrane permeability to both K+ and Cl- during regulatory volume decrease, consistent with a net loss of these ions. Neither the increase in K+ exit nor the regulatory volume decrease was affected by bumetanide, an inhibitor of anion-cation cotransport. On the other hand, the increased K+ efflux, as well as the regulatory volume decrease, was blocked by Gd3+, suggesting a putative role of stretch-activated cationic channels in the process of volume regulation. Although increases in intracellular free Ca2+ were also observed during hypotonic treatment, they occurred well after the onset of the regulatory volume decrease. Furthermore, the regulatory volume decrease was not affected by blocking the intracellular free Ca2+ increase with dimethyl 1,2-bis(2-aminophenoxy)ethane-N,N,N',N'-tetraacetic acid or by removal of extracellular Ca2+. These results indicate that the regulatory volume decrease in UC-11MG cells may involve stretch-activated channels that operate independently of changes in intracellular free Ca2+.

scholarly journals Mastoparan inhibits phosphoinositide hydrolysis via pertussis toxin-intensive G-protein in human astrocytoma cells

FEBS Letters ◽  
1990 ◽  
Vol 260 (1) ◽  
pp. 91-94 ◽  
Author(s):  
Norimichi Nakahata ◽  
Marilene Tamiko Abe ◽  
Isao Matsuoka ◽  
Hironori Nakanishi
Keyword(s):  
G Protein ◽  
Pertussis Toxin ◽  
Phosphoinositide Hydrolysis ◽  
Astrocytoma Cells ◽  
Human Astrocytoma ◽  
Human Astrocytoma Cells
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