Involvement of nitric oxide in glucose toxicity on differentiated PC12 cells: prevention of glucose toxicity by tetrahydrobiopterin, a cofactor for nitric oxide synthase

2002 ◽  
Vol 43 (1) ◽  
pp. 31-38 ◽  
Author(s):  
Kunio Koshimura ◽  
Junko Tanaka ◽  
Yoshio Murakami ◽  
Yuzuru Kato
Keyword(s):  
Nitric Oxide ◽  
Nitric Oxide Synthase ◽  
Pc12 Cells ◽  
Glucose Toxicity ◽  
Differentiated Pc12 Cells ◽  
Oxide Synthase

scholarly journals Cyclooxygenase 2 Promotes Cell Survival by Stimulation of Dynein Light Chain Expression and Inhibition of Neuronal Nitric Oxide Synthase Activity

2000 ◽  
Vol 20 (22) ◽  
pp. 8571-8579 ◽  
Author(s):  
Yu-Wen E. Chang ◽  
Rolf Jakobi ◽  
Ann McGinty ◽  
Marco Foschi ◽  
Michael J. Dunn ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Nitric Oxide Synthase ◽  
Pc12 Cells ◽  
Neuronal Nitric Oxide Synthase ◽  
Dynein Light Chain ◽  
No Donors ◽  
Differentiated Pc12 Cells ◽  
Cox 2 ◽  
Oxide Synthase ◽  
Stimulation Of

ABSTRACT Cyclooxygenase 2 (COX-2) inhibits nerve growth factor (NGF) withdrawal apoptosis in differentiated PC12 cells. The inhibition of apoptosis by COX-2 was concomitant with prevention of caspase 3 activation. To understand how COX-2 prevents apoptosis, we used cDNA expression arrays to determine whether COX-2 regulates differential expression of apoptosis-related genes. The expression of dynein light chain (DLC) (also known as protein inhibitor of neuronal nitric oxide synthase [PIN]) was significantly stimulated in PC12 cells overexpressing COX-2. The COX-2-dependent stimulation of DLC expression was, at least in part, mediated by prostaglandin E2. Overexpression of DLC also inhibited NGF withdrawal apoptosis in differentiated PC12 cells. Stimulation of DLC expression resulted in an increased association of DLC/PIN with neuronal nitric oxide synthase (nNOS), thereby reducing nNOS activity. Furthermore, nNOS expression and activity were significantly increased in differentiated PC12 cells after NGF withdrawal. This increased nNOS activity as well as increased nNOS dimer after NGF withdrawal were inhibited by COX-2 or DLC/PIN overexpression. An nNOS inhibitor or a membrane-permeable superoxide dismutase (SOD) mimetic protected differentiated PC12 cells from NGF withdrawal apoptosis. In contrast, NO donors induced apoptosis in differentiated PC12 cells and potentiated apoptosis induced by NGF withdrawal. The protective effects of COX-2 on apoptosis induced by NGF withdrawal were also overcome by NO donors. These findings suggest that COX-2 promotes cell survival by a mechanism linking increased expression of prosurvival genes coupled to inhibition of NO- and superoxide-mediated apoptosis.

scholarly journals The Ras-ERK pathway is required for the induction of neuronal nitric oxide synthase in differentiating PC12 cells

2001 ◽  
Vol 78 (3) ◽  
pp. 631-639 ◽  
Author(s):  
Christopher M. Schonhoff ◽  
Dylan A. Bulseco ◽  
Deborah M. Brancho ◽  
Luis F. Parada ◽  
Alonzo H. Ross
Keyword(s):  
Nitric Oxide ◽  
Nitric Oxide Synthase ◽  
Pc12 Cells ◽  
Neuronal Nitric Oxide Synthase ◽  
Erk Pathway ◽  
Oxide Synthase

The protective effect of GD1a ganglioside and inhibitors of nitric oxide synthase after the application of bacterial lipopolysaccharide to PC12 cells

2012 ◽  
Vol 6 (4) ◽  
pp. 278-283
Author(s):  
L. V. Bayunova ◽  
Yu. A. Vlasova ◽  
T. V. Sokolova ◽  
I. O. Zakharova ◽  
R. G. Parnova ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Nitric Oxide Synthase ◽  
Protective Effect ◽  
Pc12 Cells ◽  
Bacterial Lipopolysaccharide ◽  
Oxide Synthase ◽  
Gd1a Ganglioside
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