scholarly journals 3,4-Methylenedioxymethamphetamine Activates Nuclear Factor-κB, Increases Intracellular Calcium, and Modulates Gene Transcription in Rat Heart Cells

2005 ◽  
Vol 5 (3) ◽  
pp. 301-310 ◽  
Author(s):  
David A. Tiangco ◽  
Frank A. Lattanzio ◽  
Christopher J. Osgood ◽  
Stephen J. Beebe ◽  
Julie A. Kerry ◽  
...  
Keyword(s):  
Intracellular Calcium ◽  
Gene Transcription ◽  
Rat Heart ◽  
Nuclear Factor Κb ◽  
Heart Cells ◽  
Nuclear Factor ◽  
Rat Heart Cells

A direct requirement of nuclear factor-κB for suppression of apoptosis in ventricular myocytes

2000 ◽  
Vol 279 (3) ◽  
pp. H939-H945 ◽  
Author(s):  
Shareef Mustapha ◽  
Alla Kirshner ◽  
Danielle De Moissac ◽  
Lorrie A. Kirshenbaum
Keyword(s):  
Dna Binding ◽  
Gene Transcription ◽  
Ventricular Myocytes ◽  
Vital Staining ◽  
Fold Increase ◽  
Nuclear Factor Κb ◽  
Nuclear Factor ◽  
Cytoplasmic Factor ◽  
Tnf Α ◽  
Factor Α

Nuclear factor-κB (NF-κB) is a ubiquitously expressed cellular factor regulated by the cytoplasmic factor inhibitor protein κBα (IκBα). Activation of NF-κB by cytokines, including tumor necrosis factor-α (TNF-α), requires the phosphorylation and degradation of IκBα. An anti-apoptotic role for NF-κB has recently been suggested. In the present study, we ascertained whether death-promoting signals and apoptosis mediated by TNF-α are suppressed by NF-κB in postnatal ventricular myocytes. Stimulation of myocytes with TNF-α resulted in a 12.1-fold increase ( P < 0.01) in NF-κB-dependent gene transcription and DNA binding compared with controls. This was accompanied by a corresponding increase in the NF-κB target protein A20 as determined by Western blot analysis. Vital staining revealed that TNF-α was not cytotoxic to myocytes and did not provoke apoptosis. Adenovirus-mediated delivery of a nonphosphorylatable form of IκBα to inactivate NF-κB prevented TNF-α-stimulated NF-κB-dependent gene transcription and nuclear NF-κB DNA binding. Importantly, myocytes stimulated with TNF-α and defective for NF-κB activation resulted in a 2.2-fold increase ( P < 0.001) in apoptosis. To our knowledge, the data provide the first indication that a functional NF-κB signaling pathway is crucial for suppressing death-promoting signals mediated by TNF-α in ventricular myocytes.

scholarly journals Characterization of a strong positive cis-acting element of the human beta-myosin heavy chain gene in fetal rat heart cells.

1992 ◽  
Vol 267 (14) ◽  
pp. 9917-9924 ◽  
Author(s):  
I.L. Flink ◽  
J.G. Edwards ◽  
J.J. Bahl ◽  
C.C. Liew ◽  
M Sole ◽  
...  
Keyword(s):  
Heavy Chain ◽  
Rat Heart ◽  
Chain Gene ◽  
Heart Cells ◽  
Heavy Chain Gene ◽  
Myosin Heavy Chain Gene ◽  
Cis Acting ◽  
Fetal Rat ◽  
Rat Heart Cells

Plasma from cirrhotic patients induces inotropic changes on cultured rat heart cells

Life Sciences ◽  
1987 ◽  
Vol 41 (19) ◽  
pp. 2177-2184 ◽  
Author(s):  
Lidia E.P. de Mikulic ◽  
Marie-Claude Auclair ◽  
Catherine Vernimmen ◽  
Didier Lebrec ◽  
Esteban Mikulic
Keyword(s):  
Rat Heart ◽  
Heart Cells ◽  
Cirrhotic Patients ◽  
Rat Heart Cells

scholarly journals EFFECTS OF CORTISOL ON CULTURED RAT HEART CELLS

1973 ◽  
Vol 57 (1) ◽  
pp. 109-116 ◽  
Author(s):  
J. V. Anastasia ◽  
R. L. McCarl
Keyword(s):  
Fatty Acids ◽  
Fatty Acid ◽  
Free Fatty Acids ◽  
Fatty Acid Oxidation ◽  
Growth Medium ◽  
Rat Heart ◽  
Acid Oxidation ◽  
Heart Cells ◽  
Atp Production ◽  
Rat Heart Cells

This paper reports the determination of the ability of rat heart cells in culture to release [14C]palmitate from its triglyceride and to oxidize this fatty acid and free [14C]palmitate to 14CO2 when the cells are actively beating and when they stop beating after aging in culture. In addition, the levels of glucose, glycogen, and ATP were determined to relate the concentration of these metabolites with beating and with cessation of beating. When young rat heart cells in culture are actively beating, they oxidize free fatty acids at a rate parallel with cellular ATP production. Both fatty acid oxidation and ATP production remain constant while the cells continue to beat. Furthermore, glucose is removed from the growth medium by the cells and stored as glycogen. When cultured cells stop beating, a decrease is seen in their ability to oxidize free fatty acids and to release them from their corresponding triglycerides. Concomitant with decreased fatty acid oxidation is a decrease in cellular levels of ATP until beating ceases. Midway between initiation of cultures and cessation of beating the cells begin to mobilize the stored glycogen. When the growth medium is supplemented with cortisol acetate and given to cultures which have ceased to beat, reinitiation of beating occurs. Furthermore, all decreases previously observed in ATP levels, fatty acid oxidation, and esterase activity are restored.

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