Fluoxetine Protects against Big Endothelin-1 Induced Anti-Apoptosis by Rescuing Kv1.5 Channels in Human Pulmonary Arterial Smooth Muscle Cells
Yonsei Medical Journal
;
: 842-848, 2012.
Article
in English
| WPRIM
| ID: wpr-93569
ABSTRACT
PURPOSE:
Pulmonary Kv channels are thought to play a crucial role in the regulation of cell proliferation and apoptosis. Previous studies have shown that fluoxetine upregulated the expression of Kv1.5 and prevented pulmonary arterial hypertension in monocrotaline-induced or hypoxia-induced rats and mice. The current study was designed to test how fluoxetine regulates Kv1.5 channels, subsequently promoting apoptosis in human PASMCs cultured in vitro. MATERIALS ANDMETHODS:
Human PASMCs were incubated with low-serum DMEM, ET-1, and fluoxetine with and without ET-1 separately for 72 h. Then the proliferation, apoptosis, and expression of TRPC1 and Kv1.5 were detected.RESULTS:
In the ET-1 induced group, the upregulation of TRPC1 and down regulation of Kv1.5 enhanced proliferation and anti-apoptosis, which was reversed when treated with fluoxetine. The decreased expression of TRPC1 increased the expression of Kv1.5, subsequently inhibiting proliferation while promoting apoptosis.CONCLUSION:
The results from the present study suggested that fluoxetine protects against big endothelin-1 induced anti-apoptosis and rescues Kv1.5 channels in human pulmonary arterial smooth muscle cells, potentially by decreasing intracellular concentrations of Ca2+.
Full text:
Available
Index:
WPRIM (Western Pacific)
Main subject:
Pulmonary Artery
/
Cells, Cultured
/
Blotting, Western
/
Fluoxetine
/
Apoptosis
/
Endothelin-1
/
Reverse Transcriptase Polymerase Chain Reaction
/
Cell Proliferation
/
Flow Cytometry
/
Muscle, Smooth, Vascular
Limits:
Humans
Language:
English
Journal:
Yonsei Medical Journal
Year:
2012
Type:
Article
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