Enhancement of ATP-induced Currents by Phospholipase D1 Overexpressed in PC12 Cells
Jin-Bong PARK; Young-Rae KIM; Byeong-Hwa JEON; Seung-Kiel PARK; Sae-Ock OH; Young-Geun KIM; Sang-Do LEE; Kwang-Jin KIM; Jin-Bong PARK; Young-Rae KIM; Byeong-Hwa JEON; Seung-Kiel PARK; Sae-Ock OH; Young-Geun KIM; Sang-Do LEE; Kwang-Jin KIM; Jin-Bong PARK; Young-Rae KIM; Byeong-Hwa JEON; Seung-Kiel PARK; Sae-Ock OH; Young-Geun KIM; Sang-Do LEE; Kwang-Jin KIM.
The Korean Journal of Physiology and Pharmacology
; : 223-230, 2003.
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en Inglés
| WPRIM | ID: wpr-727898
Using phospholipase D1 (PLD1) -overexpressing PC12 (PLD1-PC12) cells, the regulatory roles of PLD1 on ATP-induced currents were investigated. In control and PLD1-PC12 cells, ATP increased PLD activity in an external Ca2+ dependent manner. PLD activity stimulated by ATP was substantially larger in PLD1-PC12 cells than in control cells. In whole-cell voltage-clamp mode, ATP induced transient inward and outward currents. The outward currents inhibited by TEA or charybdotoxin were significantly larger in PLD1-PC12 cells than in control cells. The inward currents known as Ca2+ permeable nonselective cation currents were also larger in PLD1-PC12 cells than in control cells. However, the difference between the two groups of cells disappeared in Ca2+ -free external solution, where ATP did not activate PLD. Finally, ATP-induced 45Ca uptakes were also larger in PLD1-PC12 cells than in control cells. These results suggest that PLD enhances ATP-induced Ca2+ influx via Ca2+ permeable nonselective cation channels and increases subsequent Ca2+ -activated K+ currents in PC12 cells.
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