Possible involvement of urocortin I on adaptation of the nicotine-induced oxidative stress to HL-1 cardiomyocytes

Program: Abstracts - Orals, Featured Poster Presentations, and Posters
Session: SUN 72-87-HPA Axis
Basic
Sunday, June 16, 2013: 1:45 PM-3:45 PM
Expo Halls ABC (Moscone Center)

Poster Board SUN-85
Keiichi Ikeda*1, Katsuyoshi Tojo2, Kouki Fujioka3, William C Claycomb4 and Yoshinnobu Manome3
1Jikei Univ Sch of Medicine, Tokyo, Japan, 2Jikei Univ Sch of Med, Tokyo, Japan, 3Inst DNA Med, Jikei Univ Sch Med, Tokyo, Japan, 4Louisiana State Univ Health Sci Center, New Orleans, LA
One of the adverse effects of nicotine is oxidative stress at the cellular level.  Several studies have reported that urocortin (Ucn) I exerts cellular protective actions against oxidative stress and these actions are modulated by oxidative stress.  Therefore, we examined the effects of Ucn I on nicotine-induced oxidative stress in HL-1 cardiomyocytes.  HL-1 cardiomyocytes were plated in a 96-well plate at a density of 1.5-2.0×104 cells/well with Claycomb medium containing 10% fetal bovine serum (FBS) and 0.1mmol/L epinephrine.  After FBS starvation cells were grown in Claycomb medium and norepinephrine and stimulated with nicotine and/or Ucn I.  Cells were also treated with Ucn II.  In addition, mouse Ucn I promoter-driven pGL4.14 reporter plasmid was also transfected into HL-1 cardiomyocytes and luciferase activity was stimulated with nicotine. Oxidative stress was evaluated by conversion of 2’, 7’-dichlorodihydrofluorescin diacetate (DCFH-DA) to 2’, 7’-dichlorodihydrofluorescein (DCF).  Nicotine increased production of DCF in HL-1 cardiomyocytes and this nicotine-induced increase was suppressed by Ucn I. UcnI suppressed oxidative stress in HL-1 cardiomyocytes even in the absence of nicotine. In contrast, Ucn II, a specific agonist for CRF type 2 receptor (CRFR2), could not mimic Ucn I action and nicotine increased in mouse Ucn I promoter activity about 3-fold.  The present results indicate that Ucn I suppressed nicotine-induced oxidative stress in the heart, but this anti-oxidative action of Ucn I may not be mediated via the CRFR2

Nothing to Disclose: KI, KT, KF, WCC, YM

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