Limits...
Pioglitazone improves potassium channel remodeling induced by angiotensin II in atrial myocytes.

Gu J, Hu W, Liu X - Med Sci Monit Basic Res (2014)

Bottom Line: Compared with the control group, AngII reduced Ito and Ikur current density as well as amplified Ik1 current density, which were partially prevented by pioglitazone.These results suggest that pioglitazone exhibits a beneficial effect on AngII-induced potassium channel remodeling.PPAR-γ agonists may be potentially effective up-stream therapies for AF.

View Article: PubMed Central - PubMed

Affiliation: Department of Cardiology, Shanghai Minhang District Central Hospital, Fudan University, Shanghai, China (mainland).

ABSTRACT

Background: It has been demonstrated that atrial electrical remodeling contributes toward atrial fibrillation (AF) maintenance, and that angiotensin II (AngII) is involved in the pathogenesis of atrial electrical remodeling. Peroxisome proliferator activated receptor-γ (PPAR-γ) agonists have been shown to inhibit atrial electrical remodeling, but the underlying mechanisms are poorly understood. In the present study we investigated the regulating effects of PPAR-g agonist on AngII-induced potassium channel remodeling in atrial myocytes.

Material/methods: Whole-cell patch-clamp technique was used to record transient outward potassium current (Ito), ultra-rapid delayed rectifier potassium (Ikur), and inward rectifier potassium current (Ik1). Real-time PCR was used to assess potassium channel subunit mRNA expression.

Results: Compared with the control group, AngII reduced Ito and Ikur current density as well as amplified Ik1 current density, which were partially prevented by pioglitazone. Furthermore, pioglitazone alleviated the downregulation of Ito subunit (Kv 4.2) and Ikur subunit (Kv 1.5), as well as the upregulation of Ik1 subunit (Kir 2.1 and Kir 2.2) mRNA expression stimulated by AngII.

Conclusions: These results suggest that pioglitazone exhibits a beneficial effect on AngII-induced potassium channel remodeling. PPAR-γ agonists may be potentially effective up-stream therapies for AF.

Show MeSH

Related in: MedlinePlus

Effect of pioglitazone on AngII inducing mRNA expression change of potassium channel subunit in HL-1 cells. * P<0.01 vs. control; ** P<0.01 vs. AngII.
© Copyright Policy
Related In: Results  -  Collection


getmorefigures.php?uid=PMC4206483&req=5

f4-medscimonitbasicres-20-153: Effect of pioglitazone on AngII inducing mRNA expression change of potassium channel subunit in HL-1 cells. * P<0.01 vs. control; ** P<0.01 vs. AngII.

Mentions: Since the above results revealed a functional change in potassium channel activities carrying Ito, Ikur, and Ik1 in atrial myocytes treated with AngII and/or pioglitazone, we analyzed the expression levels of the genes encoding Ito (Kv4.2), IKur (Kv1.5), and IK1 (Kir2.1 and Kir2.2). The mRNA expression of Kv4.2 and Kv1.5 in the AngII group (1 μM) was significantly decreased compared with the control group, but the mRNA expression of Kir2.1 and Kir2.2 in the AngII group (1 μM) was markedly increased compared with the control group. Pretreatment with pioglitazone (10 μM) could in part reverse the aforementioned changes (Figure 4).


Pioglitazone improves potassium channel remodeling induced by angiotensin II in atrial myocytes.

Gu J, Hu W, Liu X - Med Sci Monit Basic Res (2014)

Effect of pioglitazone on AngII inducing mRNA expression change of potassium channel subunit in HL-1 cells. * P<0.01 vs. control; ** P<0.01 vs. AngII.
© Copyright Policy
Related In: Results  -  Collection

Show All Figures
getmorefigures.php?uid=PMC4206483&req=5

f4-medscimonitbasicres-20-153: Effect of pioglitazone on AngII inducing mRNA expression change of potassium channel subunit in HL-1 cells. * P<0.01 vs. control; ** P<0.01 vs. AngII.
Mentions: Since the above results revealed a functional change in potassium channel activities carrying Ito, Ikur, and Ik1 in atrial myocytes treated with AngII and/or pioglitazone, we analyzed the expression levels of the genes encoding Ito (Kv4.2), IKur (Kv1.5), and IK1 (Kir2.1 and Kir2.2). The mRNA expression of Kv4.2 and Kv1.5 in the AngII group (1 μM) was significantly decreased compared with the control group, but the mRNA expression of Kir2.1 and Kir2.2 in the AngII group (1 μM) was markedly increased compared with the control group. Pretreatment with pioglitazone (10 μM) could in part reverse the aforementioned changes (Figure 4).

Bottom Line: Compared with the control group, AngII reduced Ito and Ikur current density as well as amplified Ik1 current density, which were partially prevented by pioglitazone.These results suggest that pioglitazone exhibits a beneficial effect on AngII-induced potassium channel remodeling.PPAR-γ agonists may be potentially effective up-stream therapies for AF.

View Article: PubMed Central - PubMed

Affiliation: Department of Cardiology, Shanghai Minhang District Central Hospital, Fudan University, Shanghai, China (mainland).

ABSTRACT

Background: It has been demonstrated that atrial electrical remodeling contributes toward atrial fibrillation (AF) maintenance, and that angiotensin II (AngII) is involved in the pathogenesis of atrial electrical remodeling. Peroxisome proliferator activated receptor-γ (PPAR-γ) agonists have been shown to inhibit atrial electrical remodeling, but the underlying mechanisms are poorly understood. In the present study we investigated the regulating effects of PPAR-g agonist on AngII-induced potassium channel remodeling in atrial myocytes.

Material/methods: Whole-cell patch-clamp technique was used to record transient outward potassium current (Ito), ultra-rapid delayed rectifier potassium (Ikur), and inward rectifier potassium current (Ik1). Real-time PCR was used to assess potassium channel subunit mRNA expression.

Results: Compared with the control group, AngII reduced Ito and Ikur current density as well as amplified Ik1 current density, which were partially prevented by pioglitazone. Furthermore, pioglitazone alleviated the downregulation of Ito subunit (Kv 4.2) and Ikur subunit (Kv 1.5), as well as the upregulation of Ik1 subunit (Kir 2.1 and Kir 2.2) mRNA expression stimulated by AngII.

Conclusions: These results suggest that pioglitazone exhibits a beneficial effect on AngII-induced potassium channel remodeling. PPAR-γ agonists may be potentially effective up-stream therapies for AF.

Show MeSH
Related in: MedlinePlus