Figure - PMC

Skip to main content

An official website of the United States government

Here's how you know

Here's how you know

Official websites use .gov
A .gov website belongs to an official government organization in the United States.

Secure .gov websites use HTTPS
A lock ( ) or https:// means you've safely connected to the .gov website. Share sensitive information only on official, secure websites.

View full-text article in PMC

. 2017 May 9;8(31):51462–51477. doi: 10.18632/oncotarget.17721

Search in PMC
Search in PubMed
View in NLM Catalog
Add to search

Copyright: © 2017 Sun et al.

This is an open-access article distributed under the terms of the Creative Commons Attribution License 3.0 (CC BY 3.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.

PMC Copyright notice

Silencing of the FoxO3a gene by siRNA prevents atrogin-1 upregulation (A) and BK_Ca β1 downregulation (B) in homocysteine-exposed PCASMCs. The role of atrogin-1 as a critical mediator of homocysteine-induced BK_Ca β1 loss is evidenced by the preserved protein level of BK_Ca β1 in homocysteine-exposed cells that are transfected with atrogin-1 siRNA (C). *p<0.05, **p<0.01; ^#p<0.05, ^##p<0.01. Silencing of the FoxO3a gene prevents homocysteine-induced inhibition of BK_Ca channel currents (D & E). Original traces and I-V curves of whole-cell K⁺ current under unstimulated condition (D - left panel) and in response to NS1619 (E - left panel) in cells from different treatment groups before and after application of the BK_Ca channel blocker iberiotoxin. *p<0.05, **p<0.01, ***p<0.001 vs. basal, ^#p<0.05, ^##p<0.01, ^###p<0.001 NS1619+Ibtx vs. NS1619. Summarized data of BK_Ca channel currents from 5 independent experiments under conditions without (D - right panel) or with NS1619 stimulation. (E - lower panel), each obtained from cell isolates of different heart. *p<0.05. Hcy: homocysteine, Ibtx: iberiotoxin.

Silencing of the FoxO3a gene by siRNA prevents atrogin-1 upregulation (A) and BK_Ca β1 downregulation (B) in homocysteine-exposed PCASMCs. The role of atrogin-1 as a critical mediator of homocysteine-induced BK_Ca β1 loss is evidenced by the preserved protein level of BK_Ca β1 in homocysteine-exposed cells that are transfected with atrogin-1 siRNA (C). *p<0.05, **p<0.01; ^#p<0.05, ^##p<0.01. Silencing of the FoxO3a gene prevents homocysteine-induced inhibition of BK_Ca channel currents (D & E). Original traces and I-V curves of whole-cell K⁺ current under unstimulated condition (D - left panel) and in response to NS1619 (E - left panel) in cells from different treatment groups before and after application of the BK_Ca channel blocker iberiotoxin. *p<0.05, **p<0.01, ***p<0.001 vs. basal, ^#p<0.05, ^##p<0.01, ^###p<0.001 NS1619+Ibtx vs. NS1619. Summarized data of BK_Ca channel currents from 5 independent experiments under conditions without (D - right panel) or with NS1619 stimulation. (E - lower panel), each obtained from cell isolates of different heart. *p<0.05. Hcy: homocysteine, Ibtx: iberiotoxin.