In vivo knockdown of nicotinic acetylcholine receptor α1 diminishes aortic atherosclerosis.

ABSTRACT:

Objective

Nicotinic acetylcholine receptor α1 (nAChRα1) was recently identified as a functional cell receptor for urokinase, a potent atherogenic molecule. Here, we test the hypothesis that nAChRα1 plays a role in the pathogenesis of atherosclerosis.

Methods

Apolipoprotein E-deficient mice were initially fed a Western diet for 8 wks. Plasmid DNA encoding scramble RNA (pscr) or siRNA (psir2) for nAChRα1 was injected into the mice (n=16) using an aortic hydrodynamic gene transfer protocol. Four mice from each group were sacrificed 7 days after the DNA injection to confirm the nAChRα1 gene silencing. The remaining mice continued on a Western diet for an additional 16 wks.

Results

The nAChRα1 was up-regulated in aortic atherosclerotic lesions. A 78% knockdown of the nAChR

SUBMITTER: Zhang G 

PROVIDER: S-EPMC3688265 | biostudies-literature | 2011 Mar

REPOSITORIES: biostudies-literature