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2017 ; 7
(ä): 43259
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Silencing salusin-? attenuates cardiovascular remodeling and hypertension in
spontaneously hypertensive rats
#MMPMID28230187
Ren XS
; Ling L
; Zhou B
; Han Y
; Zhou YB
; Chen Q
; Li YH
; Kang YM
; Zhu GQ
Sci Rep
2017[Feb]; 7
(ä): 43259
PMID28230187
show ga
Salusin-? is a bioactive peptide involved in vascular smooth muscle cell
proliferation, vascular fibrosis and hypertension. The present study was designed
to determine the effects of silencing salusin-? on hypertension and
cardiovascular remodeling in spontaneously hypertensive rats (SHR).
Thirteen-week-old male SHR and normotensive Wistar-Kyoto rats (WKY) were
subjected to intravenous injection of PBS, adenoviral vectors encoding salusin-?
shRNA (Ad-Sal-shRNA) or a scramble shRNA. Salusin-? levels in plasma, myocardium
and mesenteric artery were increased in SHR. Silencing salusin-? had no
significant effect on blood pressure in WKY, but reduced blood pressure in SHR.
It reduced the ratio of left ventricle weight to body weight, cross-sectional
areas of cardiocytes and perivascular fibrosis, and decreased the media thickness
and the media/lumen ratio of arteries in SHR. Silencing salusin-? almost
normalized plasma norepinephrine and angiotensin II levels in SHR. It prevented
the upregulation of angiotensin II and AT(1) receptors, and reduced the NAD(P)H
oxidase activity and superoxide anion levels in myocardium and mesenteric artery
of SHR. Knockdown of salusin-? attenuated cell proliferation and fibrosis in
vascular smooth muscle cells from SHR. These results indicate that silencing
salusin-? attenuates hypertension and cardiovascular remodeling in SHR.
|*Gene Silencing
[MESH]
|*Rats, Inbred SHR
[MESH]
|*Vascular Remodeling
[MESH]
|*Ventricular Remodeling
[MESH]
|Animals
[MESH]
|Blood Pressure
[MESH]
|Intercellular Signaling Peptides and Proteins/*genetics
[MESH]
|RNA, Small Interfering/administration & dosage
[MESH]