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2018 ; 42
(2
): 975-987
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MicroRNA?20b?5p promotes ventricular remodeling by targeting the TGF??/Smad
signaling pathway in a rat model of ischemia?reperfusion injury
#MMPMID29786750
Liang ZG
; Yao H
; Xie RS
; Gong CL
; Tian Y
Int J Mol Med
2018[Aug]; 42
(2
): 975-987
PMID29786750
show ga
Myocardial ischemic injury results from severe impairment of the coronary blood
supply and may lead to metabolic and ultrastructural changes, thereby causing
irreversible damage. MicroRNA (miR)?20b?5p has been demonstrated to be involved
in malignancies of the breast, colorectum, stomach, blood and oropharynx. The
present study aimed to investigate the effects of miR?20b?5p on ventricular
remodeling following myocardial ischemia?reperfusion (IR) injury in rats by
targeting small mothers against decapentaplegic homolog 7 (Smad7) via the
transforming growth factor?? (TGF??)/Smad signaling pathway. A total of 70 adult
male Sprague?Dawley rats were divided into seven groups: Sham group, IR group,
negative control group, miR?20b?5p mimics group, miR?20b?5p inhibitors group,
small interfering RNA (siRNA)?Smad7 group, and miR?20b?5p inhibitors +
siRNA?Smad7 group. Dual luciferase reporter gene assays were used to verify the
association between miR?20b?5p and Smad7. Myocardial infarction size, myocardial
collagen volume fraction and perivascular collagen area were detected separately
using triphenyltetrazolium chloride and Masson's staining. The rate of positive
expression of Smad7 was detected using immunohistochemistry, and the expression
levels of miR?20b?5p, TGF??1, Smad3 and Smad7 were detected using reverse
transcription?quantitative polymerase chain reaction and western blot analyses.
The findings revealed that miR?20b?5p inhibited Smad7. Compared with the sham
group, the other six groups had increased myocardial infarction size, myocardial
collagen, and expression of miR?20b?5p, TGF??1 and Smad3, and decreased
expression of Smad7. Compared with the IR group, the miR?20b?5p mimics group and
the siRNA?Smad7 group had increased myocardial infarction size and myocardial
collagen, increased expression of TGF??1 and Smad3, and decreased expression of
Smad7. The expression of miR?20b?5p was markedly increased in the miR?20b?5p
mimics group, but did not differ significantly from that in the siRNA?Smad7
group. The results demonstrated that miR?20b?5p promoted ventricular remodeling
following myocardial IR injury in rats by inhibiting the expression of Smad7
through activating the TGF??/Smad signaling pathway.