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2018 ; 24
(ä): 3958-3965
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Long Noncoding RNA (lncRNA) n379519 Promotes Cardiac Fibrosis in Post-Infarct
Myocardium by Targeting miR-30
#MMPMID29889825
Wang X
; Yong C
; Yu K
; Yu R
; Zhang R
; Yu L
; Li S
; Cai S
Med Sci Monit
2018[Jun]; 24
(ä): 3958-3965
PMID29889825
show ga
BACKGROUND Abnormally expressed long noncoding RNAs (lncRNAs) are recognized as
one of the key causes of cardiac diseases. However, the role of lncRNA in cardiac
fibrosis remains largely unknown. MATERIAL AND METHODS The experiment was divided
into 4 groups: a sham operation group, a myocardial infarction (MI) group, a
lentivirus group (LV-si-n379519), and a lentivirus control (LV-NC) group. The
adenovirus expression vectors LV-si-n379519 and LV-NC were constructed and
transfected into mice. Echocardiography, HE staining, and Masson staining were
performed to detect the heart function and collagen volume fraction in each
group. RT-PCR was used to detect the expression level of n379519, miR-30,
collagen I, and collagen III. In vitro, cardiac fibroblasts (CFs) were cultured
and the relationship between n379519 and miR-30 was verified using luciferase
reporter vector, n379519 siRNA, and miR-30 inhibitor. RESULTS The expression of
n379519 was markedly upregulated in the hearts of mice with MI and in the
fibrotic CFs. Knockdown of endogenous n379519 by its siRNA improved the heart
function and reduced collagen deposition and the process of cardiac fibrosis.
Further experiments showed the opposite trend of expression between n379519 and
miR-30. Bioinformatics analysis and luciferase reporter assay indicated that
n379519 directly binds to miR-30. Moreover, miR-30 inhibitor abrogated the
collagen synthesis inhibition induced by n379519. CONCLUSIONS These findings
reveal a novel function of n379519-miR-30 axis as a negative regulator for the
treatment of MI-induced cardiac fibrosis and the associated cardiac dysfunction.
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