ABSTRACT
Objective:
To investigate the regulatory effect of miR-26a in
radiation-induced
heart disease (RIHD)
mice.
Methods:
C57/BL6
mice were used to establish RIHD models. The cardiac function,
fibrosis, the expression levels of
collagen 1 (COL1) and
connective tissue growth factor (CTGF), and miR-26a were detected in RIHD
mice. Whether CTGF was the target
gene of miR-26a was verified by dual
luciferase kit. Moreover, cardiac
fibroblasts were transfected with miR-26a up and miR-26a down
lentivirus vectors to construct the miR-26a overexpression and underexpression
cell models. The expression of CTGF, proliferation, and
apoptosis of cardiac
fibroblasts were detected.
Results:
In the RIHD
mice,
heart function was decreased, myocardial
fibrosis was remodeled, the expression levels of COL1 and CTGF were up-regulated, and the expression level of miR-26a was down-regulated. Dual
luciferase reporter assay confirmed that CTGF was the target
gene regulated by miR-26a. Overexpression of miR-26a could inhibit the expression of CTGF, suppress the proliferation of cardiac
fibroblasts, promote
cell apoptosis and secrete
collagen. Underexpression of miR-26a yielded the opposite results.
Conclusion:
MiR-26a
affects the function of cardiac
fibroblasts by targeting CTGF and probably mediates the process of
radiation-induced myocardial
fibrosis, which may become a new regulatory target of RIHD.
