Enhancement of LncRNA-HFRL expression induces cardiomyocyte inflammation, proliferation, and fibrosis via the sequestering of miR-149-5p-mediated collagen 22A inhibition.

ABSTRACT:

Background

Long non-coding ribonucleic acids (lncRNAs) are believed to play crucial roles in cardiovascular diseases; however, details of the underlying mechanisms by which this occurs remain unclear.

Methods

A mouse heart failure (HF) model was established using isoproterenol (ISO), and confirmed by immunostaining and echocardiography. RNA-sequencing was performed to screen the differential lncRNA expression profiles and heart failure relative lncRNA (HFRL) was selected as the target which was validated by quantitative real-time polymerase chain reaction (qRT-PCR). In HL-1 cells, the cardiac function, inflammatory, and fibrosis-related genes expression changes were examined by qRT-PCR after silencing of HFRL by lentivirus. Meanwhile, Cell Counting Kit-8 (CCK-8) assays were

SUBMITTER: Li X 

PROVIDER: S-EPMC9347043 | biostudies-literature | 2022 May

REPOSITORIES: biostudies-literature