Key result
Knockdown of LTBP2 partially reversed isoproterenol-induced apoptosis in mouse cardiac fibroblasts by suppressing caspase-3 expression and activity.
Why the study?
The underlying mechanism of cardiac fibrosis remains unclear, and whether LTBP2 serves a role in cardiac fibrosis is unknown.
Does LTBP2 knockdown prevent isoproterenol-induced apoptosis in mouse cardiac fibroblasts?
Does LTBP2 knockdown prevent isoproterenol-induced apoptosis in mouse cardiac fibroblasts?
p-value: p=<0.01
LTBP2 knockdown reduces isoproterenol-induced apoptosis in mouse cardiac fibroblasts by suppressing caspase-3 activity, identifying a potential therapeutic target for cardiac fibrosis.
Cardiac fibrosis is a core process in the development of heart failure. However, the underlying mechanism of cardiac fibrosis remains unclear. Recently, a study found that in an isoproterenol (ISO)-induced cardiac fibrosis animal model, there is high expression of latent-transforming growth factor β-binding protein 2 (LTBP2) in cardiac fibroblasts. Whether LTBP2 serves a role in cardiac fibrosis is currently unknown. In the present study, mouse cardiac fibroblasts (MCFs) were treated with 100 µM/l ISO for 24, 48, or 72 h, and small interfering RNAs (siRNAs) were used to knockdown LTBP2. Reverse transcription-quantitative PCR and western blotting were used to determine gene and protein expression levels, respectively. Caspase-3 serves a key role in cell apoptosis and is related to cardiac fibrosis-induced heart failure. Caspase-3 activity was therefore determined using a caspase-3 assay kit, CCK8 was used to determine the rate of cell proliferation and apoptosis rates were quantified using a cell death detection ELISA kit. The present study demonstrated that cell apoptosis and LTBP2 expression increased in MCFs treated with 100 µM/l ISO in a time-dependent manner. Expression and activity of caspase-3 also increased in MCFs treated with 100 µM/l ISO for 48 h compared with the control group. In addition, ISO stimulation-induced MCF apoptosis, along with the increased expression of caspase-3 were partly abolished when LTBP2 was knocked down. In conclusion, LTBP2 expression increased in ISO-treated MCFs and accelerated mouse cardiac fibroblast apoptosis by enhancing the expression and activity of caspase-3. LTBP2 may therefore be a potential therapeutic target for treating patients with cardiac fibrosis.
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Li et al. (2021) studied Cardiac fibrosis. LTBP2 knockdown via siRNA vs. Scrambled NC siRNA was evaluated on Cell apoptosis and caspase-3 activity (p=<0.01). Knockdown of LTBP2 partially reversed isoproterenol-induced apoptosis in mouse cardiac fibroblasts by suppressing caspase-3 expression and activity.
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