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Updated: Oct 2, 2025
In Vivo Nanovector Delivery of a Heart-specific MicroRNA-sponge
Published on: June 15, 2018
miR-197 Participates in Lipopolysaccharide-Induced Cardiomyocyte Injury by Modulating SIRT1
Miaomiao Liu1, Ying Zhang1, Xiantong Cao1
1Department of Cardiovascular Surgery, First Affiliated Hospital of Xi'an Jiaotong University, Yanta, China.
Insights
MicroRNA-197 (miR-197) exacerbates sepsis-induced heart injury by downregulating SIRT1. Inhibiting miR-197 protects against this damage, suggesting miR-197 as a sepsis management marker.
Area of Science:
- Cardiovascular Biology
- Molecular Medicine
- Inflammation Research
Background:
- Sepsis-induced myocarditis is a significant cause of mortality.
- MicroRNA-197 (miR-197) is linked to inflammatory heart disease prognosis.
- The role of miR-197 in sepsis-related cardiomyocyte injury is not fully understood.
Purpose of the Study:
- To investigate the role of miR-197 in lipopolysaccharide (LPS)-induced cardiomyocyte injury.
- To explore the interaction between miR-197 and silent information regulator 1 (SIRT1) in this context.
- To evaluate miR-197 as a potential biomarker for sepsis management.
Main Methods:
- H9c2 cells were treated with LPS to mimic sepsis conditions.
- Cell viability, apoptosis, and inflammatory markers were assessed using CCK-8, flow cytometry, LDH, and ELISA assays.
- miR-197 and SIRT1 expression levels were quantified using qRT-PCR and western blotting.
Main Results:
- LPS induced miR-197 overexpression and cardiomyocyte injury, characterized by reduced viability and increased apoptosis.
- LPS downregulated Bcl-2 and SIRT1 expression while upregulating pro-apoptotic markers (Bax, cleaved caspase-3) and inflammatory cytokines (IL-6, IL-1β).
- miR-197 inhibition reversed LPS-induced injury, and this protective effect was abolished by SIRT1 silencing, indicating miR-197 mediates injury via SIRT1 modulation.
Conclusions:
- miR-197 plays a critical role in exacerbating LPS-induced cardiomyocyte injury.
- The mechanism involves the modulation of SIRT1 expression and activity.
- miR-197 may serve as a valuable molecular marker for managing sepsis-related cardiac complications.
Abstract:
Sepsis is a systemic inflammation and is capable of inducing myocarditis, which is a major leading cause of death in patients. Studies have found that miR-197 is correlated with the prognosis of patients with inflammatory heart disease, but its effect on sepsis-induced cardiomyocyte injury remains unclear. We treated H9c2 cells with lipopolysaccharide (LPS), then detected the cell viability via the cell counting kit-8 (CCK-8) assay and quantified miR-197 expression via quantitative real-time polymerase chain reaction (qRT-PCR). Then, we investigated the role of miR-197 in LPS-induced H9c2 cells by CCK-8 assay, flow cytometry, lactate dehydrogenase (LDH) measurement, enzyme-linked immunosorbent assay (ELISA), qRT-PCR, and western blot. Subsequently, silent information regulator 1 (SIRT1) was downregulated in H9c2 cells to explore its interaction with miR-197 under LPS induction. LPS induced miR-197 overexpression in H9c2 cells. LPS restrained viability, the expressions of B-cell lymphoma-2 (Bcl-2) and SIRT1, but promoted apoptosis, LDH release, and levels of interleukin-6 (IL-6), interleukin-1β (IL-1β), acetyl (AC)-p53, BCL2-associated X (Bax), and cleaved caspase-3 in H9c2 cells. miR-197 inhibition reversed the effects of LPS on H9c2 cells. The protective role of miR-197 downregulation in LPS-induced H9c2 cells was reversed by SIRT1 silencing. miR-197 contributed to LPS-induced cardiomyocyte injury by modulating SIRT1, which might be used as a molecular marker in the management of sepsis.
