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Published on: February 9, 2014
Yin Yang 1 (YY1)-induced long intergenic non-protein coding RNA 472 (LINC00472) aggravates sepsis-associated cardiac
Guixi Mo1, Jian Mo1, Xiujuan Tan1
1Department of Anesthesiology, Affiliated Hospital of Guangdong Medical University, Zhanjiang City, Guangdong Province, China.
Abstract:
As a leading complication of sepsis, sepsis-induced cardiac dysfunction (SICD) contributed to the high mortality of patients with sepsis. Long non-coding RNA (LncRNA) LINC00472 has been reported to be in sepsis-induced disease. Nonetheless, its biological function and underlying molecular in SICD remain largely unknown. In this study, in vivo and in vitro SICD models were established via LPS treatment. H&E staining was employed for the evaluation of myocardial injury. ELISA assay was performed to detect cardiac Troponin I (cTnI), creatine kinase-MB (CK-MB), interleukin (IL)-1β, and tumor necrosis factor-α (TNF-α) levels. Cardiomyocyte viability and apoptosis were assessed via CCK-8 and flow cytometry assays. The transcriptional regulation of YY1 on LINC00472 was demonstrated via ChIP assay. Besides, the interaction between YY1 and LINC00472, as well as the association between miR-335-3p and LINC00472 or MAOA were verified via luciferase reporter assay and RNA immunoprecipitation (RIP) assay. Herein, highly expressed LINC00472 was observed in both in vivo and in vitro SICD models. LINC00472 knockdown substantially attenuated LPS-induced inhibition on cardiomyocyte viability and reversed cardiomyocyte apoptosis and inflammatory response mediated by LPS treatment. YY1 induced LINC00472 upregulation, thereby promoting cardiomyocyte dysfunction induced by LPS. In addition, MAOA upregulation or miR-335-3p inhibition could partly reverse the suppressive effect on LPS-induced cardiomyocyte dysfunction mediated by LINC00472 knockdown. Based on our results, it seemed that YY1-activated LINC00472 might contribute to SICD progression via the miR-335-3p/MAOA pathway.
Insights
Sepsis-induced cardiac dysfunction (SICD) involves increased LINC00472, a long non-coding RNA. This study reveals LINC00472 promotes SICD via the miR-335-3p/MAOA pathway, offering potential therapeutic targets.
Area of Science:
- Cardiology
- Molecular Biology
- Genetics
Background:
- Sepsis-induced cardiac dysfunction (SICD) is a major cause of mortality in sepsis patients.
- The role of long non-coding RNA (LncRNA) LINC00472 in SICD pathogenesis is not well understood.
Purpose of the Study:
- To investigate the function and molecular mechanisms of LINC00472 in SICD.
- To explore the regulatory pathway involving LINC00472, YY1, miR-335-3p, and MAOA in SICD.
Main Methods:
- Established in vivo and in vitro models of SICD using lipopolysaccharide (LPS) treatment.
- Assessed myocardial injury, cardiomyocyte viability, apoptosis, and inflammatory markers (cTnI, CK-MB, IL-1β, TNF-α).
- Utilized ChIP, luciferase reporter, and RIP assays to elucidate molecular interactions and transcriptional regulation.
Main Results:
- LINC00472 was significantly upregulated in both in vivo and in vitro SICD models.
- Knockdown of LINC00472 attenuated LPS-induced cardiomyocyte dysfunction, apoptosis, and inflammation.
- YY1 was found to upregulate LINC00472, and the YY1-LINC00472 axis promoted SICD via the miR-335-3p/MAOA pathway.
Conclusions:
- YY1-activated LINC00472 plays a crucial role in the progression of SICD.
- The miR-335-3p/MAOA pathway is implicated in LINC00472-mediated cardiomyocyte dysfunction during sepsis.
