LncRNA CAIF Upregulates miR-16 Through Methylation to Suppress LPS-Induced Apoptosis of Cardiomyocytes

Background: Both lncRNA CAIF and miR-16 can inhibit LPS-induced inflammatory response. It is known that LPS plays crucial roles in sepsis. This study was therefore carried out to investigate the interactions between CAIF and miR-16 in sepsis. Methods: : Levels of CAIF (A) and miR-16 (B) in plasma samples from sepsis patients (n = 60) and healthy controls (n = 60) were measured by performing RT-qPCR. Correlations of levels of CAIF and miR-16 across plasma samples from sepsis patients (A) and healthy controls (B) were analyzed by linear regression.The effects of CAIF overexpression on miR-16 (B), and the effects of miR-16 overexpression on CAIF (C) were analyzed by RT-qPCR. Results: : We found that CAIF and miR-16 were downregulated in plasma of sepsis patients and they were positively correlated. In cardiomyocytes, LPS treatment led to downregulated CAIF and miR-16. Moreover, CAIF overexpression led to upregulated miR-16 and increased methylation of miR-16. However, miR-16 overexpression failed to significantly affect CAIF expression. Cell apoptosis analysis showed that CAIF and miR-16 overexpression suppressed LPS-induced apoptosis of cardiomyocytes. The combination of CAIF and miR-16 overexpression showed stronger effect. Conclusion: CAIF may upregulate miR-16 through methylation to suppress LPS-induced apoptosis of cardiomyocytes.