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- Title
LncRNA CAIF suppresses LPS-induced inflammation and apoptosis of cardiomyocytes through regulating miR-16 demethylation.
- Authors
Yan Wang; Yi Zhang
- Abstract
Background: The long noncoding RNA, cardiac autophagy inhibitory factor (CAIF), and microRNA (miR)-16 are reported to be involved in lipopolysaccharide (LPS)-induced inflammatory responses and cell apoptosis in many diseases. Herein, we investigated the interaction between CAIF and miR-16 in sepsis-induced chronic heart failure (CHF). Methods: The expression of CAIF and miR-16 in plasma samples from sepsisinduced CHF patients (n = 60) and healthy controls (n = 60) were measured using quantitative reverse-transcription polymerase chain reaction (qRT-PCR). The correlations between CAIF and miR-16 across plasma samples from patients with sepsis-induced CHF and healthy controls were analyzed using linear regression. The messenger RNA (mRNA) levels of inducible nitric oxide synthase, C-C motif chemokine 2 (CCL2), growth-regulated alpha protein (CXCL1), and interleukin-6 (IL-6) were evaluated using qRT-PCR while nuclear factor κB activation was evaluated using luciferase assay. Results: The expression levels of CAIF and miR-16 were downregulated in the plasma of sepsis-induced CHF patients and were positively correlated in these patients. In cardiomyocytes, LPS treatment dose-dependently decreased CAIF and miR-16 levels. CAIF overexpression increased miR-16 expression by demethylating miR-16. CAIF and/or miR-16 overexpression suppressed LPSinduced CCL2, CXCL1, and IL-6 expression at both the mRNA and protein levels. Analysis of cell apoptosis and western blot analysis showed that CAIF and/or miR-16 overexpression inhibited LPS-induced cardiomyocyte apoptosis by reducing Bax and cleaved caspase 3 levels and enhancing Bcl-2 levels. Conclusion: Our study is the first to report the abnormal expression of CAIF and miR-16 in heart disease. CAIF plays a protective role in sepsis-induced CHF by inhibiting cardiomyocyte apoptosis and inflammation, possibly by regulating miR-16 demethylation.
- Subjects
LINCRNA; DEMETHYLATION; NITRIC-oxide synthases; WESTERN immunoblotting; APOPTOSIS
- Publication
Immunity, Inflammation & Disease, 2021, Vol 9, Issue 4, p1468
- ISSN
2050-4527
- Publication type
Article
- DOI
10.1002/iid3.498