SNHG16 accelerates the proliferation of primary cardiomyocytes by targeting miRNA-770-5p
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Published on: February 24, 2017
Linshan Yang1, Yan Lu2, Jie Ming3
1Department of Cardiac Surgery, The Affiliated Hospital of Qingdao University, Qingdao, Shandong 266003, P.R. China.
Abstract:
The present study aimed to clarify the influence of long non-coding RNA small nuclear host gene 16 (lncRNA SNHG16) on cardiomyocyte proliferation following ischemia/reperfusion injury (IRI) and the potential mechanism. An IRI model in mice was established by performing ligation of the anterior descending coronary artery (LAD). Primary cardiomyocytes were isolated from newborn mice and subjected to H2O2 treatment to mimic in vitro IRI. Relative levels of SNHG16 and miRNA-770-5p in both in vivo and in vitro IRI models were examined. The regulatory effects of SNHG16 and miRNA-770-5p on the proliferative ability of H2O2-treated cardiomyocytes were assessed by Cell Counting Kit-8 (CCK-8) and 5-ethynyl-2'-deoxyuridine (EdU) assay. The binding relationship between SNHG16 and miRNA-770-5p was verified through dual-luciferase reporter gene assay. It is found that SNHG16 was time-dependently downregulated in the IRI models. Overexpression of SNHG16 enhanced the proliferative ability of the cardiomyocytes. miRNA-770-5p was found to be a direct target of SNHG16. Moreover, SNHG16 was able to negatively regulate the miRNA-770-5p level. Overexpression of miRNA-770-5p partially reversed the role of SNHG16 on accelerating cardiomyocyte proliferation. Collectively, SNHG16 accelerates the proliferative ability of cardiomyocytes following IRI by negatively regulating miRNA-770-5p.
Insights
Long non-coding RNA SNHG16 promotes cardiomyocyte proliferation after ischemia/reperfusion injury (IRI) by downregulating miRNA-770-5p. This finding offers a potential therapeutic target for heart injury recovery.
Area of Science:
- Molecular Biology
- Cardiovascular Research
- RNA Biology
Background:
- Ischemia/reperfusion injury (IRI) significantly impacts cardiomyocyte function and survival.
- Long non-coding RNAs (lncRNAs) play crucial roles in cellular responses to injury.
- Understanding the molecular mechanisms underlying cardiomyocyte protection post-IRI is critical.
Purpose of the Study:
- To investigate the role of lncRNA SNHG16 in cardiomyocyte proliferation following IRI.
- To elucidate the underlying mechanism involving miRNA-770-5p.
- To assess the therapeutic potential of modulating SNHG16 in cardiac injury.
Main Methods:
- Establishment of in vivo (mouse LAD ligation) and in vitro (H2O2-treated cardiomyocytes) IRI models.
- Quantification of SNHG16 and miRNA-770-5p expression levels.
- Assessment of cardiomyocyte proliferation using CCK-8 and EdU assays.
- Verification of the SNHG16-miRNA-770-5p interaction via dual-luciferase reporter assay.
Main Results:
- SNHG16 expression was significantly downregulated in IRI models.
- Overexpression of SNHG16 promoted cardiomyocyte proliferation.
- SNHG16 directly targets and negatively regulates miRNA-770-5p.
- Overexpression of miRNA-770-5p partially counteracted the proliferative effects of SNHG16.
Conclusions:
- lncRNA SNHG16 enhances cardiomyocyte proliferation post-IRI.
- This effect is mediated through the negative regulation of miRNA-770-5p.
- SNHG16 represents a potential therapeutic target for mitigating cardiac damage after IRI.
