Downregulation of Long Noncoding RNA LINC00261 Attenuates Myocardial Infarction through the miR-522-3p/Trinucleotide Repeat-Containing Gene 6a (TNRC6A) Axis.

BACKGROUND: Myocardial infarction (MI) is cardiac tissue necrosis caused by acute and persistent ischemic hypoxia of the coronary arteries. This study is aimed at investigating the expression of long noncoding RNA (lncRNA) LINC00261 in MI and its effect on myocardial cells. METHODS: qRT-PCR was performed to detect the expression levels of LINC00261, miR-522-3p, and TNRC6A in normal and MI cells. Western blotting analysis was performed to detect the expression of TNRC6A protein. Viability and apoptosis of myocardial cells after MI with the knockout of LINC00261 or TNRC6A were detected. The relationships among miR-522-3p, LINC00261, and TNRC6A in cardiomyocytes were evaluated using a double luciferase reporter gene assay. Hypoxic preconditioning in normal cells was used to construct a simulated MI environment to investigate the effect of LINC00261 on apoptosis of cardiac cells. RESULTS: LINC00261 and TNRC6A were upregulated, while miR-522-3p was downregulated in coronary heart disease tissues with MI. Knockout of LINC00261 can increase the viability of cardiomyocytes and inhibit cell apoptosis. LINC00261 targets miR-522-3p in cardiomyocytes. In addition, miR-522-3p targets TNRC6A in cardiomyocytes. TNRC6A regulates cell viability and apoptosis of cardiomyocytes after MI, and TNRC6A-induced MI can be reversed by overexpression of miR-522-3p. CONCLUSIONS: LINC00261 downregulated miR-522-3p in cardiomyocytes after MI by directly targeting miR-522-3p. TNRC6A is the direct target of miR-522-3p. Our results indicated that LINC00261 might serve as a therapeutic target for the treatment of MI.

[Polymorphism of SNPs in the lipoprotein lipase (LPL) in Siniperca chuatsi and their association with feed habit domestication].

Sinperca chuatsi usually refuses eating dead bait or man-made feed due to its specific feeding habit. It was showed that some S. chuatsi could be induced to take lifeless bait with domestication gradually after long-term of cultivation. High cost, serious pollution, severe diseases, and other problems of S chuatsi cultivation can be solved effectively by selecting those liable to domestication via molecular marker and treating them with artificial feed on a large scale. Lipoprotein lipase, one of the key enzymes in lipoprotein metabolic processes, provides energy by catalyzing the oxidation of triglycerides lie in the core of chylomicron and very low density lipoprotein (VLDL) into glycerin and fatty acid, and saves energy. In order to search the distribution of the alleles and genotypes of lipoprotein lipase gene (lipoprotein LPL) gene in two feed habit domestication phenotype populations, SNP genetic polymorphisms in 6 and 7 introns and 6, 7, and 8 exons of LPL in S. chuatsi were analyzed by PCR product sequencing method. Three SNPs A25T, G26T, and C29G were detected, two of which were non-synonymous mutations. It was indicated by Chi-square test that the analysis between domesticated and undomesticated populations show no significant difference (P>0.05) between the three SNPs and feed habit. However, diplotype 2 in the two population showed significant difference (P<0.05) by assembling different genotypes of the three SNPs into five diplotypes. Polymorphic analysis of partial fragment of LPL genome in S. chuatsi was accomplished successfully. Therefore, LPL gene can be considered as a candidate gene and genetic marker for feed habit domestication in S. chuatsi, which lays the foundation for the work of molecular marker and selecting breed, which has extensive application prospect.