Project description:Minipigs are animal models widely used in biomedical studies due to their physiological and anatomical similarities to humans. However, a comprehensive resource for the Korean minipig (Sus scrofa) transcriptome remains unavailable. In this study, we constructed a de novo transcriptome of the Korean minipig using RNA-seq data obtained from ten tissues across ten samples. The final assembly comprised 57,085 coding transcripts with an average length of 3,075 nucleotides and an N50 of 4,258 nucleotides. In total, 65.4% of the transcripts were annotated, and biological functions were assigned. Transcript expression profiling and principal component analysis showed that samples clustered by tissue type, reflecting transcriptomic features shared across tissues. Comparative analysis demonstrated that the novel transcriptome assembly had contiguity and completeness comparable to those available for pig and minipig breeds. Overall, this study provides a comprehensive transcriptomic resource for the Korean minipig, facilitating further functional analyses.
Project description:Minipigs are animal models widely used in biomedical studies due to their physiological and anatomical similarities to humans. However, a comprehensive resource for the Korean minipig (Sus scrofa) transcriptome remains unavailable. In this study, we constructed a de novo transcriptome of the Korean minipig using RNA-seq data obtained from ten tissues across ten samples. The final assembly comprised 57,085 coding transcripts with an average length of 3,075 nucleotides and an N50 of 4,258 nucleotides. In total, 65.4% of the transcripts were annotated, and biological functions were assigned. Transcript expression profiling and principal component analysis showed that samples clustered by tissue type, reflecting transcriptomic features shared across tissues. Comparative analysis demonstrated that the novel transcriptome assembly had contiguity and completeness comparable to those available for pig and minipig breeds. Overall, this study provides a comprehensive transcriptomic resource for the Korean minipig, facilitating further functional analyses.
Project description:Myocardial infarction (MI) is a highly prevalent cardiac emergency, which results in adverse left ventricular remodeling exacerbating progressive heart failure. Inflammation in post-MI is necessary for myocyte repair and wound healing. However, it is also a key component of subsequent heart failure pathology. Myoblasts transplantation after MI have been fulfilled a good effect on cardiac repair, but the occasion, complications of transplantation, and the underlying mechanisms have not been fully elucidated. Here, we found that myoblast transplantation decreased the expression of many pro-inflammatory genes and the activation of inflammation-related signal pathway in heart tissue of pig post MI, which mainly contributed to the improved heart function and attenuated damage of myocardial cells.
Project description:Ischemia, fibrosis, and remodeling lead to heart failure after severe myocardial infarction (MI). Myoblast sheet transplantation is a promising therapy to enhance cardiac function and induce therapeutic angiogenesis via a paracrine mechanism in this detrimental disease. We hypothesized that in a rat model of MI-induced chronic heart failure this therapy could further be improved by overexpression of the antiapoptotic, antifibrotic, and proangiogenic hepatocyte growth factor (HGF) in the myoblast sheets. We studied the ability of wild type (L6-WT) and human HGF-expressing (L6-HGF) L6 myoblast sheet-derived paracrine factors to stimulate cardiomyocyte, endothelial cell, or smooth muscle cell migration in culture. Further, we studied the autocrine effect of hHGF-expression on myoblast gene expression using microarray analysis. We induced MI in Wistar rats by left anterior descending coronary artery (LAD) ligation and allowed heart failure to develop for four weeks. Thereafter, we administered L6-WT (n=15) or L6-HGF (n=16) myoblast sheet therapy. Control rats (n=13) underwent LAD ligation and rethoracotomy without therapy and five rats underwent sham-operation in both surgeries. We evaluated cardiac function with echocardiography at 2 and 4 weeks after therapy administration. We analyzed cardiac angiogenesis and left ventricular architecture from histological sections 4 weeks after therapy. Paracrine mediators from L6-HGF myoblast sheets effectively induced migration of cardiac endothelial and smooth muscle cells but not cardiomyocytes. Microarray data revealed that hHGF-expression modulated myoblast gene expression. In vivo, L6-HGF sheet therapy effectively stimulated angiogenesis in the infarcted and non-infarcted areas. Both L6-WT and L6-HGF therapies enhanced cardiac function and inhibited remodeling in a similar fashion. In conclusion, L6-HGF therapy effectively induced angiogenesis in the chronically failing heart. Cardiac function, however, was not further enhanced by hHGF-expression. Analysis of the L6 rat skeletal myoblast cell line and myoblast cell sheets with constitutive human HGF expression.
Project description:To optimize the genome annotation, nine tissue and one pool RNA libraries (i.e. heart, liver, spleen, lung, kidney, muscle, fat, ovary, pool.) were constructed using the Illumina mRNA-spleeneq Prep Kit