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Authors = Xinyun Li

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XINYUN (8) , LI (9139)

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Open AccessArticle Cellular Localization and Regulation of Expression of the PLET1 Gene in Porcine Placenta
Int. J. Mol. Sci. 2016, 17(12), 2048; doi:10.3390/ijms17122048
Received: 18 July 2016 / Revised: 30 November 2016 / Accepted: 1 December 2016 / Published: 7 December 2016
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Abstract
The placenta expressed transcript 1 (PLET1) gene, which is expressed in placentas of pigs and mice, has been found to have a potential role in trophoblast cell fate decision in mice. Results of this study showed that the porcine PLET1 mRNA
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The placenta expressed transcript 1 (PLET1) gene, which is expressed in placentas of pigs and mice, has been found to have a potential role in trophoblast cell fate decision in mice. Results of this study showed that the porcine PLET1 mRNA and protein were expressed exclusively in trophoblast cells on Days 15, 26, 50, and 95 of gestation (gestation length in the pig is 114 days), indicating that the PLET1 could be a useful marker for porcine trophoblast cells. Additionally, PLET1 protein was found to be redistributed from cytoplasm to the apical side of trophoblast cells as gestation progresses, which suggests a role of PLET1 in the establishment of a stable trophoblast and endometrial epithelial layers. In addition, two transcripts that differ in the 3′ UTR length but encode identical protein were identified to be generated by the alternative cleavage and polyadenylation (APA), and the expression of PLET1-L transcript was significantly upregulated in porcine placentas as gestation progresses. Furthermore, we demonstrated the interaction between the miR-365-3p and PLET1 gene using luciferase assay system. Our findings imply an important role of PLET1 in the placental development in pigs. Full article
(This article belongs to the Section Biochemistry and Molecular Biology)
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Open AccessArticle RNA Sequencing Identifies Upregulated Kyphoscoliosis Peptidase and Phosphatidic Acid Signaling Pathways in Muscle Hypertrophy Generated by Transgenic Expression of Myostatin Propeptide
Int. J. Mol. Sci. 2015, 16(4), 7976-7994; doi:10.3390/ijms16047976
Received: 23 December 2014 / Revised: 18 March 2015 / Accepted: 30 March 2015 / Published: 9 April 2015
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Abstract
Myostatin (MSTN), a member of the transforming growth factor-β superfamily, plays a crucial negative role in muscle growth. MSTN mutations or inhibitions can dramatically increase muscle mass in most mammal species. Previously, we generated a transgenic mouse model of muscle hypertrophy via the
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Myostatin (MSTN), a member of the transforming growth factor-β superfamily, plays a crucial negative role in muscle growth. MSTN mutations or inhibitions can dramatically increase muscle mass in most mammal species. Previously, we generated a transgenic mouse model of muscle hypertrophy via the transgenic expression of the MSTN N-terminal propeptide cDNA under the control of the skeletal muscle-specific MLC1 promoter. Here, we compare the mRNA profiles between transgenic mice and wild-type littermate controls with a high-throughput RNA sequencing method. The results show that 132 genes were significantly differentially expressed between transgenic mice and wild-type control mice; 97 of these genes were up-regulated, and 35 genes were down-regulated in the skeletal muscle. Several genes that had not been reported to be involved in muscle hypertrophy were identified, including up-regulated myosin binding protein H (mybph), and zinc metallopeptidase STE24 (Zmpste24). In addition, kyphoscoliosis peptidase (Ky), which plays a vital role in muscle growth, was also up-regulated in the transgenic mice. Interestingly, a pathway analysis based on grouping the differentially expressed genes uncovered that cardiomyopathy-related pathways and phosphatidic acid (PA) pathways (Dgki, Dgkz, Plcd4) were up-regulated. Increased PA signaling may increase mTOR signaling, resulting in skeletal muscle growth. The findings of the RNA sequencing analysis help to understand the molecular mechanisms of muscle hypertrophy caused by MSTN inhibition. Full article
(This article belongs to the Section Biochemistry and Molecular Biology)
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Open AccessArticle Interactome Mapping Reveals Important Pathways in Skeletal Muscle Development of Pigs
Int. J. Mol. Sci. 2014, 15(12), 21788-21802; doi:10.3390/ijms151221788
Received: 15 July 2014 / Revised: 19 October 2014 / Accepted: 6 November 2014 / Published: 26 November 2014
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Abstract
The regulatory relationship and connectivity among genes involved in myogenesis and hypertrophy of skeletal muscle in pigs still remain large challenges. Presentation of gene interactions is a potential way to understand the mechanisms of developmental events in skeletal muscle. In this study, genome-wide
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The regulatory relationship and connectivity among genes involved in myogenesis and hypertrophy of skeletal muscle in pigs still remain large challenges. Presentation of gene interactions is a potential way to understand the mechanisms of developmental events in skeletal muscle. In this study, genome-wide transcripts and miRNA profiling was determined for Landrace pigs at four time points using microarray chips. A comprehensive method integrating gene ontology annotation and interactome network mapping was conducted to analyze the biological patterns and interaction modules of muscle development events based on differentially expressed genes and miRNAs. Our results showed that in total 484 genes and 34 miRNAs were detected for the duration from embryonic stage to adult in pigs, which composed two linear expression patterns with consensus changes. Moreover, the gene ontology analysis also disclosed that there were three typical biological events i.e., microstructure assembly of sarcomere at early embryonic stage, myofibril formation at later embryonic stage and function establishments of myoblast cells at postnatal stage. The interactome mappings of different time points also found the down-regulated trend of gene expression existed across the whole duration, which brought a possibility to introduce the myogenesis related miRNAs into the interactome regulatory networks of skeletal muscle in pigs. Full article
(This article belongs to the Section Biochemistry and Molecular Biology)
Open AccessArticle The Inflammation-Related Gene S100A12 Is Positively Regulated by C/EBPβ and AP-1 in Pigs
Int. J. Mol. Sci. 2014, 15(8), 13802-13816; doi:10.3390/ijms150813802
Received: 10 June 2014 / Revised: 7 July 2014 / Accepted: 23 July 2014 / Published: 8 August 2014
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Abstract
S100A12 is involved in the inflammatory response and is considered an important marker for many inflammatory diseases in humans. Our previous studies indicated that the S100A12 gene was abundant in the immune tissues of pigs and was significantly upregulated during infection with Haemophilus
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S100A12 is involved in the inflammatory response and is considered an important marker for many inflammatory diseases in humans. Our previous studies indicated that the S100A12 gene was abundant in the immune tissues of pigs and was significantly upregulated during infection with Haemophilus parasuis (HPS) or porcine circovirus type 2 (PCV2). In this study, the mechanism of transcriptional regulation of S100A12 was investigated in pigs. Our results showed that S100A12, CCAAT/enhancer-binding protein beta (C/EBPβ) and activator protein-1 (AP-1) genes were up-regulated in PK-15 (ATCC, CCL-33) cells when treated with LPS or Poly I: C. Additionally, the promoter activity and expression level of the S100A12 gene were significantly upregulated when C/EBPβ or AP-1 were overexpressed. We utilized electromobility shift assays (EMSA) to confirm that C/EBPβ and AP-1 could directly bind the S100A12 gene promoter. We also found that the transcriptional activity and expression levels of C/EBPβ and AP-1 could positively regulate each other. Furthermore, the promoter activity of the S100A12 gene was higher when C/EBPβ and AP-1 were cotransfected than when they were transfected individually. We concluded that the S100A12 gene was cooperatively and positively regulated by C/EBPβ and AP-1 in pigs. Our study offers new insight into the transcriptional regulation of the S100A12 gene. Full article
(This article belongs to the Section Biochemistry and Molecular Biology)

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