Publications by authors named "Hui-Li Tong"

The extracellular matrix (ECM) is known to regulate tissue development and cell morphology, movement, and differentiation. SPARCL1 is an ECM protein, but its role in mouse cell differentiation has not been widely investigated. The results of western blotting and immunofluorescence showed that SPARCL1 is associated with the repair of muscle damage in mice and that SPARCL1 binds to bone morphogenetic protein 7 (BMP7) by regulating BMP/transforming growth factor (TGF)-β cell signaling.

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TCEA3 is a member of the transcription elongation factor family that not only promotes transcription but may also participate in other cytoplasmic processes. However, its mechanisms of action remain unclear. Our previous study indicated that TCEA3 may affect muscle differentiation.

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The mechanism by which bta-miR-378 regulates bovine skeletal muscle-derived satellite cell (bMDSC) myogenesis remains unknown. In this study, stem-loop RT-PCR was used to assess bta-miR-378 expression during the proliferation and differentiation of bMDSCs. The results showed that bta-miR-378 expression did not obviously change during bMDSC proliferation but increased significantly when bMDSCs began to differentiate.

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C2C12 murine myoblasts are a common model for studying muscle differentiation. Platelet endothelial aggregation receptor-1 (PEAR1), an epidermal growth factor repeat-containing transmembrane receptor, is known to participate in platelet contact-induced activation. In the present study, we demonstrated that PEAR1 is involved in the differentiation of C2C12 murine myoblasts.

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ELOVL3 is involved in elongating saturated and monounsaturated fatty acids, and is a critical enzyme for lipid accumulation in brown adipocytes during the early phase of tissue recruitment. In addition, ELOVL3 is related to increased fatty acid oxidation in brown adipocytes. However, the potential functions of ELOVL3 in bovine cells remain unclear.

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Background: The differentiation of skeletal muscle-derived satellite cells (MDSCs) is important in controlling muscle growth, improving livestock muscle quality, and healing of muscle-related disease. MicroRNAs (miRNAs) are a class of gene expression regulatory factors, which play critical roles in the regulation of muscle cell differentiation. This study aimed to compare the expression profile of miRNAs in MDSC differentiation, and to investigate the miRNAs which are involved in MDSC differentiation.

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Our group previously identified miR-2425-5p, a unique bovine miRNA; however, its biological function and regulation in muscle-derived satellite cells (MDSCs) remain unclear. Herein, stem-loop RT-PCR results showed that miR-2425-5p increased during MDSCs proliferation, but decreased during differentiation. Cell proliferation was examined using EdU assays, cyclin B1 (CCNB1) and proliferating cell nuclear antigen (PCNA) western blot (WB) and flow cytometry analysis.

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The transcription factor, early growth response 1 (EGR1), has important roles in various cell types in response to different stimuli. EGR1 is thought to be involved in differentiation of bovine skeletal muscle-derived satellite cells (MDSCs); however, the precise effects of EGR1 on differentiation of MDSCs and its mechanism of action remain unknown. In the present study, a time course of EGR1 expression and the effects of EGR1 on MDSC differentiation were determined.

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Bovine muscle-derived satellite cells (MDSCs) are important for animal growth. In this study, the effect of transcription elongation factor A3 (TCEA3) on bovine MDSC differentiation was investigated. Western blotting, immunofluorescence assays, and cytoplasmic and nuclear protein isolation and purification techniques were used to determine the expression pattern and protein localization of TCEA3 in bovine MDSCs during in vitro differentiation.

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MicroRNAs (miRNAs) play critical roles in the proliferation of bovine preadipocytes. miR-2400 is a novel and unique miRNA from bovines. In the present study, we separated and identified preadipocytes from bovine samples.

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In this study, we utilized high throughput RNA sequencing to obtain a comprehensive gene expression profile of muscle-derived satellite cells (MDSCs) upon induction of differentiation. MDSCs were cultured in vitro and RNA was extracted for sequencing prior to differentiation (MDSC-P), and again during the early and late differentiation (MDSC-D1, and MDSC-D3, respectively) stages. Sequence tags were assembled and analyzed by digital gene expression profile to screen for differentially expressed genes, Gene Ontology annotation, and pathway enrichment analysis.

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MicroRNAs play critical roles in skeletal muscle development as well as in regulation of muscle cell proliferation and differentiation. Previous study in our laboratory showed that the expression level of miR-2400, a novel and unique miRNA from bovine, had significantly changed in skeletal muscle-derived satellite cells (MDSCs) during differentiation, however, the function and expression pattern for miR-2400 in MDSCs has not been fully understood. In this report, we firstly identified that the expression levels of miR-2400 were down-regulated during MDSCs differentiation by stem-loop RT-PCR.

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Signal transducer and activator of transcription 5a (Stat5a) transduces signals of extracellular cytokines and growth factors to the nucleus of mammary gland epithelial cells and thereby regulates gene transcription during pregnancy, lactation, and weaning. However, its function on the milk production of dairy cows needs further investigation. In this experiment, the effects of Stat5a on lactation ability of dairy cow mammary gland epithelial cells (DCMECs) were analyzed.

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To study milk synthesis in dairy goat mammary gland, we had established an in vitro lactating dairy goat mammary epithelial cell (DGMEC) line. Mammary tissues of Guan Zhong dairy goats at 35 d of lactation were dispersed and cultured in a medium containing epithelial growth factor, insulin-like growth factor-1, insulin transferrin serum, and fetal bovine serum. Epithelial cells were enriched by digesting with 0.

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