Tao Qin

Tianjin University of Science and Technology, T’ien-ching-shih, Tianjin Shi, China

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Publications (5)8.42 Total impact

  • Tong Cun Zhang · Yao Meng · Nan Wang · Feng Lin · Tao Qin · Zhe Sun · Man Li ·
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    ABSTRACT: NF-H (a member of neurofilaments) is a protein widely expressed in all kinds of neurons after birth and can be used as one of the symbols of mature neurons. Constuction of NF-H promoter luciferase reporter plasmid will provide the theory basis for researching the effect of other transcription factors on regulating NF-H transcription. Here, human NF-H promoter luciferase reporter plasmid were successfully constructed. Then the effects of some key transcription factors were investigated by luciferase reporter assays in COS-7 cells. The results showed that retinoid X receptor α (RXRα) can enhance transcriptional activity of NF-H. Furthermore, ERK 1/2 (extracellular signal-regulated kinase 1/2) and STAT3 (signal transducer and activator of transcription 3) also show obvious impact in activating NF-H transcription.
    04/2014; 915-916:942-946. DOI:10.4028/www.scientific.net/AMR.915-916.942
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    ABSTRACT: Mesenchymal stem cells (MSCs) have multilineage differentiation potential and can differentiate into neuron cells under appropriate environment in vitro and in vivo. Retinoic acid (RA), a vitamin A derivative, is known to facilitate the neuronal differentiation of MSCs. However, the mechanism by which RA induced MSC differentiation into neuron-like cells is not completely understood. Here, we show that RA can induce neural-like differentiation of bone marrow-derived MSCs, as evidenced by the increase of neuron specific markers expression and the gradually decreased resting membrane potential. Of note, myocardin-related transcription factor-A (MRTF-A), a major co-activator of serum response factor (SRF), was significantly activated and its nuclear localization was observed during RA-induced neural-like differentiation. MRTF-A is recently reported to function in the development of the nervous system. Our results demonstrated that dominant-negative form of MRTF-A (DN-MRTF-A) or shRNA-MRTF-A strongly inhibited upregulation of neural markers in response to RA. Furthermore, reporter assays with NF-H promoter indicated that RA and MRTF-A can synergistically activate NF-H transcription and enhance the mRNA expression of NF-H. These findings reveal that MRTF-A is key regulator in all-trans RA-induced neural-like differentiation of bone marrow-derived MSCs.
    Gene 03/2013; 523(2). DOI:10.1016/j.gene.2013.03.043 · 2.14 Impact Factor
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    ABSTRACT: Several reports demonstrated that mesenchymal stem cells (MSCs) might differentiate into smooth muscle cells (SMCs) in vitro and in vivo. It has been shown that myocardin protein is a strong inducer of smooth muscle genes and MSCs can differentiate into SMCs in response to transforming growth factor-β (TGF-β). However, the relationship or link between myocardin and TGF-β3-induced MSC differentiation has not been fully elucidated. Here, we demonstrated that both myocardin and TGF-β3 were able to induce differentiation of rat bone marrow-derived MSCs toward smooth-muscle-like cell types, as evidenced by increasing expression of SMC-specific genes. Of note, myocardin cooperated with Smad2 to synergistically activate SM22α promoter and significantly enhance the expression of SM22α. Report assays with site-direct mutation analysis of SM22α promoter demonstrated that myocardin and Smad2 coactivated SM22α promoter mainly depending on CArG box and less on smad binding elements (SBE) sites as well. These findings reveal the cooperation of myocardin and Smad2 in process of MSC differentiation into SMCs.
    International Union of Biochemistry and Molecular Biology Life 04/2012; 64(4):331-9. DOI:10.1002/iub.1003 · 3.14 Impact Factor
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    ABSTRACT: Myocardin is a remarkably potent transcriptional coactivator expressed specifically in cardiac muscle lineages and smooth muscle cells during postnatal development. Myocardin shares homology with myocardin-related transcription factor-A (MRTF-A), which are expressed in a broad range of embryonic and adult tissues. Our previous results show that myocardin induces cardiac hypertrophy. However, the effects of MRTF-A in cardiac hypertrophy remain poorly understood. Our present work further demonstrates that myocardin plays an important role in inducing hypertrophy. At the same time, we find that overexpression of MRTF-A in neonatal rat cardiomyocytes might induce cardiomyocyte hypertrophy. Furthermore, MRTF-A expression is induced in phenylephrine, angiotensin-II, and transforming growth factor-β-stimulated cardiac hypertrophy, whereas a dominant-negative form of MRTF-A or MRTF-A siRNA strongly inhibited upregulation of hypertrophy genes in response to hypertrophic agonists in neonatal rat cardiomyocytes. Our studies indicate that besides myocardin, MRTF-A might play an important role in cardiac hypertrophy. Our findings provide novel evidence for the future studies to explore the roles of MRTFs in cardiac hypertrophy.
    International Union of Biochemistry and Molecular Biology Life 01/2011; 63(1):54-61. DOI:10.1002/iub.415 · 3.14 Impact Factor
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    ABSTRACT: ObjectiveTo observe the effect of all-trans retinoic acid (ATRA) on inducing human glioma MO59K cells differentiation and further explore the underlying molecular mechanisms. MethodsThe expression of glial fibrillary acidic protein (GFAP) was detected by immunocytochemistry staining. The mRNA levels of GFAP, retinoid X receptor α (RXRα), p21 were examined by semi-quantitative RT-PCR analysis. Luciferase activity assay was performed in the COS-7, MO59K cells to measure p21 promoter transcription activity. ResultsATRA could significantly enhance the expression and mRNA level of GFAP by immunostaining and RT-PCR (P < 0.05). Simultaneously, the mRNA levels of RXRα and p21 were remarkably increased in dose-dependent manner by RT-PCR (P < 0.05). Furthermore, luciferase assay confirmed that ATRA and RXRα could transactivate p21 promoter in COS-7 and glioma cells (P < 0.05). ConclusionATRA can induce differentiation of human glioma cells. The RXRα and p21 were activated during ATRA-induced differentiation process. This effect may be caused by directly RXRα-induced p21 gene transactivation. Our findings provide novel evidence for the future studies to explore the molecular mechanism of transcriptional regulation for glioma cell differentiation and cellular therapeutic approaches for glioblastoma. Key Wordsglioma cells–all-trans retinoic acid–Retinoid X receptor α –P21
    Clinical Oncology and Cancer Research 01/2011; 8(1):42-46. DOI:10.1007/s11805-011-0558-8