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RISS 인기검색어
- 검색키워드
- 저자 : Liming Xuan (검색결과 4 건)
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Yu, Liming,Tu, Qisheng,Han, Qianqian,Zhang, Lan,Sui, Lei,Zheng, Leilei,Meng, Shu,Tang, Yin,Xuan, Dongying,Zhang, Jin,Murray, Dana,Shen, Qingping,Cheng, Jessica,Kim, Sung-Hoon,Dong, Lily Q.,Valverde, P Wiley (John WileySons) 2015 Stem Cells Vol.33 No.1
<P>Adiponectin (APN) is an adipocyte-secreted adipokine that exerts well-characterized antidiabetic properties. Patients with type 2 diabetes (T2D) are characterized by reduced APN levels in circulation and impaired stem cell and progenitor cell mobilization from the bone marrow for tissue repair and remodeling. In this study, we found that APN regulates the mobilization and recruitment of bone marrow-derived mesenchymal stem cells (BMSCs) to participate in tissue repair and regeneration. APN facilitated BMSCs migrating from the bone marrow into the circulation to regenerate bone by regulating stromal cell-derived factor (SDF)-1 in a mouse bone defect model. More importantly, we found that systemic APN infusion ameliorated diabetic mobilopathy of BMSCs, lowered glucose concentration, and promoted bone regeneration in diet-induced obesity mice. In vitro studies allowed us to identify Smad1/5/8 as a novel signaling mediator of APN receptor (AdipoR)-1 in BMSCs and osteoblasts. APN stimulation of MC3T3-E1 osteoblastic cells led to Smad1/5/8 phosphorylation and nuclear localization and increased SDF1 mRNA expression. Although APN-mediated phosphorylation of Smad1/5/8 occurred independently from adaptor protein, phosphotyrosine interaction, pleckstrin homology domain, and leucine zipper containing 1, it correlated with the disassembly of protein kinase casein kinase 2 and AdipoR1 in immunoprecipitation experiments. Taken together, this study identified APN as a regulator of BMSCs migration in response to bone injury. Therefore, our findings suggest APN signaling could be a potential therapeutic target to improve bone regeneration and homeostasis, especially in obese and T2D patients.</P>
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Shi Liuliu,Yao Shichuan,Xuan Liming,Dai Ren 대한기계학회 2018 JOURNAL OF MECHANICAL SCIENCE AND TECHNOLOGY Vol.32 No.5
The influence of the velocity ratio (VR) between the jet and main flow on the wake structure and aerodynamic loss of the trailing edge jet is studied using particle image velocimetry and numerical simulations. Three different velocity ratios, namely, VR = 0.5, 1.0, 1.5, are chosen for this comparative study. The Reynolds number (Re h ) based on the slot height (h) and the mainstream velocity (U 0 ) are 3380. Results show that the influence of jet on wake structure is significant such that the wake region shrinks and the turbulent kinetic energy is enhanced as the velocity ratio increases. The distribution area of strong vorticity is enlarged with increasing velocity ratio. By using proper orthogonal decomposition and fast Fourier transfer analysis, the variation of velocity ratio demonstrates significant impact on vortex shedding and turbulent kinetic energy. The aerodynamic loss coefficient is nearly constant between VR = 0.5 and 1.0, but increases by 3.25 % as the velocity ratio increases from 1.0 to 1.5.
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Han, Qianqian,Yang, Pishan,Wu, Yuwei,Meng, Shu,Sui, Lei,Zhang, Lan,Yu, Liming,Tang, Yin,Jiang, Hua,Xuan, Dongying,Kaplan, David L.,Kim, Sung Hoon,Tu, Qisheng,Chen, Jake Mary Ann Liebert 2015 Tissue engineering. Part A Vol.21 No.15
<P>Epigenetic regulation of gene expression is a central mechanism that governs cell stemness, determination, commitment, and differentiation. It has been recently found that PHF8, a major H4K20/H3K9 demethylase, plays a critical role in craniofacial and bone development. In this study, we hypothesize that PHF8 promotes osteoblastogenesis by epigenetically regulating the expression of a nuclear matrix protein, special AT-rich sequence-binding protein 2 (SATB2) that plays pivotal roles in skeletal patterning and osteoblast differentiation. Our results showed that expression levels of PHF8 and SATB2 in preosteoblasts and bone marrow stromal cells (BMSCs) increased simultaneously during osteogenic induction. Overexpressing PHF8 in these cells upregulated the expression of SATB2, Runx2, osterix, and bone matrix proteins. Conversely, knockdown of PHF8 reduced the expression of these genes. Furthermore, ChIP assays confirmed that PHF8 specifically bound to the transcription start site (TSS) of the SATB2 promoter, and the expression of H3K9me1 at the TSS region of SATB2 decreased in PHF8 overexpressed group. Implantation of the BMSCs overexpressing PHF8 with silk protein scaffolds promoted bone regeneration in critical-sized defects in mouse calvaria. Taken together, our results demonstrated that PHF8 epigenetically modulates SATB2 activity, triggering BMSCs osteogenic differentiation and facilitating bone formation and regeneration in biodegradable silk scaffolds.</P>
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Identification of pathways and genes associated with cerebral palsy
Qingwen Zhu,Yufei Ni,Jing Wang,Honggang Yin,Qin Zhang,Lingli Zhang,Wenjun Bian,Bo Liang,Lingyin Kong,Liming Xuan,Naru Lu 한국유전학회 2018 Genes & Genomics Vol.40 No.12
Cerebral palsy (CP) is a non-progressive neurological disease, of which susceptibility is linked to genetic and environmental risk factors. More and more studies have shown that CP might be caused by multiple genetic factors, similar to other neurodevelopmental disorders. Due to the high genetic heterogeneity of CP, we focused on investigating related molecular pathways. Ten children with CP were collected for whole-exome sequencing by next-generation sequencing (NGS) technology. Customized processes were used to identify potential pathogenic pathways and variants. Three pathways (axon guidance, transmission across chemical synapses, protein–protein interactions at synapses) with twenty-three genes were identified to be highly correlated with CP. This study showed that the three pathways associated with CP might be the molecular mechanism of pathogenesis. These findings could provide useful clues for developing pathway-based pharmacotherapies. Further studies are required to confirm potential roles for these pathways in the pathogenesis of CP.
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