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| 1 | Changes of number of cells expressing proliferation and progenitor cell markers with age in rabbit intervertebral discs显示文摘在 intervertebral 磁盘(IVD ) 以内的正常新生进程的基本知识对内在的生物学的理解重要。在 IVD 的祖先和干细胞的存在被验证了。然而,有年龄的祖先和干细胞的数字的变化仍然是未知的。在这研究,房间增长和祖先房间变化有在从二不同年龄的兔子的 IVD 房间的年龄的标记用流动 cytometry, immunohistochemistry,即时聚合酶链反应,和西方的污点分析被调查。原子抗原(PCNA ) 为增长被选择为一个标记的增殖的房间,和 Notch1, Jagged1, C 工具包, CD166 被选择为干细胞标记。房间周期分析证明在小兔子的 G2/M 阶段的那个房间数字比成熟兔子的显著地高。染色的 Immunohistochemical 在年轻、成熟的体环 fibrosus (AF ) 表明了 PCNA, C 工具包, CD166, Notch1,和 Jagged1 的表示。在小兔子的这些房间标记的蛋白质表情都比在成熟兔子的那些显著地高。PCNA 的表示层次, CD166, C 工具包, Jagged1 在 AF,和 PCNA 是显著地更高的,在从小兔子的原子核 pulposus 的 C 工具包比那些从成熟兔子。这些调查结果证明增长和祖先房间在兔子 IVD 和在兔子 IVD 房间与年龄表示增长和祖先房间标记减少的房间的数字存在。被设计维持内长的祖先房间并且刺激他们的增长的方法能在阻止或禁止退化圆盘疾病是成功的。 | Miersalijiang Yascn Qinming Fei JianZhang WilliamCHutton JianDong XiaoxingJiang FengZhang | 2013 | Acta Biochimica et Biophysica Sinica2013，45，5： | 14 |
| 2 | Osteogenic growth peptide enhances the proliferation of bone marrow mesenchymal stem cells from osteoprotegerin-deficient mice by CDK2/cyclin A显示文摘支持骨头形成是在骨质疏松症治疗的基本策略之一,破裂修理。作为骨头形成上的激发器之一, osteogenic 生长肽(OGP ) 在 vitro 并且在 vivo, osteoprotegerin (OPG ) 在被建议了被包含增加造骨细胞的增长和区别。在这研究,我们在骨头髓上评估了 OGP 的效果从在由 3-(4,5-dimethylthiazol-2-yl ) 的 vitro 的 OPG 缺乏的老鼠的间充质的干细胞(MSC )-2,5-diphenyltetrazolium 溴化物试金,碱的磷酸酶(高山) 活动试金,即时聚合酶链反应,和西方的污点分析。结果证明 OGP 刺激了 MSC 增长并且在 mRNA 和蛋白质层次两个都在 MSC 增加了 CDK2 和 cyclin A 的表示。然而, OGP 的 differentiative 效果都没作为高山活动和 Runx2 的表示层次被显示出, Osterix 没被 OGP 显著地增加。我们的学习建议 OGP 可以由刺激 MSC 增长而非区别在 OPG 缺乏的老鼠增加骨头形成,并且可能由触发 CDK2/cyclin 一条小径。 | Qinming Fei Changjun Guo Xiaoya Xu Jianjun Gao Jian Zhang Tongyi Chen Dafu Cui | 2010 | Acta Biochimica et Biophysica Sinica2010，42，11： | 11 |
| 3 | Isolation and identification of stem cells from degenerated human intervertebral discs and their migration characteristics显示文摘间充质的干细胞(MSC ) 从 intervertebral 圆盘的三个部件独立被孤立并且识别,即体环 fibrosus (AF ) ,原子核 pulposus (NP ) ,和软骨终板(CEP ) 。然而,很少研究被执行了比较这些三种干细胞的性质,他们为他们的潜在的临床的应用程序必要的特别移植能力。在这研究,分别地, MSC 人的堕落磁盘从 AF, NP,和 CEP 被孤立并且在经过 3 点由表面标记和 multilineage 区别试金识别了。干细胞的这三种类型作为 AF-MSCs, NP-MSCs,和 CEP-MSCs 被说出。然后,他们的生物特征以增长,经过,殖民地形成,移植,和侵略能力被比较。结果证明房间的所有三种类型作为 MSC 被识别并且在增长,经过,和殖民地形成能力有类似的特征。当 NP-MSCs 显示出最低迁居能力时, CEP-MSCs 显示出最高的迁居和侵略力量,建议那 CEP-MSCs 并且几乎,没有侵略力量有移植和侵略的最强大的性质什么时候与 AF-MSCs 和 NP-MSCs 相比。比的, CXCR4 的表示才在 CEP-MSCs 是更高的在。 | Shuhao Liu Haifeng Liang Soo-min Lee Zheng Li Jian Zhang Qinming Fei | 2017 | Acta Biochimica et Biophysica Sinica2017，49，2： | 10 |
| 4 | Truncated Human LMP-1 Triggers Differentiation of C2C12 Cells to an Osteoblastic Phenotype in vitro显示文摘秘鲁利玛机场之代号矿化作用 protein-1 (LMP-1 ) 是被显示了在 vitro 并且在 vivo.LMP-1 导致骨头形成的新奇细胞内部的 osteoinductiveprotein 包含 anN 终端 PDZ 领域和三个 C 终端秘鲁利玛机场之代号领域。在这研究,我们调查了是否人的 LMP-1 的一种截断的形式( hLMP-l [ t ]),缺乏三个C终端秘鲁利玛机场之代号领域, weretransiently 触发 pluripotent myoblastic C2C12 房间的区别到造骨细胞 lineage.C2C12 房间有 Ad5-hLMP-l (t)绿色的 transduced 荧光灯的蛋白质和截断的蛋白质被检验。结果证明 thathLMP-l (t) 在 C2C12 文化堵住了 myotube 形成并且显著地提高了碱性磷酸酶(高山) 活动。另外,形态基因的蛋白质(BMP )-2 和 BMP-7 基因也是的高山, osteocalcin,和骨头的表情增加了。这些关键 osteogenic 标记的正式就职建议 hLMP-l (t)能触发 pluripotent myoblastic C2C12 房间区分 intoosteoblastic 系,因此扩大我们 LMP-1 和 LMP-1 (t)提高的以前的观察在房间的文化的 theosteoblastic 显型已经承诺了 osteoblasticlineage.Therefore , C2C12 房间是为 osteoblastic 显型和 LMP-1 行动的机制的学习感应的 LMP-1 的考试的一个适当模型系统。 | Qinming FEI | 2007 | Acta Biochimica et Biophysica Sinica2007，39，9： | 8 |
| 5 | Effect of silicon-doped calcium phosphate cement on angiogenesis based on controlled macrophage polarization显示文摘Vascularization is an important early indicator of osteogenesis involving biomaterials. Bone repair and new bone formation are associated with extensive neovascularization. Silicon-based biomaterials have attracted widespread attention due to their rapid vascularization. Although calcium phosphate cement (CPC) is a mature substitute for bone, the application of CPC is limited by its slow degradation and insufficient promotion of neovascularization. Calcium silicate (CS) has been shown to stimulate vascular endothelial proliferation. Thus, CS may be added to CPC (CPC–CS) to improve the biocompatibility and neovascularization of CPC. In the early phase of bone repair (the inflammatory phase), macrophages accumulate around the biomaterial and exert both anti- and pro-inflammatory effects. However, the effect of CPC–CS on macrophage polarization is not known, and it is not clear whether the effect on neovascularization is mediated through macrophage polarization. In the present study, we explored whether silicon-mediated macrophage polarization contributes to vascularization by evaluating the CPC–CS-mediated changes in the immuno-environment under different silicate ion contents both in vivo and in vitro. We found that the silicon released from CPC–CS can promote macrophage polarization into the M2 phenotype and rapid endothelial neovascularization during bone repair. Dramatic neovascularization and osteogenesis were observed in mouse calvarial bone defects implanted with CPC–CS containing 60% CS. These findings suggest that CPC–CS is a novel biomaterial that can modulate immune response, promote endothelial proliferation, and facilitate neovascularization and osteogenesis. Thus, CPC–CS shows potential as a bone substitute material. | Soomin Lee Zheng Li Dehua Meng Qinming Fei Libo Jiang Tengfei Fu Ze Wang Shuhao Liu Jian Zhang | 2021 | Acta Biochimica et Biophysica Sinica2021，53，11： | 0 |
| 6 | Glycolytic enzyme PKM2 regulates cell senescence but not inflammation in the process of osteoarthritis显示文摘Chondrocyte senescence is an important mechanism underlying osteoarthritis in the senile population and is characterized by reduced expressions of the extracellular matrix proteins.The involvement of glycolysis and the tricarboxylic acid cycle in the development of osteoarthritis is inclusive.The present study aims to investigate the role of the glycolytic enzyme M2 isoform of pyruvate kinase(PKM2)in chondrocytes in senescence and inflammation.Primary chondrocytes are isolated from the knee joints of neonatal mice.Small interfering RNAs(siRNAs)against PKM2 are transfected using lipofectamine.RNA sequencing is conducted in primary chondrocytes with the PKM2 gene deleted.Cell apoptosis,autophagy,reactive oxygen species measurement,and senescent conditions are examined.The glycolytic rate in cells is measured by Seahorse examination.Interleukin 1-β(IL-1β)increases the protein expressions of matrix metallopeptidases(MMP)13 and PKM2 and reduces the protein expression of collagen type II(COL2A1)in primary chondrocytes.Silencing of PKM2 alters the protein expressions of MMP13,PKM2,and COL2A1 in the same pattern in quiescent and stimulated chondrocytes.RNA sequencing analysis reveals that PKM2 silencing reduces senescent biomarker p16INK4a expression.Compared with low-passage chondrocytes,high-passage chondrocytes exhibit increased expression of p16INK4a and reduced expression of COL2A1.Silencing of PKM2 reduces SA-β-Gal signals and increases COL2A1 expression in high-passage chondrocytes.Seahorse assay reveals that PKM2 deletion favors the tricarboxylic acid cycle in mitochondria in low-but not in high-passage chondrocytes.In summary,the glycolytic enzyme PMK2 modulates chondrocyte senescence but does not participate in the regulation of inflammation. | Bo Liu Chenzhong Wang Ziyu Weng Yi Yang Hong Zhao Yueqi Zhang Qinming Fei Yi Shi Chi Zhang | 2023 | Acta Biochimica et Biophysica Sinica2023，55，9： | 0 |
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