PDGF启动子区DNA甲基化在Hcy致VSMCs增殖的作用机制研究

目的:探讨血小板源性生长因子(Platelet-derived growth factor,PDGF)DNA甲基化在同型半胱氨酸((homocysteine,Hcy)致血管平滑肌细胞(vascular smooth muscle cells,VSMCs)增殖的作用机制。方法:正常人脐动脉VSMCs体外培养,随机分为对照组、治疗组(Hcy100μmol/L+叶酸30μmol/L)、Hcy干预组(50、100、200、500μmol/L)总计6组,以MTT检测VSMCs的增殖率,巢式降落式PCR(nMS-PCR)法检测PDGF启动子区DNA甲基化的改变。结果:不同浓度Hcy干预的VSMCs与对照组和治疗组相比,随着Hcy浓度的增加VSMCs增殖率增加。治疗组与对照组比所有结果均无明显变化。PDGF甲基化水平增高,100μmol/L、200μmol/L Hcy组与对照组比较差异有统计学意义(P0.01和P0.05),而治疗组与对照组比较差异无统计学意义(P0.05)。结论:Hcy可导致人VSMCs PDGF启动子区域甲基化异常从而促进VSMCs的增殖。     

NG2 cells (polydendrocytes): Listeners to the neural network with diverse properties

NG2 cells (polydendrocytes) are the fourth major non‐neuronal cell type in the central nervous system parenchyma. They exhibit diverse properties, ranging from their well‐established role as oligodendrocyte precursors to their ability to respond to neurotransmitters released by synaptic and non‐synaptic mechanisms. The functional diversity of NG2 cells has prompted the question of whether they represent a single cellular entity or multiple distinct cell populations. This review first summarizes recent findings on the nature and mechanism underlying the diversity of NG2 cells with regard to their proliferative and differentiation behavior. This will be followed by a synopsis of observations on how their microenvironment, particularly neuronal activity, influences their dynamic behavior, and how these changes in NG2 cells could in turn influence neural function and animal behavior. GLIA 2014;62:1195–1210     

原发性脑瘤的分子遗传学研究进展

［摘要］ 原发性脑瘤是发生于神经系统常见的疾病,高度恶性的胶质瘤占原发性脑瘤的40%,主要分为I型胶质母细胞瘤（继发性胶质母细胞瘤）和II型胶质母细胞瘤（原发性胶质母细胞瘤）,二者的产生有着不同的遗传学改变。I型胶质母细胞瘤的产生途径是从一种恶性程度较低的星形细胞瘤（II级,主要为p53基因突变和血小板来源的生长因子/受体过表达）至恶性的间变型星型细胞瘤（III级,主要为Rb基因突变,CDK4基因扩增,9p、11p、13q和19q的等位基因缺失）,再到胶质母细胞瘤（IV级,最常见的遗传学改变是7号和20号染色体的获得,10号染色体的丢失以及PTEN和LRRC4基因的缺失,PDGFα及其受体的过表达）的渐进的发展过程;而II型胶质母细胞瘤则是一种没有恶性程度渐进过程的原发性胶质母细胞瘤,表皮生长因子受体基因的扩增是最常见的遗传学改变。     

Intercellular communication via gap junctions in activated rat hepatic stellate cells

BACKGROUND AND AIMS: Gap junctional communication was studied in quiescent and activated hepatic stellate cells. METHODS: Connexin expression and intercellular dye transfer were studied in rat hepatic stellate cells in culture and in vivo. RESULTS: Protein expression of connexin 43 was up-regulated in activated hepatic stellate cells in vivo and in vitro and was mainly localized on the cell surface, whereas connexin 26 was found intracellularly. In contrast to hepatocytes, hepatic stellate cells do not express connexin 32. Confluent hepatic stellate cells in culture communicate via gap junctions, resulting in lucifer yellow transfer and propagation of intracellular calcium signals. Phorbol ester induces a protein kinase C-dependent hyperphosphorylation and degradation of connexin 43 and inhibits intercellular communication on a short-term time scale. At the long-term level, vitamin D(3) , lipopolysaccharide, thyroid hormone T(3), dexamethasone, platelet-derived growth factor, endothelin 1, and interleukin 1beta up-regulate connexin 43 protein and messenger RNA expression and enhance intercellular communication. Slight down-regulation of connexin 43 is observed in response to vitamin A. Connexin 43 induction by endothelin 1 is inhibited by both endothelin A and endothelin B receptor antagonists. In coculture systems, hepatic stellate cells communicate with each other, which is suggestive of a syncytial organization, but no communication was found between hepatic stellate cells and other liver cell types. As shown by immunohistochemistry and electron microscopy, gap junctions are formed between activated hepatic stellate cells in vivo. CONCLUSIONS: Gap junctional communication occurs between hepatic stellate cells, is enhanced after activation, and underlies complex regulation by cytokines, hormones, and vitamins.     

川芎嗪对PDGF-BB诱导的大鼠血管平滑肌细胞增殖和骨桥蛋白mRNA表达的影响

目的:探讨川芎嗪对血小板源生长因子(PDGF BB)诱导的大鼠血管平滑肌细胞(VSMC)增殖及骨桥蛋白mRNA表达的影响。方法:大鼠胸主动脉平滑肌细胞体外培养,PDGF BB刺激VSMC ,采用MTT法和流式细胞仪测定川芎嗪对VSMC增殖的影响,逆转录聚合酶联反应(RT PCR)测定VSMC骨桥蛋白mRNA的表达水平。结果:川芎嗪可显著地抑制VSMC增殖(P <0 .0 1) ,使细胞生长停滞于G0 /G1期;PDGF BB诱导骨桥蛋白mRNA呈高表达,川芎嗪下调了这种表达。结论:川芎嗪能抑制体外的VSMC增殖,提示川芎嗪可能作为防治血管成形术后再狭窄的一种药物。     

骨康含药血清对成骨细胞PDGF-AA表达影响的实验研究

目的 观察中药骨康含药血清对新生大鼠成骨细胞血小板衍生生长因子-AA（PDGF—AA）基因表达的调控作用。方法 将实验动物随机分成中药组、罗盖全组和蒸馏水组3组，通过体外分离和培养成骨细胞体系，运用逆转录法测定含药血清对成骨细胞PDGF-AA mRNA表达的影响。结果 用10％的血清培养成骨细胞第7d时，与空白血清组相比，骨康含药血清组和罗盖全含药血清组对成骨细胞PDGF—AA mRNA表达的平均影响率分别为149．4％和177．7％。结论 中药骨康含药血清能明显增强成骨细胞PDGF—AA mRNA的表达。     

慢性肝炎不同证型与细胞因子PDGF TGF-β相关性研究

目的:研究和探讨慢性肝炎患者血清PDGF、TGF-β含量与慢性肝炎不同证型之间的关系.方法:根据辨证设慢性肝炎肝郁脾虚、湿热中阻、瘀血阻络3组各30例和正常对照组30例,采用酶联免疫吸附法(ELISA)检测不同证型慢性肝病患者血清PDGF、TGF-β的含量.结果:肝郁脾虚等3组PDGF、TGF-β含量阳性率均高于正常对照组,差异有显著性;瘀血阻络证组高于肝郁脾虚、湿热中阻,差异有显著性;定量水平结果亦与其相符;肝炎程度不同,其PDGF、TGF-β水平也不同,差异有显著性.结论:慢性肝炎不同证型肝纤维化程度不同,与PDGF、TGF-β水平有较强的关联.