肝脏内皮细胞和枯否细胞的细胞生物学

内皮细胞 肝窦内皮细胞(LSEC)构成连续但有筛孔的肝窦内衬。筛孔使窦腔和Disse间隙之形成开放性连接。肝窦腔和含有实质细胞表面的Disse间隙之间通过筛孔转运和交换各种物质。筛孔大小的改变将影响物质的运送。细胞弛缓素B、二甲基亚硝胺、乙醇,双泛酰硫乙胺和细胞外基质可调节筛孔直径与数量。LSEC的细胞支架对筛孔的调节也起重要作用。     

外源性p16基因对人肺癌细胞生物学特性的影响

目的：研究外原性p16基因对肺癌细胞生物学特性的影响。方法：利用脂质体介导的基因转染方法将外源性p16基因转入p16基因缺陷的人肺腺癌细胞株A549中,用逆转录聚合酶链反应（RT－PCR）及免疫组化的方法检测p16基因的表达,同时观察转染后细胞恶性生长的变化。结果：外源性p16基因在A549细胞中能稳定表达,转染后A549细胞生长速度明显减慢,在软琼脂上形成克隆的能力降低。流式细胞仪检测显示A549细胞G1期阻滞并发生了凋亡,接种裸鼠后致瘤性降低,肿瘤生长明显减慢。结论：外源性p16基因导入人肺癌细胞株A549中可稳定表达并抑制细胞的恶性生长,同时诱导调亡。     

电场对细胞生物学行为的影响

电场的生物学效应对胚胎发育、组织损伤修复、肿瘤发生有一定作用。本文综述电场对细胞生物学行为的影响及其机制的研究进展。     

砷对细胞的生物学影响研究进展

大量的研究表明,长期暴露在含砷高的环境中,可以引起慢性砷中毒,甚至致癌.近年来,随着细胞生物学的兴起与发展,人们得以通过近代物理学、试验生物学、生物化学以及分子生物学的技术和方法,从细胞整体水平、亚微结构水平和分子水平对细胞结构及基本生命活动规律进行深入研究.目前,通过对砷生物学毒性的深入研究发现,砷作用于生物细胞后可以导致细胞染色体异常、基因突变以及通过改变某些基因的功能诱导癌症的发生.特别是近期大量研究发现,砷化合物具有诱导肿瘤细胞凋亡的作用,但其详细机制仍不十分清楚.现就砷对细胞的生物学影响方面的研究进展作一综述.     

131I的生物学特点和碘化钾在核事故中的应用

日本3·11福岛核事故释放出大量 131I,引起公众关注.本文讨论 131I的生物学特点和碘化钾在核事故中的应用.碘化钾有很好的保护甲状腺的作用,但要根据卫生当局的指令,注意服用的时机和剂量.

Abstract：

Japan 3·11 Fukushima nuclear accident releases a huge amount of radioiodine-131 and attracts public concern with it. This article discusses the feature of radioiodine-131 and the use of potassium iodide in nuclear accident.The potassium iodide has a good role in protecting thyroid.It should pay attention on taking time and dosage based on instruction issued by public health authority.     

肺泡Ⅱ型细胞钠通道的生物学特点及调节机制

为了实现有效的气体交换，肺泡必须保持开放和相对干燥。肺泡上皮细胞在维护肺泡的正常功能时起着十分重要的作用。肺泡上皮细胞主要由扁平的Ⅰ型上皮细胞(ATI)和立方型的Ⅱ型细胞(ATⅡ)组成。在成人肺中，占肺泡上皮细胞总数的67％的Ⅱ型细胞，虽然仅仅覆盖肺泡表面积的3％，但是，ATⅡ除了是ATI的前期细胞以及分泌肺泡表面活性物质外，另一个重要功能是主动转运Na ，从而促使肺泡腔内的液体向细胞间隙转运，促进肺水的吸收。     

弓形虫组织包囊细胞生物学的研究进展

本文简述了弓形虫在中间宿主体内进行速殖子与缓殖子转化及影响这一过程的因素。     

舒张性心力衰竭的细胞生物学机制

舒张性心力衰竭主要指舒张功能异常的充血性心力衰竭.舒张性心力衰竭十分常见,且预后也接近于收缩性心力衰竭.舒张性心力衰竭的发生机制比较复杂,钙超载为导致舒张性心力衰竭的主要因素,围绕其细胞生物学发病机制的研究渐成为热点.     

HepaRG cells: a human model to study mechanisms of acetaminophen hepatotoxicity

Acetaminophen (APAP) overdose is the leading cause of acute liver failure in Western countries. In the last four decades much progress has been made in our understanding of APAP-induced liver injury through rodent studies. However, some differences exist in the time course of injury between rodents and humans. To study the mechanism of APAP hepatotoxicity in humans, a human-relevant in vitro system is needed. Here we present evidence that the cell line HepaRG is a useful human model for the study of APAP-induced liver injury. Exposure of HepaRG cells to APAP at several concentrations resulted in glutathione depletion, APAP-protein adduct formation, mitochondrial oxidant stress and peroxynitrite formation, mitochondrial dysfunction (assessed by JC-1 fluorescence), and lactate dehydrogenase (LDH) release. Importantly, the time course of LDH release resembled the increase in plasma aminotransferase activity seen in humans following APAP overdose. Based on propidium iodide uptake and cell morphology, the majority of the injury occurred within clusters of hepatocyte-like cells. The progression of injury in these cells involved mitochondrial reactive oxygen and reactive nitrogen formation. APAP did not increase caspase activity above untreated control values and a pancaspase inhibitor did not protect against APAP-induced cell injury. CONCLUSION: These data suggest that key mechanistic features of APAP-induced cell death are the same in human HepaRG cells, rodent in vivo models, and primary cultured mouse hepatocytes. Thus, HepaRG cells are a useful model to study mechanisms of APAP hepatotoxicity in humans.     

Transdifferentiation of hepatocyte-like cells from the human hepatoma HepaRG cell line through bipotent progenitor

Hepatic tumors, exhibiting mature hepatocytes and undifferentiated cells merging with cholangiocyte and hepatocyte phenotypes, are frequently described. The mechanisms by which they occur remain unclear. We report differentiation and transdifferentiation behaviors of human HepaRG cells isolated from a differentiated tumor developed consecutively to chronic HCV infection. We demonstrate that, in vitro, proliferating HepaRG cells differentiate toward hepatocyte-like and biliary-like cells at confluence. If hepatocyte-like cells are selectively isolated and cultured at high cell density, they proliferate and preserve their differentiation status. However, when plated at low density, they transdifferentiate into hepatocytic and biliary lineages through a bipotent progenitor. In accordance, transplantation of either undifferentiated or differentiated HepaRG cells in uPA/SCID mouse damaged liver gives rise mainly to functional human hepatocytes infiltrating mouse parenchyma. Analysis of the differentiation/transdifferentiation process reveals that: (1) the reversible differentiation fate of HepaRG cells is related to the absence of p21(CIP1) and p53 accumulation in differentiated cells; (2) HepaRG bipotent progenitors express the main markers of in vivo hepatic progenitors, and that cell differentiation process is linked to loss of their expression; (3) early and transient changes of beta-catenin localization and HNF3beta expression are correlated to Notch3 upregulation during hepatobiliary commitment of HepaRG cells. CONCLUSION: Our results demonstrate the great plasticity of transformed hepatic progenitor cells and suggest that the transdifferentiation process could supply the pool of hepatic progenitor cells. Moreover, they highlight possible mechanisms by which transdifferentiation and proliferation of unipotent hepatocytes might cooperate in the development of mixed and differentiated tumors.     

The biology of hairy cells

The evidence that hairy cells are activated clonal late B cells is presented. The largely non-specific (i.e. not confined to hairy-cell leukaemia) chromosome and genetic abnormalities are then described. Next, the features of malignant-cell activation are considered, including the distinctive morphology of hairy cells and their expression of activation-related antigens and activated adhesion receptors. Also, signalling and cytokine production are discussed in the context of malignant-cell activation. It is then demonstrated that many of the distinctive clinicopathological features of hairy-cell leukaemia can be explained in terms of the interaction of the activated malignant cells with other types of cell and tissue matrix. Finally, the biological basis of the hairy cell's unusually high sensitivity to IFN-alpha and nucleoside analogues is discussed.     

Induction of vesicular steatosis by amiodarone and tetracycline is associated with up-regulation of lipogenic genes in HepaRG cells

Drug-induced liver injury occurs in general after several weeks and is often unpredictable. It is characterized by a large spectrum of lesions that includes steatosis and phospholipidosis. Many drugs such as amiodarone and tetracycline have been reported to cause phospholipidosis and/or steatosis. In this study, acute and chronic hepatic effects of these two drugs were investigated using well-differentiated human hepatoma HepaRG cells. Accumulation of typical lipid droplets, labeled with Oil Red O, was observed in hepatocyte-like HepaRG cells after repeat exposure to either drug. Amiodarone caused the formation of additional intracytoplasmic vesicles that did not stain in all HepaRG cells. At the electron microscopic level, these vesicles appeared as typical lamellar bodies and were associated with an increase of phosphatidylethanolamine and phosphatidylcholine. A dose-dependent induction of triglycerides (TG) was observed after repeat exposure to either amiodarone or tetracycline. Several genes known to be related to lipogenesis were induced after treatment by these two drugs. By contrast, opposite deregulation of some of these genes (FASN, SCD1, and THSRP) was observed in fat HepaRG cells induced by oleic acid overload, supporting the conclusion that different mechanisms were involved in the induction of steatosis by drugs and oleic acid. Moreover, several genes related to lipid droplet formation (ADFP, PLIN4) were up-regulated after exposure to both drugs and oleic acid. CONCLUSION: Our results show that amiodarone causes phospholipidosis after short-term treatment and, like tetracycline, induces vesicular steatosis after repeat exposure in HepaRG cells. These data represent the first demonstration that drugs can induce vesicular steatosis in vitro and show a direct relationship between TG accumulation and enhanced expression of lipogenic genes.     

Developmental and regenerative biology of multipotent cardiovascular progenitor cells

Our limited ability to improve the survival of patients with heart failure is attributable, in part, to the inability of the mammalian heart to meaningfully regenerate itself. The recent identification of distinct families of multipotent cardiovascular progenitor cells from endogenous, as well as exogenous, sources, such as embryonic and induced pluripotent stem cells, has raised much hope that therapeutic manipulation of these cells may lead to regression of many forms of cardiovascular disease. Although the exact source and cell type remains to be clarified, our greater understanding of the scientific underpinning behind developmental cardiovascular progenitor cell biology has helped to clarify the origin and properties of diverse cells with putative cardiogenic potential. In this review, we highlight recent advances in the understanding of cardiovascular progenitor cell biology from embryogenesis to adulthood and their implications for therapeutic cardiac regeneration. We believe that a detailed understanding of cardiogenesis will inform future applications of cardiovascular progenitor cells in heart failure therapy and regenerative medicine.