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各路牛人帮忙翻译英文论文，谢谢！！！！！！
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先谢过各位了！！！！！！！！！！！！！急用急用啊~~~~~~~ Introduction During early development of mouse, the stomach in 12.5-day-old embryo (E12.5) is comprised entirely of monolayer epithelium, adjacent to a layer of mesenchyme. At E13.5 anterior stomach epithelium (in forestomach region) is differentiated to squamous multilayer epithelium, while epithelia progenitors in posterior region proliferate by symmetrical division. The resulting multilayer round epithelia are then organized into numerous gastric units, which are lined by monolayer epithelium. Progenitor cells locating in isthmus region of gastric units proliferate then asymmetrically producing daughter cells that differentiate during an up and down migration from the isthmus to different cell lineages (Fukuda and Yasugi, 2005; van den Brink, 2007). Epithelia cell differentiation requires several events to establish polarized domains with specialized function. Establishment of epithelial cell polarity is initially directed by cell adhesion molecules,followed by organization of cytoskeleton and sorting of polarized proteins to basolateral and apical compartments (Perez-Moreno et al., 2003). Protein clustering at the cortical (peripheral) membrane occurs, in part, through binding to cytoplasmic domain of cell adhesion molecules. Genetic studies in Drosophila and mouse revealed that the distribution of the polarized proteins to apical and basolateral compartments mediates the orientation of mitotic spindle. During mitotic division of monolayer epithelium of embryonic epidermis, the mitotic spindle is oriented along the planar axis (Lu et al., 2001; Lechler et al., 2005). By contrast, in the areas that show the differentiation of squamous multilayer epithelium, spindles are oriented perpendicularly to the basement membrane (Seery, 2002). One group of proteins involved in cell adhesion are the immunoglobulin superfamily proteins (IGSF). Cell adhesion molecules of IGFS superfamily have one or more Ig-like domains in their extracellular region that are implicated in cell-cell adhesion and one cytoplasmic C-terminal region. The cytoplasmic domain is linked to the actin cytoskeleton through many peripheral membrane proteins, including members of catenin, PAR und ZO protein family,which strengthen the cell-cell adhesion activity of cell adhesion molecules and establish the epithelial cell polarization. Loss of cell-cell adhesion and cell polarity is commonly observed in advanced tumours and correlates with their invasion into adjacent tissues and the formation of metastases (Cumbiner, 2000; Lechler et al., 2005; Wodarz and Näthke, 2007). Autoimmune gastritis (AIG) is a stomach-specific autoimmune disease, which is characterized by a chronic mononuclear cell infiltration predominantly in the gastric glands and causing loss of parietal and zymogenic cells. Patients with AIG often have complications such as gastric cancer pernicious anaemia accompanied by achlorhydria. A hallmark of AIG is the production of circulating autoantibodies, which are responsible for deplation of parietal and zymogenic cells of the stomach. We have isolated and characterized the Vsig1 gene. The VSIG1 is characterized by the presence of two Ig-like domains, a V-type and a C2-type Ig-like domain, and is related in polypeptide sequence to the JAM/CTX subfamily proteins, which are regulating the tight junction formation and cell polarity. The Vsig1 is predominantly expressed in stomach. The cellular distribution of VSIG1 in embryonic stomach was determined by immunohistological experiments. Only negligible staining could be discerned in the epithelium of E12.5 (embryonic day 12.5) stomach. At E13.5, VSIG1 expression is restricted to the symmetrically dividing cells of the posterior epithelium and is lacking in the epithelium of anterior region, which is developed later to squamous epithelium. In E14.5 and E17.5 stomach, a much stronger expression of VSIGl was observed in primordial buds of the glandular epithelium of gastric units. The temporal and spatial profile of VSIGl expression suggests a potential role in regulation of cytodifferentiation of stomach epithelium to monolayer glandular epithelium (Oidovsambuu et al., 2011). To clarify the in vivo function of VSIGl in stomach development, we have disrupted the X-linked Vsigl in XY ES cells and generated Vsigl-/Y↔ Vsigl+/Y chimeric mice. We found that some regions of glandular epithelium in the posterior stomach contain VSIG1-negative cells. Hematoxylin-Eosin (H&E) staining revealed that VSIG1-deficient epithelium was morphologically different from adjacent Vsigl+/Y epithelium and had an atypical morphology of the squamous multilayer epithelium, which is normally localized in the forestomach. These results indicate that VSIG1-deficiency disrupts the symmetric division of posterior epithelium leading to transdifferentiation of the stratified monolayer epithelia of the glandular stomach to squamous multilayer epithelia (Oidovsambuu et al., 2011). To investigate the in vivo role of murine Vsig1 gene during later stages of embryonic development and adult life, we started to generate Vsig1 conditional knockout mice using inducible Cre/LoxP system. Analyses of Vsig1-deficient mice during embryonic and postnatal development revealed the transdifferentiation of the monolayer glandular epithelium to monolayer squamous epithelium in the first half region of glandular stomach confirming the results observed in Vsigl-/Y↔ Vsigl+/Y chimeric stomach. Immunohistological and molecular analyses of stomach of adult Vsig1 knockout mice showed the depletion of parietal and zymogenic cells in gastric glands and hyperproliferation of gastric epithelium. Further results revealed that depletion of parietal cells is a result of increased production of anti-parietal cell antibodies in serum of Vsig1-deficient mouse stomach. These results indicate the development of autoimmune gastritis (AIG). Furthermore, we found increased incidence of tumor development in different tissues of Vsig1-deficient mice, which are older than 12 months. |
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cory0931
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以下为第一和最后一段的翻译，仅供参考； 简介 在小鼠胚胎发育早期，第12.5天（E12.5）的胚胎时，胃是有单层上皮组成的，邻近是一层间充质。E13.5时，胃前部上皮分化为多层扁平上皮，其上皮祖细胞（干细胞）是通过对称分裂增殖的。产生的多层圆形的上皮细胞随后组成了无数的胃单位，并通过单层上皮相互连接。而此后，位于胃峡部的上皮祖细胞不对称分裂，产生的子细胞再在向上和向下的异性过程中分化为不同的细胞谱系(Fukuda and Yasugi, 2005; van den Brink, 2007)。 …… …… …… 为了研究体外鼠类的Vsig1基因在胚胎发育晚期和成年期的作用，我们使用可诱导的Cre/LoxP系统构建了Vsig1基因敲除小鼠。对Vsig1基因缺失小鼠的胚胎期和出生后的研究表明，在腺胃的前半部分单层腺上皮转化为多层扁平上皮与Vsigl-/Y↔ Vsigl+/Y嵌合体胃的研究结果一致。免疫组织化学技术和分子分析技术研究Vsig1基因敲除的成年小鼠，发现胃腺的胃壁细胞和泌酶细胞在胃上皮的过度增殖现象消失了。进一步的研究表明，Vsig1基因缺失的胃壁细胞过度增殖的消除是由缺失该基因的小鼠胃部血清中抗胃壁细胞抗体的产量增加造成的。这些结果表明了自身免疫性胃炎（AIG）的发生；而且，我们还发现在年龄大于12个月的Vsig1基因缺失的小鼠中，有不同程度肿瘤发生率的增加。 |
5楼2013-03-17 20:29:33
