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各路牛人幫忙翻譯英文論文，謝謝�。。。。。�
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先謝過各位了�。。。。。。。。。。。�！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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以下為第一和最后一段的翻譯，僅供參考； 簡(jiǎn)介 在小鼠胚胎發(fā)育早期，第12.5天（E12.5）的胚胎時(shí)，胃是有單層上皮組成的，鄰近是一層間充質(zhì)。E13.5時(shí)，胃前部上皮分化為多層扁平上皮，其上皮祖細(xì)胞（干細(xì)胞）是通過對(duì)稱分裂增殖的。產(chǎn)生的多層圓形的上皮細(xì)胞隨后組成了無數(shù)的胃單位，并通過單層上皮相互連接。而此后，位于胃峽部的上皮祖細(xì)胞不對(duì)稱分裂，產(chǎn)生的子細(xì)胞再在向上和向下的異性過程中分化為不同的細(xì)胞譜系(Fukuda and Yasugi, 2005; van den Brink, 2007)。 …… …… …… 為了研究體外鼠類的Vsig1基因在胚胎發(fā)育晚期和成年期的作用，我們使用可誘導(dǎo)的Cre/LoxP系統(tǒng)構(gòu)建了Vsig1基因敲除小鼠。對(duì)Vsig1基因缺失小鼠的胚胎期和出生后的研究表明，在腺胃的前半部分單層腺上皮轉(zhuǎn)化為多層扁平上皮與Vsigl-/Y↔ Vsigl+/Y嵌合體胃的研究結(jié)果一致。免疫組織化學(xué)技術(shù)和分子分析技術(shù)研究Vsig1基因敲除的成年小鼠，發(fā)現(xiàn)胃腺的胃壁細(xì)胞和泌酶細(xì)胞在胃上皮的過度增殖現(xiàn)象消失了。進(jìn)一步的研究表明，Vsig1基因缺失的胃壁細(xì)胞過度增殖的消除是由缺失該基因的小鼠胃部血清中抗胃壁細(xì)胞抗體的產(chǎn)量增加造成的。這些結(jié)果表明了自身免疫性胃炎（AIG）的發(fā)生；而且，我們還發(fā)現(xiàn)在年齡大于12個(gè)月的Vsig1基因缺失的小鼠中，有不同程度腫瘤發(fā)生率的增加。 |
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