Physiological and pathological role of inositol phospholipids

在这项研究中，我们分析了PTEN主要在支气管肺泡上皮细胞，NKT细胞和尿路上皮细胞的功能如下：1 90%的支气管肺泡上皮特异性Pten突变小鼠出生后不久死于缺氧，存活的小鼠发生自发性肺腺癌。肺组织学检查显示支气管肺泡上皮细胞和肌成纤维细胞前体增生，表面活性蛋白的产生受损。支气管肺泡干细胞（BASCs），肺腺癌的假定发起人的数量也增加了。这些结果表明，Pten对于正常肺形态发生和预防肺癌发生都是必不可少的，可能是因为这种肿瘤抑制因子是BASC稳态所必需的。2 NKT细胞中Pten突变导致Va 14 iNKT细胞发育失败。此外，Pten缺陷型Va 14 iNKT细胞在应答中表现出增殖和细胞因子分泌减少。 ...更多信息 对αGalCer刺激的影响。在体内，Va 14 iNKT细胞介导的对黑色素瘤细胞转移到肺的保护在Pten不存在的情况下受损。因此，Pten/PI 3 K通路对于Va 14 iNKT细胞的稳态和抗肿瘤监视功能是必不可少的。3小鼠中Pten的所有尿路上皮特异性无效突变均表现出尿路上皮增生。随着时间的推移，10%的突变小鼠自发发展为有蒂乳头状移行细胞癌（TCC）。在人类中，超过一半的原发性膀胱癌患者在肿瘤细胞的细胞质或细胞核中表现出PTEN蛋白表达减少或缺失。因此，PTEN缺乏可能导致膀胱癌。4此外，我们报道了电信号通过磷脂酰肌醇-3-OH激酶-γ和PTEN控制皮肤伤口愈合;当靶向由大鼠胰岛素启动子驱动时，PTEN是身体大小和葡萄糖代谢的关键决定因素;在中性粒细胞中，PI（3，4，5）P3磷酸酶对细胞极性和运动性的控制由SHIP而不是PTEN控制。少

In this study, we have analyzed the functions of PTEN mainly in bronchioalveolar epithelial cells, NKT cells, and urothelial epithelial cells as follows;1 Ninety percent of bronchioalveolar epithelium-specific Pten mutant mice died of hypoxia soon after birth, and surviving mice developed spontaneous lung adenocarcinomas. Histological examinations of the lungs revealed hyperplasia of bronchioalveolar epithelial cells and myofibroblast precursors, and impaired production of surfactant proteins. Numbers of bronchioalveolar stem cells(BASCs), putative initiators of lung adenocarcinomas, were also increased. These results indicate that Pten is essential for both normal lung morphogenesis and the prevention of lung carcinogenesis, possibly because this tumor suppressor is required for BASC homeostasis.2 A failure in the development of Va14iNKT cells occurs by Pten mutation in NKT cells. In addition, Pten-deficient Va14iNKT cells show reduced proliferation and cytokine secretion in response … More to αGalCer stimulation in vitro. In vivo, Va14iNKT cell-mediated protection against the metastasis of melanoma cells to the lung was impaired in the absence of Pten. Thus, the Pten/PI3K pathway is indispensable for the homeostasis and antitumor surveillance function of Va14iNKT cells.3 All urothelium-specific null mutation of Pten in mice exhibited urothelial hyperplasia. With time, 10% of mutant mice spontaneously developed pedicellate papillary transitional cell carcinomas(TCC). In humans, more than half of primary bladder cancer patients exhibited decreased or absent expression of PTEN protein in either the cytoplasm or nucleus of tumor cells. Thus, PTEN deficiency may contribute to bladder cancer.4 Furthermore, we reported that electrical signals control skin wound healing through phosphatidylinositol-3-OH kinase-gamma and PTEN; PTEN is a critical determinant of body size and glucose metabolism when targeting is driven by the rat insulin promoter; and control of cell polarity and motility by PI(3,4,5) P3 phosphatase is governed by SHIP rather than PTEN in neutrophils. Less