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| 1 | Increased susceptibility of aging gastric mucosa to injury:The mechanisms and clinical implications显示文摘This review updates the current views on aging gastric mucosa and the mechanisms of its increased susceptibility to injury.Experimental and clinical studies indicate that gastric mucosa of aging individuals-'aging gastropathy'-has prominent structural and functional abnormalities vs young gastric mucosa.Some of these abnormalities include a partial atrophy of gastric glands,impaired mucosal defense(reduced bicarbonate and prostaglandin generation,decreased sensory innervation),increased susceptibility to injury by a variety of damaging agents such as ethanol,aspirin and other non-steroidal anti-inflammatory drugs(NSAIDs),impaired healing of injury and reduced therapeutic efficacy of ulcer-healing drugs.Detailed analysis of the above changes indicates that the following events occur in aging gastric mucosa:reduced mucosal blood flow and impaired oxygen delivery cause hypoxia,which leads to activation of the early growth response-1(egr-1)transcription factor.Activation of egr-1,in turn,upregulates the dual specificity phosphatase,phosphatase and tensin homologue deleted on chromosome ten(PTEN)resulting in activation of pro-apoptotic caspase-3 and caspase-9 and reduced expression of the anti-apoptosis protein,survivin.The imbalance between pro-and anti-apoptosis mediators results in increased apoptosis and increased susceptibility to injury.This paradigm has human relevance since increased expression of PTEN and reduced expression of survivin were demonstrated in gastric mucosa of aging individuals.Other potential mechanisms operating in aging gastric mucosa include reduced telomerase activity,increase in replicative cellular senescence,and reduced expression of vascular endothelial growth factor and importin-α-a nuclear transport protein essential for transport of transcription factors to nucleus.Aging gastropathy is an important and clinically relevant issue because of:(1)an aging world population due to prolonged life span;(2)older patients have much greater risk of gastroduodenal ulcers and gastrointestinal complications(e.g.,NSAIDs-induced gastric injury)than younger patients;and(3)increased susceptibility of aging gastric mucosa to injury can be potentially reduced or reversed pharmacologically. | Andrzej S Tarnawski Amrita Ahluwalia Michael K Jones | 2014 | World Journal of Gastroenterology2014，20，16： | 16 |
| 2 | Role of phosphatase PTEN in the activation of extracellular signal-regulated kinases induced by estradiol in endometrial carcinoma cells显示文摘Objectives To study extracellular signal-regulated kinase (ERK) activation in the endometrial carcinoma cell line Ishikawa with stimulation by 17-β-estradiol, and to elucidate the role of phosphatase and tensin homologue (PTEN) and estrogen receptor (ER) subtype on the activation of ERKs. Methods Western blot was used to examine the expression of PTEN and PTEN (G129E) in Ishikawa cells after stable transfection as well as ERK activation in Ishikawa-EGFP, Ishikawa- PTEN and Ishikawa- PTEN (G129E) stimulated with various doses of 17-β-estradiol for different lengths of time. Western blot was also used for examining the expression of ERα and ERβ in NIH3T3 fibroblasts after transient transfection of pCXN2hERα and pCXN2hERβ. Then, ERK activation was examined after stimulation with 17-β-estradiol. Results 17-β-estradiol activated ERK cascades (mainly ERK2) in Ishikawa cells. The activation of ERK increased gradually as concentration of 17-β-estradiol also increased. The maximal activation of ERK2 took place 5 min after stimulation with 17-β-estradiol. The activation of ERK2 was inhibited markedly by PTEN, but not by PTEN (G129E). 17-β-estradiol activated ERK cascades in NIH3T3 fibroblasts after transient transfection of pCXN2hERα. Conclusions 17-β-estradiol activate ERK cascades in Ishikawa cells by integrating with ERα. Lipid phosphatase PTEN has an inhibitory role on the activation of ERK stimulated by 17-β-estradiol in Ishikawa cells. | 张育军 魏丽惠 王建六 孙铁铮 | 2003 | Chinese Medical Journal2003，，3： | 13 |
| 3 | Involvement of phosphatase and tensin homolog-induced putative kinase 1–Parkin-mediated mitophagy in septic acute kidney injury显示文摘Background:Studies have reported mitophagy activation in renal tubular epithelial cells(RTECs)in acute kidney injury(AKI).Phosphatase and tensin homolog-induced putative kinase 1(PINK1)and E3 ubiquitin-protein ligase Parkin are involved in mitophagy regulation;however,little is known about the role of PINK1-Parkin mitophagy in septic AKI.Here we investigated whether the PINK1-Parkin mitophagy pathway is involved in septic AKI and its effects on cell apoptosis in vitro and on renal functions in vivo.Methods:Mitophagy-related gene expression was determined using Western blot assay in human RTEC cell line HK-2 stimulated with bacterial lipopolysaccharide(LPS)and in RTECs from septic AKI rats induced by cecal ligation and perforation(CLP).Autophagy-related ultrastructural features in rat RTECs were observed using electron microscopy.Gain-and loss-of-function approaches were performed to investigate the role of the PINK1-Parkin pathway in HK-2 cell mitophagy.Autophagy activators and inhibitors were used to assess the effects of mitophagy modulation on cell apoptosis in vitro and on renal functions in vivo.Results:LPS stimulation could significantly induce LC3-II and BECN-1 protein expression(LC3-II:1.72±0.05 vs.1.00±0.05,P<0.05;BECN-1:5.33±0.57 vs.1.00±0.14,P<0.05)at 4 h in vitro.Similarly,LC3-II,and BECN-1 protein levels were significantly increased and peaked at 2 h after CLP(LC3-II:3.33±0.12 vs.1.03±0.15,P<0.05;BECN-1:1.57±0.26 vs.1.02±0.11,P<0.05)in vivo compared with those after sham operation.Mitochondrial deformation and mitolysosome-mediated mitochondria clearance were observed in RTECs from septic rats.PINK1 knockdown significantly attenuated LC3-II protein expression(1.35±0.21 vs.2.38±0.22,P<0.05),whereas PINK1 overexpression markedly enhanced LC3-II protein expression(2.07±0.21 vs.1.29±0.19,P<0.05)compared with LPS-stimulated HK-2 cells.LPS-induced proapoptotic protein expression remained unchanged in autophagy activator-treated HK-2 cells and was significantly attenuated in PINK1-overexpressing cells,but was remarkably upregulated in autophagy inhibitor-treated and in PINK1-depleted cells.Consistent results were observed in flow cytometric apoptosis assay and in renal function indicators in rats.Conclusion:PINK1-Parkin-mediated mitophagy might play a protective role in septic AKI,serving as a potential therapeutic target for septic AKI. | Xin-Gui Dai Wei Xu Tao Li Jia-Ying Lu Yang Yang Qiong Li Zhen-Hua Zeng Yu-Hang Ai | 2019 | Chinese Medical Journal2019，，19： | 9 |
| 4 | Impact of KRAS mutation and PTEN expression on cetuximab-treated colorectal cancer显示文摘AIM:To investigate the prognostic value of KRAS mutation,and phosphatase and tensin (PTEN) expression in Chinese metastatic colorectal cancer metastatic colorectal cancer (mCRC) patients treated with cetuximab.METHODS:Ninety Chinese mCRC patients treated with cetuximab were evaluated for KRAS mutation and PTEN protein expression by DNA sequencing of codons 12 and 13 and immunohistochemistry,respectively.We then selected 61 patients treated with cetuximab,either in combination with chemotherapy,or alone as a second-line or third-line regimen to assess whether KRAS mutation or PTEN protein expression is associated with the response and the survival time of mCRC patients treated with cetuximab.RESULTS:KRAS mutation was found in 30 (33.3%) tumor samples from the 90 patients,and positive PTEN expression was detected in 58 (64.4%) of the 90 patients.Among the 61 patients who were treated with cetuximab as a second-line or third-line regimen,the resistance to cetuximab was found in 22 patients with KRAS mutation and in 39 patients without KRAS mutation,with a response rate of 4.5% and 46.1% respectively (P=0.001),a shorter median progression-free survival (PFS) time of 14 ± 1.3 wk and 32 ± 2.5 wk respectively (P < 0.001),a median overall survival (OS) time of 11 ± 1.2 mo and 19 ± 1.8 mo respectively (P < 0.001),as well as in 24 patients with negative PTEN expression and in 37 patients with positive PTEN expression respectively (P < 0.001),with a responsive rate of 4.2% and 48.6% respectively,a shorter median PFS survival time of 17 ± 2.0 wk and 28 ± 1.9 wk respectively (P=0.07),and a median OS time of 11 ± 1.3 mo and 18 ± 1.9 mo respectively (P=0.004).Combined KRAS mutation and PTEN expression analysis showed that the PFS and OS time of patients with two favorable prognostic factors were longer than those of patients with one favorable prognostic factor or no favorable prognostic factor (P < 0.001).CONCLUSION:KRAS mutation and PTEN protein expression are significantly correlated with the response rate and survival time of Chinese mCRC patients treated with cetuximab. | Fang-Hua Li,Zhuang-Hua Li,Hui-Yan Luo,Miao-Zhen Qiu,Yu-Hong Li,Rui-Hua Xu,State Key Laboratory of Oncology in Southern China,Department of Medical Oncology,Sun YatSen University Cancer Center,Guangzhou 510060,Guangdong Province,China Fang-Hua Li,Department of Medical Oncology,Shengli Oil Field Central Hospital,Dongying 257034,Shandong Province,China Lin Shen,Department of GI Oncology,Peking University School of Oncology,Beijing Cancer Hospital and Institute,Beijing 100142,China Hui-Zhong Zhang,State Key Laboratory of Oncology in Southern China,Department of Pathology,Sun Yat-Sen University Cancer Center,Guangzhou 510060,Guangdong Province,China | 2010 | World Journal of Gastroenterology2010，16，46： | 9 |
| 5 | HBx-induced reactive oxygen species activates hepatocellular carcinogenesis via dysregulation of PTEN/Akt pathway显示文摘AIM:To investigate the role of hepatitis B virus X-protein(HBx)-induced reactive oxygen species(ROS)on liver carcinogenesis in HBx transgenic mice and HepG2-HBx cells.METHODS:Cell growth rate was analyzed,and through western blotting,mitogenic signaling was observed.Endogenous ROS from wild and HBx transgenic mice and HepG2-Mock and HBx cells were assayed by FACS-calibur.Identification of oxidized and reduced phosphatase and tensin homolog(PTEN)was analyzed through N-ethylmaleimide alkylation,nonreducing electrophoresis.RESULTS:We observed that the cell-proliferation-related phosphoinositide 3-kinase/Akt pathway is activated by HBx in vivo and in vitro.Increased ROS were detected by HBx.Tumor suppressor PTEN,via dephosphorylation of Akt,was oxidized and inactivated by increased ROS.Increased oxidized PTEN activated the mitogenic pathway through over-activated Akt.However,treatment with ROS scavenger N-acetyl cysteine can reverse PTEN to a reduced form.Endogenously produced ROS also stimulated HBx expression.CONCLUSION:HBx induced ROS promoted Akt pathways via oxidized inactive PTEN.HBx and ROS maintained a positive regulatory loop,which aggravated carcinogenesis. | Hye-Lin Ha Dae-Yeul Yu | 2010 | World Journal of Gastroenterology2010，16，39： | 8 |
| 6 | Anti-miRNA-221 sensitizes human colorectal carcinoma cells to radiation by upregulating PTEN显示文摘AIM:To investigate the regulative effect of miRNA(miR)-221 on colorectal carcinoma(CRC)cell radiosensitivity and the underlying mechanisms.METHODS:A human CRC-derived cell line was cultured conventionally and exposed to different doses of X-rays(0,2,4,6 and 8 Gy).The total RNA and protein of the cells were extracted 24 h after irradiation,and the alteration of miR-221 and phosphatase and tensin homolog deleted on chromosome 10(PTEN)gene mRNA expression was detected by real-time reverse transcriptase polymerase chain reaction(PCR).The protein alteration of PTEN in the cells was detected by Western blotting.Caco2 cells were pretreated with or without anti-PTEN-siRNA prior to the addition of premiR-221 or anti-miR-221 using Lipofectamine 2000.Colony formation assay and flow cytometry analysis were used to measure the surviving cell fraction and the sensitizing enhancement ratio after irradiation.Ad-ditionally,PTEN 3′-untranslated region fragment was PCR amplified and inserted into a luciferase reporter plasmid.The luciferase reporter plasmid construct was then transfected into CRC cells together with premiR-221 or anti-miR-221,and the luciferase activity in the transfected cells was detected.RESULTS:The X-ray radiation dose had a significant effect on the expression of miR-221 and PTEN protein in human Caco2 cells in a dose-dependent manner.The miR-221 expression level improved gradually with the increase in irradiation dose,while the PTEN protein expression level reduced gradually.miR-221 expression was significantly reduced in the anti-miR-221 group compared with the pre-miR-221 and negative control groups(P<0.01).Anti-miR-221 upregulated expression of PTEN protein and enhanced the radiosensitivity of Caco2 cells(P<0.01).Moreover,the inhibitory effect was dramatically abolished by pretreatment with anti-PTEN-siRNA,suggesting that the enhancement of radiosensitivity was indeed mediated by PTEN.A significant increase of luciferase activity was detected in CRC cells that were cotransfected with the luciferase reporter plasmid construct and anti-miR-221(P<0.01).CONCLUSION:Anti-miR-221 can enhance the radiosensitivity of CRC cells by upregulating PTEN. | Qi Xue Kai Sun Hai-Jun Deng Shang-Tong Lei Jing-Qing Dong Guo-Xin Li | 2013 | World Journal of Gastroenterology2013，19，48： | 6 |
| 7 | Diffuse intestinal ganglioneuromatosis an uncommon manifestation of Cowden syndrome显示文摘Diffuse intestinal ganglioneuromatosis is a hamartomatous polyposis characterized by a disseminated, intramural or transmural proliferation of neural elements involving the enteric plexuses. It has been associated with MEN Ⅱ, neurofibromatosis type 1 and hamartomatous polyposis associated with phosphatase and tensin homolog mutation. We report the case of a female patient with a history of a breast and endometrial tumor who presented in a colonoscopy performed for rectal bleeding diffuse ganglioneuromatosis, which oriented the search for other characteristic findings of Cowden syndrome given the personal history of the patient. The presence of an esophagogastric polyposis was also noted. Cowden syndrome is characterized by skin lesions, but it is rarely diagnosed by these lesions, because they are usually overlooked. Intestinal polyposis is not a major diagnostic criterion but it is very useful for early diagnosis. The combination of colonic polyposis and glucogenic acanthosis should orient the diagnosis to Cowden syndrome. | Maria Teresa Herranz Bachiller Jesus Barrio Andrés Fernando Pons Noelia Alcaide Suárez Rafael Ruiz-Zorrilla Lorena Sancho del Val Sara Lorenzo Pelayo Carlos De La Serna Higuera Ramon Atienza Sánchez Manuel Perez Miranda | 2013 | World Journal of Gastrointestinal Oncology2013，5，2： | 5 |
| 8 | phosphatase and tensin homolog is a differential diagnostic marker between nonalcoholic and alcoholic fatty liver disease显示文摘AIM: To investigate the protein expression of phosphatase and tensin homolog(PTEN) in human liver biopsies of patients with alcoholic and non-alcoholic liver disease.METHODS: PTEN protein expression was assessed by immunohistochemistry in formalin-fixed, paraffinembedded liver sections of patients with non-alcoholic fatty liver disease(NAFLD)(n = 44) or alcoholic liver disease(ALD)(n = 25). Liver resections obtained from 3 healthy subjects candidate for partial liver donation served as controls. Histological evaluations were performed by two experienced pathologists, and diagnoses established based on international criteria. The intensity of the PTEN staining in nuclei was compared between steatotic and non-steatotic areas of each liver fragment analyzed. For each liver specimen, the antibody-stained sections were examined and scored blindly by three independent observers, who were unaware of the patients' clinical history.RESULTS: In healthy individuals, PTEN immunostaining was intense in both the cytoplasm and nuclei of all hepatocytes. However, PTEN was strongly downregulated in both the nucleus and the cytoplasm of hepatocytes from steatotic areas in patients with NAFLD, independently of the disease stage. In contrast, no changes in PTEN protein expression were observed in patients with ALD, regardless of the presence of steatosis or the stage of the disease. The degree of PTEN downregulation in hepatocytes of patients with NAFLD correlated with the percentage of steatosis(r = 0.3061, P = 0.0459) and the BMI(r = 0.4268, P = 0.0043). Hovewer, in patients with ALD, PTEN expression was not correlated with the percentage of steatosis with or without obesity as a confounding factor(P = 0.5574). Finally, PTEN expression level in steatotic areas of ALD patients was significantly different from that seen in steatotic areas of NAFLD patients(P < 0.0001).CONCLUSION: PTEN protein expression is downregulated early in NAFLD, but not in ALD. PTEN immunohistochemical detection could help in the differential diagnosis of NAFLD and ALD. | Andrea Sanchez-Pareja Sophie Clément Marion Peyrou Laurent Spahr Francesco Negro Laura Rubbia-Brandt Michelangelo Foti | 2016 | World Journal of Gastroenterology2016，22，14： | 2 |
| 9 | Micro RNA-21 promotes phosphatase gene and protein kinase B/phosphatidylinositol 3-kinase expression in colorectal cancer显示文摘AIM: To explore the regulatory mechanism of the target gene of micro RNA-21(mi R-21), phosphatase gene(p TEN), and its downstream proteins, protein kinase B(AKT) and phosphatidylinositol 3-kinase(p I3K), in colorectal cancer(CRC) cells. METHODS: Quantitative real-time p CR(q RT-p CR) and Western blot were used to detect the expression levels of mi R-21 and p TEN in HCT116, HT29, Colo32 and SW480 CRC cell lines. Also, the expression levels of p TEN m RNA and its downstream proteins AKT and p I3 K in HCT116 cells after downregulating mi R-21 were investigated. RESULTS: Comparing the mi R-21 expression in CRC cells, the expression levels of mi R-21 were highest in HCT116 cells, and the expression levels of mi R-21 were lowest in SW480 cells. In comparing mi R-21 and p TEN expression in CRC cells, we found that the protein expression levels of mi R-21 and p TEN were inversely correlated(p < 0.05); when mi R-21 expression was reduced, m RNA expression levels of p TEN did not significantly change(p > 0.05), but the expression levels of its protein significantly increased(p < 0.05). In comparing the levels of p TEN protein and downstream AKT and p I3 K in HCT116 cells after downregulation of mi R-21 expression, the levels of AKT and p I3 K protein expression significantly decreased(p < 0.05). CONCLUSION: p TEN is one of the direct target genesof mi R-21. Thus, phosphatase gene and its downstream AKT and p I3 K expression levels can be regulated by regulating the expression levels of mi R-21, which in turn regulates the development of CRC. | Wei-Zhong Sheng Yu-Sheng Chen Chuan-Tao Tu Juan He Bo Zhang Wei-Dong Gao | 2016 | World Journal of Gastroenterology2016，22，24： | 2 |
| 10 | PTEN参与神经干细胞调控及脊髓损伤修复的研究进展显示文摘1997年,第10号染色体缺失的磷酸酶与张力蛋白同源物基因(phosphatase and tensin homolog deleted on chromosome 10,PTEN)由国外3个独立的研究小组先后克隆命名,这是目前发现的第一个具有磷酸酶活性的抑癌基因,其编码的蛋白在细胞内具有脂质磷酸酶和蛋白磷酸酶的双重活性。PTEN具有广泛的生物学功能,通过细胞内多个信号通路来调控细胞的生长、分化、迁移、凋亡等过程。 | 宋志文 余常麟 丁亚 邹红军 刘锦波 | 2016 | 中国脊柱脊髓杂志2016，26，6： | 2 |
| 11 | Curcumin cytotoxicity is enhanced by PTEN disruption in colorectal cancer cells显示文摘AIM:To investigate the effects of phosphatase and tensin homolog deleted on chromosome 10(PTEN) deficiency on the cytotoxicity of chemotherapeutic agents toward colorectal cancer cells.METHODS:PTEN-deficient colorectal cancer(CRC) cells were generated by human somatic cell gene targeting using the adeno-associated virus system. The cytotoxic effects of compounds including curcumin,5-fluorouracil(5-FU),dihydroartemisinin(DHA),irinotecan(CPT-11)and oxaliplatin(OXA) on cancer cells were determined using the MTT assay. Enhanced cytotoxicity of curcumin in PTEN-deficient CRC cells was observed,and this was confirmed using clonogenic assays. Apoptosis and cell cycle progression were analyzed by flow cytometry.Levels of apoptosis and cell cycle-related proteins were examined by Western blotting.RESULTS:We developed an isogenic set of CRC cell lines that differed only in their PTEN status. Using this set of cell lines,we found that disruption of the PTEN gene had no effect on the sensitivity of CRC cells to5-FU,CPT-11,DHA,or OXA,whereas PTEN disruption increased the sensitivity of CRC cells to curcumin. Loss of PTEN did not alter the curcumin-induced apoptosis in CRC cells. However,PTEN deficiency led to an altered pattern of curcumin-mediated cell cycle arrest.In HCT116 PTEN+/+cells,curcumin caused a G2/M phase arrest,whereas it caused a G0/G1 phase arrest in HCT116 PTEN-/-cells. Levels of cell cycle-related proteins were consistent with these respective patterns of cell cycle arrest.CONCLUSION:Curcumin shows enhanced cytotoxicity toward PTEN-deficient cancer cells,suggesting that it might be a potential chemotherapeutic agent for cancers harboring PTEN mutations. | Lin Chen Wen-Feng Li Hong-Xiao Wang Hai-Na Zhao Jia-Jia Tang Chang-Jie Wu Li-Ting Lu Wan-Qin Liao Xin-Cheng Lu | 2013 | World Journal of Gastroenterology2013，19，40： | 2 |
| 12 | 高糖条件下Tensin在人肾脏系膜细胞上的表达显示文摘目的:探讨在高糖刺激的条件下,Tensin在人类肾脏系膜细胞上的表达及变化。方法:体外培养系膜细胞,用含不同浓度的葡萄糖(5mmol/L,30mmol/L)刺激细胞48h、72h和5d。用免疫荧光法观察tensin在人类肾脏系膜细胞上表达及变化,ELISA法检测上清液中纤连蛋白含量。结果:高糖刺激下系膜细胞tensin的表达随着培养时间的延长逐渐增多,且纤连蛋白的分泌也随培养时间的延长而增加。结论:高糖刺激下tensin在人类肾脏系膜细胞的细胞膜上表达增加,在细胞外基质增多的发生机制中起重要作用。 | 黄立娟 杜波 宋辉 | 2009 | 细胞与分子免疫学杂志2009，25，8： | 1 |
| 13 | Axon regeneration induced by environmental enrichment-epigenetic mechanisms显示文摘Environmental enrichment is known to be beneficial for cognitive improvement.In many animal models of neurological disorders and brain injury,EE has also demonstrated neuroprotective benefits in neurodegenerative diseases and in improving recovery after stroke or traumatic brain injury.The exact underlying mechanism for these phenomena has been unclear.Recent findings have now indicated that neuronal activity elicited by environmental enrichment induces Ca2+influx in dorsal root ganglion neurons results in lasting enhancement of CREB-binding protein-mediated histone acetylation.This,in turn,increases the expression of pro-regeneration genes and promotes axonal regeneration.This mechanism associated with neuronal activity elicited by environmental enrichment-mediated pathway is one of several epigenetic mechanisms which modulate axon regeneration upon injury that has recently come to light.The other prominent mechanisms,albeit not yet directly associated with environmental enrichment,include DNA methylation/demethylation and N6-methyladenosine modification of transcripts.In this brief review,I highlight recent work that has shed light on the epigenetic basis of environmental enrichment-based axon regeneration,and discuss the mechanism and pathways involved.I further speculate on the implications of the findings,in conjunction with the other epigenetic mechanisms,that could be harness to promote axon regeneration upon injury. | Bor Luen Tang | 2020 | Neural Regeneration Research2020，15，1： | 1 |
| 14 | Diabetic neuropathy research: from mouse models to targets for treatment显示文摘Diabetic neuropathy is one of the most serious complications of diabetes, and its increase shows no sign of stopping. Furthermore, current clinical treatments do not yet approach the best effectiveness. Thus, the development of better strategies for treating diabetic neuropathy is an urgent matter. In this review, we first discuss the advantages and disadvantages of some major mouse models of diabetic neuropathy and then address the targets for mechanism-based treatment that have been studied. We also introduce our studies on each part. Using stem cells as a source of neurotrophic factors to target extrinsic factors of diabetic neuropathy, we found that they present a promising treatment. | Vuong M. Pham Shinji Matsumura Tayo Katano Nobuo Funatsu Seiji Ito | 2019 | Neural Regeneration Research2019，14，11： | 1 |
| 15 | 糖尿病肾病大鼠肾脏Tensin表达的变化显示文摘目的 观察tensin在糖尿病肾病(DN)大鼠肾脏中的表达,探讨其在DN肾小球纤维化中的作用。方法 链脲佐菌素(STZ)诱导大鼠DN,间接免疫荧光组织化学方法观察DN大鼠肾脏tensin的表达。结果 糖尿病肾病大鼠的肾脏tensin表达明显增加(与正常对照组相比P〈0.01,有统计学意义),阳性表达主要位于系膜细胞胞浆内。结论 tensin在糖尿病肾病大鼠系膜细胞中高表达可能参与了糖尿病肾病过程中肾小球纤维化的形成。 | 黄立娟 杜波 姜德友 | 2009 | 国际免疫学杂志2009，32，2： | 0 |
| 16 | C-terminal tensin-like (CTEN) knockin alleviates cystic kidney defects in Tensin-1 knockout mice显示文摘Tensin-1(TNS1)is a 220 kD focal adhesion protein that binds to actin filaments,integrin receptors,small GTPases,tyrosine-phosphorylated proteins,and lipids.1 These binding activities enable TNS1 to link the actin cytoskeleton to integrins and transduce outside-in and inside-out signals at focal adhesion sites,thereby regulating cell attachment,migration,proliferation,and mechanical sensing.1 Lack of TNS1 in kidney epithelial cells results in multiple lumen,instead of single lumen,phenotypes in the three-dimensional(3D)culture. | Chun-Lung Chiu Shiao-Ya Hong Ying Tan Yuh-Ru Julie Lee Yi-Ping Shih Clifford GTepper Su Hao Lo | 2023 | Genes & Diseases2023，10，3： | 0 |
| 17 | Biomarkers for glioblastoma multiforme: status quo显示文摘Background:Glioblastoma(GBM)is the most frequent and most malignant central nervous system(CNS)tumor.GBM shows poor prognosis with a median overall survival of 14.6 months,despite current surgical and adjuvant therapies.O(6)-methylguanine-DNA methyltransferase(MGMT)methylation is the strongest molecular prognosticator for GBM with therapeutic implications in adjuvant treatment.Isocitrate dehydrogenase(IDH)mutation is the most recently introduced molecular marker and is important for the GBM classification because distinguishes primary(de novo)from secondary GBM.In the last two decades huge advances in the understanding of biopathological bases of gliomagenesis have been made but,to date,there is a lack of biopathological markers endowed of some prognostic and predictive value for GBM.Aim:In the present review we analyzed the role,as possible prognosticators,of epidermal growth factor receptor(EGFR)variant III(EGFRvIII),phosphatase and tensin homolog(PTEN)deletion and other alteration of the receptor tyrosine kinase(RTK)pathway,and vascular endothelial growth factor(VEGF)expression.We included in the review studies considering both the prognostic value and the predictive value for response to therapy of the above-mentioned biomarkers.Relevance for patients:These factors have a paramount importance in gliomagenesis and are potential targets for individualized therapies.EGFR can be targeted by tyrosine kinase inhibitors(TKIs).mTOR,whose activation is triggered by PTEN loss,is the target of rapalogs and VEGF is the target of the molecular antibody bevacizumab.Unfortunately,current evidence is insufficient to draw a definite prognostic/predictive role for these biomarkers in GBM.Further understanding the gliomagenesis pathways and looking for biomarkers endowed with translational relevance are necessary efforts in order to find the appropriate,tailored therapy for each specific GBM patient. | Nicola Montano Quintino Giorgio D’Alessandris Alessandro Izzo Eduardo Fernandez Roberto Pallini | 2016 | Journal of Clinical & Translational Research2016，2，1： | 0 |
| 18 | 第10号染色体缺失的磷酸酶和张力蛋白的同源基因通过减少上皮-间充质转化来抑制胆管癌细胞QBC939的迁移能力显示文摘目的 探讨第10号染色体缺失的磷酸酶和张力蛋白的同源基因(PTEN)对胆管癌细胞株QBC939迁移能力的抑制作用及其机制.方法 取4μg PTEN质粒转染胆管癌细胞株QBC939,转染72 h后,采用Transwell迁移实验和Western blot检测上调PTEN对QBC939细胞迁移能力和上皮-间充质转化(EMT)中重要的分子标志物表达的影响.结果 人胆管癌细胞株QBC939经PTEN质粒转染72 h后,其通过基质膜细胞数目比较对照组数目减半(P<0.01),迁移能力减弱,与EMT相关分子标志物Slug、Snail、波形蛋白(Vimentin)蛋白表达水平降低,磷酸肌醇3激酶(PI3K)/蛋白激酶B(Akt)信号通路中的磷酸化Akt (p-Akt)蛋白表达也明显减少.结论 PTEN可以通过抑制EMT进而影响胆管癌细胞迁移,PTEN对EMT的抑制作用可能是由PI3K/Akt信号通路调节的. | 向丹 郑富霖 李明 提爱军 张龙 李文岗 | 2015 | 中华实验外科杂志2015，32，11： | 0 |
| 19 | 肾消康对糖尿病肾病大鼠肾损伤的保护作用及对tensin表达的影响显示文摘目的:探讨肾消康对糖尿病肾病(DN)的保护作用及机理。方法:建立糖尿病肾病大鼠模型,以肾消康治疗,观察各组大鼠的血糖、尿素氮、肌酐、24h尿微量白蛋白的数值及tensin的表达。结果:正常大鼠肾脏tensin表达很弱,DN大鼠肾脏tensin表达明显增强(与正常对照组相比P<0.01,有统计学意义),肾消康对DN大鼠肾脏组织tensin的表达有下调作用(与模型组相比P<0.01,有统计学意义)。同时肾消康能有效降低血糖、尿素氮、肌酐、尿微量白蛋白。结论:肾消康能够调节血糖水平,下调ten-sin的表达,降低尿素氮、肌酐、尿微量白蛋白,从而防止肾纤维化及延缓肾衰。 | 黄立娟 杜波 姜德友 | 2009 | 中医药信息2009，26，3： | 0 |
| 20 | Tensin的研究进展显示文摘Tensin是一种位于胞浆灶性粘附区的磷酸蛋白,它包含了一个磷酸酪氨酸结合(PTB)区域和一个Src同源区2区域(SH2)。Tensin通过整合素、纽蛋白和灶性粘附激酶(FAK)的粘附复合物影响肾小球系膜细胞产生细胞外基质,它在肌肉再生、细胞迁移中起关键作用。因此,tensin可以作为对肾脏疾病、创口愈合、癌症等进行干预治疗的靶点。 | 黄立娟 杜波 | 2009 | 国际免疫学杂志2009，32，3： | 0 |
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