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Functional characterization of the keratinocyte growth factor system in human fetal gastrointestinal tract

PEDIATRIC RESEARCH 2000年第4期48卷 504-510页

作者： Chailler, P Basque, JR Corriveau, L Ménard, D Univ Sherbrooke Fac Med Dept Anat & Biol Cellulaire MRC Grp Funct Dev & Physiopathol Digest Tract Sherbrooke PQ J1H 5N4 Canada

Keratinocyte growth factor (KGF) is a paracrine growth factor whose mRNA has been detected in human adult and rodent gut tissues together with its associated receptor. Our objectives were to assess the presence of immunoreactive KGF ligand and receptor proteins in human fetal gastrointestinal (GI) tract segments and to evaluate the role of exogenous KGF on cell proliferation and intestinal digestive functions. KGF (26-28 kD doublet) was identified in esophagus, stomach, small intestine, and colon by Western blot. Its receptor (135 kD) was ubiquitously detected in proliferative and differentiated epithelial cells of each GI segment by use of indirect immunofluorescence (anti-bek, anti-K-sam). The addition of KGF to explants cultured in serum-free conditions greatly stimulated DNA synthesis in all GI tract tissues. The growth factor up-regulated intestinal sucrase-isomaltase and gamma-glutamyl-transpeptidase activities in jejunal exp]ants, whereas it down-regulated these activities in colon explants. It is suggested that the KGF system likely represents an important paracrine pathway that is able to stimulate cell proliferation in all segments of the human fetal GI tract and to differentially regulate intestinal digestive functions.

关键词：印迹法蛋白质结肠/化学结肠/胚胎学结肠/酶学培养技术 DNA/生物合成消化系统/化学消化系统/胚胎学上皮细胞/化学食管/化学食管/胚胎学成纤维细胞生长因子10 成纤维细胞生长因子7 成纤维细胞生长因子荧光抗体技术间接孕龄生长物质/分析生长物质/药理学小肠/化学小肠/胚胎学空肠/酶学受体成纤维细胞生长因子 2型受体成纤维细胞生长因子受体生长因子/分析胃/化学胃/胚胎学蔗糖酶异麦芽糖酶复合物/代谢 γ-谷氨酰转移酶/代谢女(雌)性人类妊娠

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Basic fibroblast growth factor stimulates repair of wounded hepatocyte monolayer: Modulatory role of protein kinase A and extracellular matrix

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JOURNAL OF LABORATORY AND CLINICAL MEDICINE 1999年第4期134卷 363-371页

作者： Ma, TY Kikuchi, M Sarfeh, IJ Shimada, H Hoa, NT Tarnawski, AS DVA Med Ctr Dept Med & Surg Div Gastroenterol Long Beach CA 90822 USA Univ Calif Irvine Irvine CA 92717 USA Yokohama City Univ Dept Surg 2 Yokohama Kanagawa 232 Japan

The two important repair mechanisms after hepatocyte injury are proliferation and migration of the nearby healthy hepatocytes. Although previous studies have shown that basic fibroblast growth factor (bFGF) levels are markedly elevated after liver injury, the role of bFGF in the repair of the wounded hepatocytes is not well understood. The aim of this study was to delineate the role of bFGF in the repair of the wounded hepatocyte monolayers. Specifically, we examined the role of bFGF in cellular proliferation and migration of hepatocytes with an in vitro wound model. Standardized excisional wounds were created in clone 9 rat hepatocyte monolayers by a razor blade, and the extent of epithelial proliferation and migration was measured. After wound formation, bFGF (30 ng/mL) significantly stimulated proliferation of hepatocytes at the wound margin. bFGF also stimulated the migration of hepatocytes at the wound front. bFGF stimulation of hepatocyte migration correlated with increased formation of actin stress fibers and bFGF-receptor protein level. The bFGF stimulation of hepatocyte migration was abolished by various protein kinase A activating agents including 3-isobutyl-1-methylxanthine, 8-bromoadenosine-3', 5'-cyclic monophosphate, forskolin, and cholera toxin. In addition, protein kinase A activating agents almost completely prevented bFGF-induced actin stress fiber formation in the cells at the wound front. Varying the basement membrane composition of the extracellular matrix had a selective enhancing effect on the basal rates of hepatocyte migration (collagen IV greater than or equal to laminin > collagen I > fibronectin > control (plastic)). bFGF treatment resulted in a similar additive increase in hepatocyte migration across all coated surfaces studied. We conclude that bFGF promotes hepatocyte wound repair by stimulating both proliferation and migration of the hepatocyte at the margin of the wound.

关键词： 1-甲基-3-异丁基黄嘌呤/药理学 8-溴环腺苷一磷酸/药理学肌动蛋白类/代谢印迹法蛋白质细胞分裂/药物作用细胞运动/药物作用细胞培养的霍乱毒素/药理学环AMP依赖性蛋白激酶类/代谢上皮细胞/化学上皮细胞/细胞学上皮细胞/酶学细胞外基质/酶学成纤维细胞生长因子2/药理学福司柯林/药理学肝/细胞学丝裂霉素/药理学核酸合成抑制剂/药理学磷酸二酯酶抑制剂/药理学受体成纤维细胞生长因子/分析应力物理氚/诊断应用伤口愈合动物大鼠

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Cell type-specific regulation of fetal fibronectin expression in amnion: Conservation of glucocorticoid responsiveness in human and nonhuman primates

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BIOLOGY OF REPRODUCTION 2000年第6期62卷 1812-1817页

作者： Ma, YH Lockwood, CJ Bunim, AL Giussani, DA Nathanielsz, PW Guller, S NYU Sch Med Dept Obstet Gynecol New York NY 10016 USA Univ Cambridge Dept Physiol Cambridge England Cornell Univ Dept Physiol Lab Pregnancy & Newborn Res Ithaca NY 14853 USA

The appearance of oncofetal fibronectin (FFN) in cervical and vaginal secretions is predictive of human labor. Levels of FFN in amnion increase with the onset of labor in rhesus monkeys. Since glucocorticoid (GC) levels in serum and amniotic fluid increase in association with parturition, we compared GC-mediated regulation of FFN expression in cultures of amnion epithelial cells and fibroblasts isolated from human and baboon amnions. Cells were maintained with and without dexamethasone (DEX), and levels of FFN in the conditioned media were determined by ELISA. We observed that DEX treatment suppressed FFN levels in both human and baboon amnion epithelial cells, whereas it increased FFN levels in amnion fibroblasts. DEX treatment reduced FFN revels in cytotrophoblasts from human placenta and increased FFN levers in placental fibroblasts. Northern blots revealed that DEX reduced levers of fibronectin (FN) mRNA in amnion epithelial cells and cytotrophoblasts, whereas it increased FN mRNA in amnion and placental fibroblasts. We conclude that CC differentially regulates FFN expression in epithelial and mesenchymal cells from amnion and placenta. In addition, this pattern of cell type-specific FFN regulation by CC is conserved in human and nonhuman primates and may be responsible for parturition-dependent changes in FFN expression in gestational tissues.

关键词：羊膜/化学细胞培养的培养基条件性地塞米松/药理学上皮细胞/化学胎儿/代谢成纤维细胞/化学纤连蛋白类/分析纤连蛋白类/遗传学基因表达调控/药物作用糖皮质激素类/药理学恒河猴胎盘/化学 RNA 信使/分析动物女(雌)性人类妊娠

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Effects of extracellular Mg²⁺ on transepithelial capacitance and Na⁺ transport in A6 cells under different osmotic conditions

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PFLUGERS ARCHIV-EUROPEAN JOURNAL OF PHYSIOLOGY 2000年第5期439卷 504-512页

作者： Jans, D Simaels, J Cucu, D Zeiske, W Van Driessche, W Katholieke Univ Leuven Physiol Lab B-3000 Louvain Belgium Univ Bucharest Fac Biol Biophys Lab Bucharest 76208 Romania

The electrophysiological characteristics of monolayers of cultured renal epithelial A6 cells were studied under short-circuit conditions. Replacing basolateral isosmotic (260 mOsm/kg H2O) media by hyposmotic (140 mOsm/kg H2O) solutions transiently increased the transepithelial capacitance (C-T) by 57.3 +/- 2.3% after 16 min. The transepithelial Na+ current (I-Na) increased concomitantly from 4.2 +/- 0.7 to 26.1 +/- 2.6 mu A/cm(2) with a time course that was noticeably slower, reaching its maximum after 60 min of hypotonicity. The transepithelial conductance (C-T) increased synchronously with I-Na. Analysis of blocker-induced noise in I-Na, using the amiloride analogue 6-chloro-3,5-diaminopyrazine-2-carboxamide (CDPC), showed that the hypotonic shock increased Na+ channel density (N-T) at the apical border. The presence of 10 mM Mg2+ on both sides of the epithelium suppressed the hypotonicity-induced C-T increase to 14.3 +/- 0.5%, whereas the I-Na increase was even larger than without Mg2+. Both effects of Mg2+ were located at an extracellular, basolateral site. because apical administration was without effect. whereas the acute basolateral addition of Mg2+ at the moment of the hypotonic shock was sufficient. Interaction between Mg2+ and Ca2+ influenced the behaviour of C-T. At constant osmolality (200 mOsm/kg H2O) 10 mM Mg2+ increased I-Na, leaving C-T unaffected, whereas 10 mM Ca2+ stimulated both I-Na and C-T. In the presence of mM Mg2+, however, the Ca2+-induced C-T increase was abolished. The failure of C-T to increase during stimulation of I-Na by Mg2+ suggests that the divalent cation activates pre-existing channels in the apical membrane. Noise analysis showed that the natriferic effects of Mg2+ were also mediated by an increase in N-T. The moderate initial increase in C-T in the presence of Mg2+ under hypotonic conditions, occur-ring in parallel with increases in G(T) and I-Na reflects most lihrly Na+ channel insertion induced by the hypotonic treatment. How

关键词：伪迹生物转运/药物作用生物转运/生理学钙/药理学细胞极性/药物作用细胞极性/生理学上皮细胞/化学上皮细胞/药物作用上皮细胞/代谢胞吐作用/生理学低渗溶液/药理学离子通道闸门/药物作用离子通道闸门/生理学肾/细胞学镁/药理学容积渗克分子浓度膜片钳术钠/代谢钠通道/代谢水电解质平衡/生理学动物

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Asbestos and cigarette smoke cause increased DNA strand breaks and necrosis in bronchiolar epithelial cells in vivo

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FREE RADICAL BIOLOGY AND MEDICINE 2000年第8期28卷 1295-1299页

作者： Jung, M Davis, WP Taatjes, DJ Churg, A Mossman, BT Univ Vermont Coll Med Dept Pathol Burlington VT 05405 USA Univ British Columbia Dept Pathol Vancouver BC Canada

Coexposures to asbestos and cigarette smoke cause increased risks of lung cancer in asbestos workers. Although these carcinogens cause DNA damage to epithelial cells in vitro via generation of reactive oxygen species (ROS), it is unclear whether they cause injury to bronchiolar epithelial cells (i.e., the target cells of lung cancers in vivo). We exposed rats to amosite asbestos, cigarette smoke, and the two agents in combination for 1, 2, and 14 d. Numbers of cells exhibiting DNA strand breaks in comparison to sham rats were then evaluated in lungs using the terminal deoxynucleotidyl transferase (TDT)-mediated dUTP-biotin nick end labeling (TUNEL) method and by transmission electron microscopy (TEM). Increases in TUNEL-positive, necrotic epithelial cells occurred after exposure to asbestos alone and in an additive fashion after smoke and asbestos in combination. These results indicate that DNA strand breakage and necrosis are prominent mechanisms of injury by asbestos fibers and cigarette smoke in vivo to epithelial cells of the respiratory tract, thus validating in vitro observations from a number of laboratories. (C) 2000 Elsevier Science Inc.

关键词：细胞凋亡/药物作用石棉铁/毒性支气管/细胞学支气管/药物作用辅致癌作用 DNA损伤药物协同作用上皮细胞/化学上皮细胞/药物作用原位缺口末端标记坏死植物有毒大鼠 Sprague-Dawley 活性氧烟/副作用烟草动物男(雄)性大鼠

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λ-Carrageenan-induced inhibition of gap-junctional intercellular communication in rat liver epithelial cells

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NUTRITION AND CANCER-AN INTERNATIONAL JOURNAL 2000年第1期36卷 122-128页

作者： Suzuki, J Na, HK Upham, BL Chang, CC Trosko, JE Michigan State Univ Dept Pediat & Human Dev Natl Food Safety & Toxicol Ctr E Lansing MI 48824 USA

lambda-Carrageenan, a food additive extracted from red seaweed, is widely used as an emulsifier, stabilizer, or thickener. Previously, it has been shown that carrageenan could play a role in carcinogenesis. However, the mechanism by which it might influence the multimechanism, multistep process of carcinogenesis is not known. Gap-junctional intercellular communication (GJIC) has been associated with maintaining homeostatic regulation of cell proliferation and differentiation. Most cancer cells have dysfunctional GJIC, and many tumor-promoting chemicals, growth factors, and oncogenes can downregulate GJIC. The experiments in this study were designed to test the hypothesis that carrageenan might function as a tumor-promoting chemical by inhibiting GJIC. To test this hypothesis, nontumorigenic vat liver epithelial cells were exposed to carrageenan, and GJIC was measured. Western blot analysis and immunofluorescent staining were used to monitor the phosphorylation and localization of connexin 43. The data revealed inhibition of GJIC by carrageenan similar to that by the well-documented tumor promoter phorbol ester. However the phosphorylation and localization of connexin 43 were not altered. Although the mechanism by which carrageenan inhibits GJIC is unknown, carrageenan's influence on the carcinogenic process might be via its ability to be a tumor promoter.

关键词：抗体单克隆角叉菜胶/药理学细胞分裂/药物作用细胞系细胞存活/药物作用连接蛋白43/分析连接蛋白43/代谢上皮细胞/化学上皮细胞/超微结构荧光抗体技术缝隙接合部/化学缝隙接合部/药物作用组织细胞化学肝/化学肝/超微结构磷酰化动物大鼠

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Effect of estradiol on estrogen receptor expression in rat uterine cell types

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BIOLOGY OF REPRODUCTION 2000年第1期62卷 168-177页

作者： Nephew, KP Long, XH Osborne, E Burke, KA Ahluwalia, A Bigsby, RM Indiana Univ Sch Med Program Neural Sci Bloomington IN 47405 USA Indiana Univ Sch Med Dept Obstet & Gynecol Indianapolis IN 46202 USA

In rodent uterus, both up- and down-regulation of estrogen receptor alpha (ER alpha) messenger ribonucleic acid (mRNA) and protein levels by estradiol has been demonstrated;however, it is not known which of the uterine compartments (endometrial epithelium, stroma, myometrium) respond to estradiol with autoregulation of ER alpha. The purpose of the present study was to investigate and compare the kinetics and cell type-specific effects of estradiol on uterine ER alpha expression in immature and adult rats. Ovariectomized female rats were injected s.c, with sesame oil or estradiol-17 beta. Uteri were collected and analyzed far changes in ER alpha mRNA using RNase protection assays (RPA) and in situ hybridization using radiolabeled probes specific for ER alpha. Immunohistochemical analysis was performed with a polyclonal antibody specific to ER alpha. Expression of ER alpha in the uterine epithelial cells decreased at 3 and 6 h after estradiol administration to immature and adult rats, respectively. At 24 h, ER alpha mRNA levels in the immature and mature rat uterus were higher than pretreatment levels but returned to baseline by 72 h. Pretreatment with cycloheximide did not block the 3-h repressive effect of estradiol, suggesting that the estradiol-induced decrease in ER alpha mRNA occurs independent of new protein synthesis. A decrease in ER alpha mRNA and protein was also observed in uterine epithelia at 3 and 6 h after an estradiol injection to immature and adult rats, and intensity of both the in situ hybridization signal and the immunostaining in the epithelium increased at 24 and 72 h. However, the periluminal stromal cells in the adult uterus and the majority of stromal cells of the immature uterus appeared to have increased ER alpha expression. The results indicate that down-regulation of ER alpha in the epithelia and up-regulation of stromal ER alpha play a role in early events associated with estradiol-induced cell proliferation of the uterine epithelia.

关键词：放线菌酮/药理学上皮细胞/化学雌二醇/药理学雌激素受体α 基因表达/药物作用免疫组织化学原位杂交卵巢切除术蛋白质合成抑制药/药理学 RNA 信使/分析 RNA 信使/代谢大鼠 Sprague-Dawley 受体雌激素/遗传学核糖核酸酶类间质细胞/化学组织分布子宫/化学子宫/代谢动物女(雌)性大鼠

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Expression of inducible nitric oxide synthase and p53 in oral epithelial dysplasia

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ORAL SURGERY ORAL MEDICINE ORAL PATHOLOGY ORAL RADIOLOGY AND ENDODONTOLOGY 2000年第5期90卷 624-629页

作者： Brennan, PA Conroy, B Spedding, AV St Richards Hosp Chichester England Queen Alexandra Hosp Portsmouth Hants England

Aims. Nitric oxide (NO) has been studied in a variety of human cancers and is implicated in both tumor promotion and inhibition. Downregulation of the enzyme iNOS by wild-type p53 (but not mutant) protein has been shown to occur in normal cells and some tumors, but the relationship has not been reported in oral epithelial dysplasia. Methods and results. An immunohistochemical study was conducted with antibodies to iNOS and p53 (clone DO-7) in 36 cases of oral dysplasia of varying severity. Statistical analysis showed a significant correlation between iNOS staining and grade of dysplasia (P < .001) and between p53 and iNOS staining (P < .001). Conclusions. This preliminary study has shown that iNOS expression correlates with severity of dysplasia, and it is also increased in those cases showing positive staining for p53. Further research is required to fully establish the relationship between iNOS and p53 in both dysplasia and oral squamous cell carcinoma.

关键词：印迹法蛋白质减量调节电泳聚丙烯酰氨凝胶酶诱导上皮细胞/化学上皮细胞/酶学基因 p53 免疫组织化学口腔黏膜/化学口腔黏膜/酶学口腔黏膜/病理学口腔肿瘤/酶学口腔肿瘤/遗传学一氧化氮合酶/分析一氧化氮合酶/生物合成癌前状态/酶学癌前状态/遗传学肿瘤抑制蛋白质p53/分析肿瘤抑制蛋白质p53/生物合成人类

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Expression of the chemokine eotaxin and its receptor, CCR3, in human endometrium

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BIOLOGY OF REPRODUCTION 2000年第2期62卷 404-411页

作者： Zhang, J Lathbury, LJ Salamonsen, LA Prince Henrys Inst Med Res Clayton Vic 3168 Australia

Eosinophils are present in human endometrium only immediately before and during menstruation, suggesting a role in that process. The expression of the eosinophil chemoattractant, eotaxin, and its receptor, CCR3, within the human endometrium were investigated by immunohistochemical analysis of tissue sections spanning the entire menstrual cycle. Eotaxin was localized to perivascular cells in the late secretory phase, and it was also identified in eosinophils, However, the highest levels of this chemokine were present in both luminal and glandular epithelial cells during the proliferative and secretory phases of the cycle. Treatment of endometrial tissue with monensin, which blocks protein secretion, increased epithelial immunoreactive eotaxin, substantiating synthesis in these cells. Although the CCR3 receptor was expressed by eosinophils, it was also strongly expressed by endometrial epithelial cells. The CCR3 receptor on purified, cultured endometrial epithelial cells was functional, as assessed by a transient Ca2+ flux in response to eotaxin. These analyses demonstrate that eotaxin is expressed by endometrial cells and may therefore be involved in the recruitment of eosinophils into this tissue premenstrually. However, the observation that this chemokine and the CCR3 molecule are strongly expressed by epithelial cells throughout the cycle suggests that these proteins may have additional important functions within the endometrium.

关键词：印迹法蛋白质钙/代谢细胞分离细胞培养的趋化因子 CC 趋化因子类/生理学趋化因子嗜酸细胞/生物合成细胞因子类/生物合成子宫内膜/代谢嗜酸细胞/生理学上皮细胞/化学上皮细胞/代谢免疫组织化学月经/生理学受体趋化因子/生物合成间质细胞/化学间质细胞/代谢成年人女(雌)性人类

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Foveolar differentiation of mouse gastric mucosa in vitro

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AMERICAN JOURNAL OF PATHOLOGY 2003年第6期162卷 1905-1912页

作者： Ootani, A Toda, S Fujimoto, K Sugihara, H Saga Med Sch Dept Pathol Saga 8498501 Japan Saga Med Sch Dept Internal Med Saga 8498501 Japan

We report a novel method that allows the culture of highly differentiated gastric surface mucous cells. isolated mouse gastric epithelial cells and fibroblasts were co-cultured in a three-dimensional collagen gel system, and the reconstructed mucosal surface treated with an air-liquid interface. Cultured cells were examined by histology, immunohistochemistry, and electron microscopy. Isolated epithelial cells were positive for MUC5AC, and showed immature mucous cell features (pre-pit cell stage) on cell-free collagen gel. However, when given fibroblastic support, the epithelial cells differentiated into mature surface mucous cells (pit cell stage), and showed a tall columnar cell shape, basal round nuclei, and mucus-filled cytoplasm. In the fine structure, the cells showed Junctional complexes, basal Lamina, and glycogen and secretary granules. Further treatment by the air-liquid interface environment modified the differentiated state of the pit cells (pit top cell stage);resulting in the expression of cathepsin E, the disappearance of glycogen granules and the apical accumulation of secretory granules along with an increase in apoptotic cells. This culture model should provide a useful tool for studying gastric epithelial cell biology and various diseases of the gastric mucosa.

关键词：动物新生细胞凋亡细胞培养技术/方法细胞分化细胞分裂细胞培养的胶原上皮细胞/化学上皮细胞/细胞学上皮细胞/超微结构成纤维细胞/细胞学胃黏膜/化学胃黏膜/细胞学胃黏膜/超微结构免疫组织化学小鼠近交C57BL 显微镜检查电子黏蛋白类/分析动物小鼠

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