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Epithelial Proliferation (epithelial + proliferation)

Distribution by Scientific Domains

Medical Sciences	83%
Life Sciences	12%

Distribution within Medical Sciences

Gastroenterology & Hepatology	19%
11 Other Subdomains	62%

Selected Abstracts

DOSE-DEPENDENT EFFECT OF LUMINAL BUTYRATE ON EPITHELIAL PROLIFERATION IN THE DISTAL COLON OF RATS

JOURNAL OF GASTROENTEROLOGY AND HEPATOLOGY, Issue 2001
S Sengupta
Butyrate, a major product of bacterial fermentation of dietary fibre, is trophic to the colonic epithelium, when deprived of dietary fibre or faecal stream. However, the dose,response relationship of butyrate to this trophic effect is not known. The mechanism of this effect is still debated and how it relates to the antitumorigenic action of butyrate is unclear. Aim, To characterise the dose,response relationship of the effect of butyrate delivered topically to the distal colon on fibre-deprived atrophic colonic epithelium in rats. Methods, Sixty-four male Sprague,Dawley rats were maintained on a fibre-free AIN 93G diet for 3 weeks to induce mucosal atrophy in the colon. The rats then underwent laparotomy for colonic intubation, in which a polyethylene tube was positioned at the proximal end of the distal colon via a caecotomy. After recovering from surgery, they were randomly divided into five groups, which were given for 4 days twice daily infusions of 0.5 mL butyrate at doses of 0, 10, 20, 40 or 80 mm (at which complete reversal of atrophy has been previously observed). Prior to sacrifice, the rats were injected intraperitoneally with vincristine to induce mitotic arrest. Crypt column heights and mitotic arrests were quantified by light microscopy. Results, All treatment groups were healthy and stress-free. The mucosa of vehicle-infused rats was atrophic (mean 38 cells/crypt). Effects of twice daily infusions of butyrate were first observed on cell proliferation (number of mitotic arrests per crypt column) at 10 mm, and increased linearly to 80 mm. Crypt column height increased linearly from 20 mm to 80 mm, at which a mean of 45 cells/crypt were observed (the number usually observed in chow-fed healthy rats). The mitotic index (number of mitotic arrests per 100 crypt cells) also increased linearly from 10 mm. Conclusions, Butyrate's trophic effect showed a linear dose,dependent relationship. Although a maximal effect was not convincingly demonstrated, the results indicate that very small amounts of butyrate are required to affect epithelial proliferation. Since much higher luminal delivery is required to suppress tumorigenesis in this model, the mechanism by which butyrate exerts its trophic and antitumorigenic effects are likely to be different. [source]

Aggressiveness and Quantification of Epithelial Proliferation of Middle Ear Cholesteatoma by MIB1

THE LARYNGOSCOPE, Issue 2 2003
Y. Mallet MD
Abstract Objective To assess an easy method that predicts cholesteatoma aggressiveness. Study Design An experimental prospective study. Methods Monoclonal antibody MIB1 was used to determine epithelium proliferation in 91 cholesteatomatous ears. Clinical and surgical parameters were compared with proliferation activity to determine pathological and clinical correlation. Results Statistical correlations were established between hyperproliferation of the cholesteatoma and severe bone erosion (leading to major cholesteatoma complications) and between hyperproliferation and middle ear inflammation (associated with more surgical difficulties and a higher risk of recurrence). A high proliferation index was also found in children's cholesteatoma, which is known to have more aggressive behavior. Conclusion Immunohistochemical use of the MIB1 antibody is a simple technique that can help to determine the aggressiveness of a cholesteatoma. [source]

Regulation of keratinocyte growth factor and scatter factor in cyclosporin-induced gingival overgrowth

JOURNAL OF ORAL PATHOLOGY & MEDICINE, Issue 7 2004
P. L. Hyland
Background:, Epithelial proliferation is a histological characteristic of drug-induced gingival overgrowth. Keratinocyte growth factor (KGF) and scatter factor (SF) are fibroblast-derived growth factors with potent mitogenic and motogenic effects on epithelial cells, and, therefore, could be involved in the pathogenesis of gingival overgrowth. The aims of this study were to investigate: (i) the effects of cyclosporin on KGF and SF expression by gingival fibroblasts; and (ii) the expression levels of KGF and SF mRNA in normal and overgrown gingival tissue. Methods:, The KGF and SF protein production was determined by enzyme-linked immunosorbent assay. Relative levels of KGF and SF mRNA expression were determined using semi-quantitative reverse transcriptase polymerase chain reaction. Expression levels in biopsies of normal and overgrown gum were also determined. Results:, In overgrown fibroblasts, 500 ng/ml cyclosporin significantly inhibited KGF and SF mRNA and protein while 2000 ng/ml cyclosporin induced a stimulatory effect. In normal cells cyclosporin significantly increased both KGF and SF. KGF and SF mRNA was detected in both normal and overgrown tissues with a tendency towards increased expression levels in overgrown tissue. Conclusion:, These results suggest that KGF and SF may have an important role in cyclosporin-induced gingival overgrowth. [source]

Protection of the Peyer's patch-associated crypt and villus epithelium against methotrexate-induced damage is based on its distinct regulation of proliferation

THE JOURNAL OF PATHOLOGY, Issue 1 2002
Ingrid B. Renes
Abstract The crypt and villus epithelium associated with Peyer's patches (PPs) is largely spared from methotrexate (MTX)-induced damage, compared with the non-patch (NP) epithelium. To assess the mechanism(s) preventing damage to the PP epithelium after MTX treatment, epithelial proliferation, apoptosis, and cell functions were studied in a rat-MTX model. Small intestinal segments containing PPs were excised after MTX treatment. Epithelial proliferation and apoptosis were assessed by detection of incorporated BrdU and cleaved caspase-3, respectively. Epithelial functions were determined by the expression of cell type-specific gene products at mRNA and protein level. Before and after MTX treatment, the number of BrdU-positive cells was higher in PP crypts than in NP crypts. BrdU incorporation was diminished in NP crypts, while in PP crypts incorporation was hardly affected. In PP and NP crypts, similar and increased levels of cleaved caspase-3-positive cells were observed after MTX. The enterocyte markers, sucrase-isomaltase, sodium-glucose co-transporter 1, glucose transporters 2 and 5, and intestinal and liver fatty acid binding protein, were down-regulated after MTX in NP epithelium but not in PP epithelium. In contrast, expression of the goblet cell markers, Muc2 and trefoil factor 3, and the Paneth cell marker, lysozyme, was maintained after MTX in both PP and NP epithelium. In conclusion, as MTX-induced apoptosis was similar in PP and NP crypts, the protection of the PP epithelium seems to be based on differences in the regulation of epithelial proliferation. Enterocyte function in the PP epithelium was unaffected by MTX treatment. Goblet and Paneth cell function was maintained in both NP and PP epithelium. Copyright © 2002 John Wiley & Sons, Ltd. [source]

Neurokinin-1 receptor activation induces reactive oxygen species and epithelial damage in allergic airway inflammation

CLINICAL & EXPERIMENTAL ALLERGY, Issue 12 2007
J. Springer
Summary Background An induction of reactive oxygen species (ROS) is characteristic for inflammation but the exact pathways have not been identified for allergic airway diseases so far. Objective The aim of this study was to characterize the role of the tachykinin NK-1 receptor on ROS production during allergen challenge and subsequent inflammation and remodelling. Methods Precision-cut lung slices of ovalbumin (OVA)-sensitized mice were cultivated and ROS-generation in response to OVA challenge (10 ,g/mL) was examined by the 2,,7,-dichloroflourescein-diacetate method. Long-term ROS effects on epithelial proliferation were investigated by 5-bromo-2,-deoxyuridine incorporation (72 h). In vivo, the results were validated in OVA-sensitized animals which were treated intra-nasally with either placebo, the tachykinin neurokinin 1 (NK-1) receptor antagonist SR 140333 or the anti-oxidant N -acetylcystein (NAC) before allergen challenge. Inflammatory infiltration and remodelling were assessed 48 h after allergen challenge. Results ROS generation was increased by 3.7-fold, which was inhibited by SR 140333. [Sar9,Met11(O2)]-Substance P (5 nm) caused a tachykinin NK-1 receptor-dependent fourfold increase in ROS generation. Epithelial proliferation was decreased by 68% by incubation with [Sar9,Met11(O2)]-SP over 72 h. In-vivo, treatment with SR 140333 and NAC reduced epithelial damage (91.4% and 76.8% vs. placebo, respectively, P<0.01) and goblet cell hyperplasia (67.4% and 50.1% vs. placebo, respectively, P<0.05), and decreased inflammatory cell influx (65.3% and 45.3% vs. placebo, respectively, P<0.01). Conclusion Allergen challenge induces ROS in a tachykinin NK-1 receptor-dependent manner. Inhibition of the tachykinin NK-1 receptor reduces epithelial damage and subsequent remodelling in vivo. Therefore, patients may possibly benefit from treatment regime that includes radical scavengers or tachykinin NK-1 receptor antagonists. [source]

E2F4 expression is required for cell cycle progression of normal intestinal crypt cells and colorectal cancer cells

JOURNAL OF CELLULAR PHYSIOLOGY, Issue 2 2009
Hugo Garneau
The generation of knock-out mice for E2F4 gene expression has suggested a role for this transcription factor in establishing and/or maintaining the intestinal crypt compartment. Having previously demonstrated that E2F4 is cytoplasmic in quiescent-differentiated cells but nuclear in growth factor-stimulated proliferative cells, the present study was aimed at determining the role of E2F4 in the control of human intestinal epithelial proliferation. Results herein demonstrate that lentiviral infection of an shRNA which specifically knocked-down E2F4 expression slowed down G1/S phase transition and the proliferation rate of normal human intestinal epithelial cells (HIEC) and of colon cancer cells. Protein expression of Cdk2, cyclins D1 and A, Cdc25A and c-myc was markedly down-regulated in shE2F4-expressing cells; by contrast, expression of the cell cycle inhibitors p21Cip/Waf and p27Kip1 was increased. In addition, the expression of many genes involved in DNA synthesis was down-regulated in shE2F4-expressing cells, whereas no modulation in E2F1 expression was observed. A decrease in E2F4 in colon cancer cell lines also resulted in a reduction in soft-agar growth capacity. Immunofluorescence experiments in human fetal intestine revealed that cells expressing high nuclear levels of E2F4 also expressed cyclin A protein. Lastly, E2F4 and its target cyclin A were up-regulated and mostly nuclear in human colorectal tumor cells in comparison to the corresponding benign epithelium. These results indicate that nuclear E2F4 may be determinant in the promotion of proliferation of human intestinal epithelial crypt cells and colorectal cancer cells. J. Cell. Physiol. 221: 350,358, 2009. © 2009 Wiley-Liss, Inc. [source]

Beneficial effects of growth hormone on bacterial translocation during the course of acute necrotizing pancreatitis in rats

JOURNAL OF DIGESTIVE DISEASES, Issue 1 2001
Wang Xingpeng
OBJECTIVE: Because bacterial translocation from the gut is one of the important sources of bacterial infection in acute necrotizing pancreatitis (ANP), and growth hormone (GH) has the ability to promote intestinal epithelial proliferation, we investigated the effects of GH on bacterial translocation in a rat ANP model. METHODS: Acute necrotizing pancreatitis was induced in rats via injection of 5% sodium taurocholate into the biliopancreatic duct. The rats with ANP were treated with either human recombinant GH or a placebo. Laparotomized animals without ANP induction (sham operation) served as controls. Twenty-four hours after the operation, blood was drawn for bacterial culture and determinations of amylase, lipase and endotoxin. Peritoneal fluid and specimens of mesenteric lymph nodes (MLN), liver, pancreas and spleen were taken for bacterial culture by standard techniques. Intestinal mucosal permeability was assessed by measuring the movement of [125I]-labeled albumin from blood to the intestinal lumen. Insulin-like growth factor-1 (IGF-1) mRNA was detected in the liver and ileum by reverse transcription,polymerase chain reaction (RT-PCR). Morphological changes in the pancreas and ileum were also analyzed. RESULTS: Administration of GH significantly decreased the activity of serum amylase and lipase, decreased the plasma endotoxin level and reduced the incidence of bacterial translocation. Moreover, the survival rate of ANP rats was improved. The severity of inflammation in the pancreas and ileum was reduced by GH treatment. Ileal mucosal thickness, villus height and crypt depth in GH-treated rats were obviously increased as compared with those of ANP rats. The intestinal permeability was markedly decreased in the GH group as compared with the ANP group. GH treatment resulted in upregulation of IGF-1 mRNA expression in ileum, but not in liver. CONCLUSIONS: These results suggest that exogenous GH has beneficial effects in maintaining the integrity of the intestinal mucosal barrier and reducing the incidence of bacterial translocation in rats with ANP. One of the mechanisms might be the upregulation of IGF-1 mRNA in the intestine by GH. [source]

Can Renal Acute Tubular Necrosis Be Differentiated from Autolysis at Autopsy?,

JOURNAL OF FORENSIC SCIENCES, Issue 2 2009
Linda Kocovski B.Sc.
Abstract:, We investigate the morphological characteristics that may differentiate between ischemic acute tubular necrosis (ATN) and autolysis in postmortem samples. Renal tissue from 57 postmortem cases with an antemortem diagnosis of ATN and 57 age-/sex-matched control cases were examined for 10 morphological characteristics: epithelial proliferation (Ki-67 immunoperoxidase positivity), fibrin thrombi, tubular epithelial whorls, mitoses, casts, autolysis, tubulorrhexis, epithelial flattening, interstitial inflammation, and interstitial expansion. Tubular epithelial whorls were found in 16 ATN cases and were absent in controls. These findings suggest that specific morphological criteria may distinguish ischemic ATN from autolysis. Diagnoses of ATN may be confirmed using these combined criteria as contributing to cause of death and/or to ascertain previously undiagnosed cases of ATN postmortem. [source]

DOSE-DEPENDENT EFFECT OF LUMINAL BUTYRATE ON EPITHELIAL PROLIFERATION IN THE DISTAL COLON OF RATS

The effects of high-dose esomeprazole on gastric and oesophageal acid exposure and molecular markers in Barrett's oesophagus

ALIMENTARY PHARMACOLOGY & THERAPEUTICS, Issue 8 2010
A. Abu-Sneineh
Aliment Pharmacol Ther 2010; 32: 1023,1030 Summary Background, Acid reflux is often difficult to control medically. Aim, To assess the effect of 40 mg twice daily esomeprazole (high-dose) on gastric and oesophageal pH and symptoms, and biomarkers relevant to adenocarcinoma, in patients with Barrett's oesophagus (BO). Methods, Eighteen patients, treated with proton pump inhibitors as prescribed by their treating doctor, had their therapy increased to high-dose esomeprazole for 6 months. Results, At entry into the study, 9/18 patients had excessive 24-h oesophageal acid exposure, and gastric pH remained <4 for >16 h in 8/18. With high-dose esomeprazole, excessive acid exposure occurred in 2/18 patients, and gastric pH <4 was decreased from 38% of overall recording time and 53% of the nocturnal period to 15% and 17%, respectively (P < 0.001). There was a reduction in self-assessed symptoms of heartburn (P = 0.0005) and regurgitation (P < 0.0001), and inflammation and proliferation in the Barrett's mucosa. There was no significant change in p53, MGMT or COX-2 expression, or in aberrant DNA methylation. Conclusions, High-dose esomeprazole achieved higher levels of gastric acid suppression and control of oesophageal acid reflux and symptoms, with significant decreases in inflammation and epithelial proliferation. There was no reversal of aberrant DNA methylation. [source]

Gastric epithelial cell proliferation and apoptosis in Helicobacter pylori-infected mice

ALIMENTARY PHARMACOLOGY & THERAPEUTICS, Issue 2000
T. Yamaguchi
Summary Background: Helicobacter pylori causes gastritis and is strongly associated with gastroduodenal ulcer and gastric cancer. The bacterium is associated with an increased rate of epithelial proliferation, which can be reversed by eradication of the organism. The mechanism of this response is not known, but this epithelial proliferation is one of the risk factors for developing gastric carcinoma. Recently, apoptosis also was found to be increased in the gastric mucosa of persons carrying H. pylori. Methods: cagA -positive H. pylori isolated from a human gastric ulcer was inoculated into BALB/C mice. At 4, 6, 12, 18 and 24 weeks, mice were injected with bromodeoxyuridine 5 mg/kg and killed 1 h later. Proliferation was analysed by histochemical staining for BrdU; apoptosis was examined by the TUNEL assay. Results: The number of BrdU-labelled cells in the antrum was significantly increased by H. pylori infection beginning 12 weeks after infection. The number of apoptotic cells in this tissue was increased significantly by 6 weeks after inoculation. Conclusion: The proliferation observed in H. pylori infection may be a response to increased apoptosis. [source]

Novel renoprotective actions of erythropoietin: New uses for an old hormone (Review Article)

NEPHROLOGY, Issue 4 2006
DAVID W JOHNSON
SUMMARY: Erythropoietin (EPO) has been used widely for the treatment of anaemia associated with chronic kidney disease and cancer chemotherapy for nearly 20 years. More recently, EPO has been found to interact with its receptor (EPO-R) expressed in a large variety of non-haematopoietic tissues to induce a range of cytoprotective cellular responses, including mitogenesis, angiogenesis, inhibition of apoptosis and promotion of vascular repair through mobilization of endothelial progenitor cells from the bone marrow. Administration of EPO or its analogue, darbepoetin, promotes impressive renoprotection in experimental ischaemic and toxic acute renal failure, as evidenced by suppressed tubular epithelial apoptosis, enhanced tubular epithelial proliferation and hastened functional recovery. This effect is still apparent when administration is delayed up to 6 h after the onset of injury and can be dissociated from its haematological effects. Based on these highly encouraging results, at least one large randomized controlled trial of EPO therapy in ischaemic acute renal failure is currently underway. Preliminary experimental and clinical evidence also indicates that EPO may be renoprotective in chronic kidney disease. The purpose of the present article is to review the renoprotective benefits of different protocols of EPO therapy in the settings of acute and chronic kidney failure and the potential mechanisms underpinning these renoprotective actions. Gaining further insight into the pleiotropic actions of EPO will hopefully eventuate in much-needed, novel therapeutic strategies for patients with kidney disease. [source]

Ki-67 expression in non-tumour epithelium adjacent to oral cancer as risk marker for multiple oral tumours

ORAL DISEASES, Issue 1 2010
MA González-Moles
Objective:, The aim of this study was to determine whether the differential assessment of epithelial proliferation is useful to diagnose premalignant fields and assess the risk of multiple tumours. Material and methods:, We analysed 83 oral carcinomas with associated non-tumour epithelium classified as distant or close according to its distance (> or <1 cm) from the invasion point, and as squamous hyperplasia, mild, moderate, severe dysplasia or carcinoma in situ. Twenty-five healthy oral mucosa samples were used as controls. An immunohistochemical technique was applied using Mib-1. Ki-67 in premalignant epithelium was assessed in basal layer, parabasal layer, medium and upper third. Results:, Parabasal expression was significantly higher or showed a tendency to be higher in close and distant epithelia with any histological grade than in the controls. Parabasal Ki-67 significantly differed between distant epithelia associated with multiple vs single tumours (P < 0.001) and between distant epithelia associated with multiple tumours vs controls (P < 0.001). This difference was not observed between distant epithelia associated with single tumours and controls (P = 0.175). The cut-off point that differentiated epithelia associated with multiple tumours was >50% of Ki-67 + parabasal cells in distant epithelia, which yielded 0.88 sensitivity and 0.79 specificity. Conclusions:, The concept of a precancerous field may be linked to an increase in the proliferative activity of parabasal cells. [source]

Immunohistochemical Studies on Oestrogen Receptor Alpha (ER,) and the Proliferative Marker Ki-67 in the Sow Uterus at Different Stages of the Oestrous Cycle

REPRODUCTION IN DOMESTIC ANIMALS, Issue 1 2003
S Sukjumlong
Contents In order to better understand physiological changes during the different stages of the oestrous cycle, immunohistochemistry was used in the present study to investigate the distribution of oestrogen receptor alpha (ER,) as well as the proliferative marker Ki-67, in the sow uterus during the oestrous cycle. Uterine samples were collected from multiparous sows with normal reproductive performance at selected stages of the oestrous cycle: at late dioestrus (d 17), prooestrus (d 19), oestrous (d 1), early dioestrus (d 4) and dioestrus (d 11,12), respectively. The tissue samples were fixed in 10% formaldehyde, embedded in paraffin and subjected to immunohistochemistry using monoclonal antibodies against ER, (C-311) and Ki-67 (MM-1). In general, the immunostaining of both ER, and Ki-67 was confined to nuclei of the target cells. Variations were seen, not only at the different stages of the oestrous cycle, but also in the different tissue compartments of the uterus. In the epithelia, the strongest ER, staining and highest amount of positive Ki-67 cells were found at early dioestrus. In the myometrium, the highest levels of staining of both ER, and Ki-67 positive cells were found at pro-oestrus and oestrus. For the proliferative marker, Ki-67, no positive cells were found at dioestrus and late dioestrus in the epithelium and myometrium. In the connective tissue stroma (subepithelial layer), the highest number of ER, positive cells were found at oestrus, which was significantly different compared with other stages (p,0.05), whereas the levels of Ki-67 positive cells were relatively low and did not differ between the stages examined. Significant correlations between the number of ER, positive cells in the stroma and Ki-67 positive cells in the epithelia were observed. This suggests indirect regulatory mechanisms on epithelial proliferation via ER, in the stroma. In conclusion, these findings in the sow uterus show that the presence of ER, as well as Ki-67 protein varies not only between different stages of the oestrous cycle but also between different tissue compartments of the uterus. These findings indicate various regulatory mechanisms and stress the importance of localising ER, and proliferating cells in different uterine tissues. [source]

Effects of melatonin on the oxidant/antioxidant status and lung histopathology in rabbits exposed to cigarette smoke

RESPIROLOGY, Issue 4 2006
Mehmet UNLU
Objectives and background: To evaluate the effects of cigarette smoking on the histopathology and the oxidant/antioxidant status of the lungs and to test the potential antioxidant benefits of melatonin on these induced changes. Methodology: Rabbits were exposed to cigarette smoke in a glass chamber for 1 h daily for 1 month with or without intraperitoneal melatonin injection. A melatonin control group was given intraperitoneal melatonin only. A control group was exposed to clean air only. At the end of 1 month, animals were sacrificed and lung tissues were examined histopathologically. Blood levels of protein sulphydryls, carbonyls, prostaglandin F2, (PGF2,), malondialdehyde (MDA), glutathione peroxidase and superoxide dismutase (SOD) were measured. Results: Intraparenchymal vascular congestion and thrombosis, intraparenchymal haemorrhage, respiratory epithelial proliferation, number of macrophages in the alveolar and bronchial lumen, alveolar destruction, emphysematous changes and bronchoalveolar haemorrhage scores were significantly increased in rabbits exposed to cigarette smoke compared with the control group. Protein sulphydryls and SOD levels were significantly decreased; carbonyls, PGF2, and MDA levels were significantly increased in the smoke exposed rabbits. Administration of melatonin to rabbits exposed to cigarette smoke caused a reduction in the bronchoalveolar haemorrhage score and blood carbonyls levels. Other parameters were unaffected by melatonin. Conclusion: Exposure to cigarette smoke causes severe histopathological changes and negatively affects the oxidant/antioxidant status in the lungs of rabbits. A low daily dose of melatonin has some protective effects on histopathological changes and oxidant/antioxidant status of the lungs in smoke exposed rabbits. [source]

Long-term infection with Helicobacter felis and inactivation of the tumour suppressor gene p53 cumulatively enhance the gastric mutation frequency in Big Blue® transgenic mice

THE JOURNAL OF PATHOLOGY, Issue 4 2003
Peter J Jenks
Abstract The aims of this study were to determine whether colonization with Helicobacter felis resulted in the accumulation of mutations within murine gastric tissue and whether the degree of genetic damage was increased by p53 deficiency. Female C57BL/6 mice carrying either the lambda/lacI transgene (Big Blue® transgenic mice) or the lambda/lacI transgene and deficient in one allele of the p53 tumour suppressor gene (TSG-p53®/Big Blue®) were inoculated with H felis. Seven months after inoculation, mutations in the target lacI gene were assessed using the Big Blue® transgenic mutagenesis assay system in these animals and in controls. There was an approximately two-fold increase in lacI mutations in gastric mucosa harvested from mice infected with H felis and also from non-infected mice heterozygous for the p53 allele relative to wild-type mice. The mutation frequency in mice infected with H felis and deficient in one allele of p53 was increased approximately three-fold. Active gastric inflammation was significantly greater in H felis -infected p53 hemizygous mice compared with H felis p53 wild-type mice. Gastric epithelial proliferation was similarly increased with infection in both of these latter groups of mice. In infected mice, there was a significant correlation between the mutation frequency and the degree of active gastric inflammation. These data suggest a synergistic action between infection with H felis and p53 deficiency in the accumulation of mutations within gastric tissue. Active neutrophil infiltration in gastric Helicobacter infection may contribute to the increased levels of mutation observed. Copyright © 2003 John Wiley & Sons, Ltd. [source]

Protection of the Peyer's patch-associated crypt and villus epithelium against methotrexate-induced damage is based on its distinct regulation of proliferation

FGF17 is an autocrine prostatic epithelial growth factor and is upregulated in benign prostatic hyperplasia

THE PROSTATE, Issue 1 2004
Nathaniel Polnaszek
Abstract BACKGROUND Fibroblast growth factors (FGFs) are known to play an important role in the growth of prostatic epithelial cells. Benign prostatic hyperplasia (BPH) is characterized by increased epithelial and stromal proliferation within the transition zone of the prostate. FGF2, FGF7, and FGF9 are expressed in BPH tissue but expression of FGF17 has not been previously characterized in human prostate tissue. METHODS Expression of FGF17 in human prostate tissue and primary cultures of prostatic epithelial and stromal cells was determined by reverse-transcriptase polymerase chain reaction (RT-PCR). Growth response to FGF17 was assessed by addition of recombinant FGF17 to immortalized normal and neoplastic epithelial cell lines and primary cultures of prostatic stromal cells in the presence of insulin. Quantitative analysis of expression of FGF17 relative to keratin 18 and/or ,-actin in normal and hyperplastic prostate and prostate carcinoma was carried out by real-time quantitative RT-PCR. RESULTS FGF17 is expressed by prostatic epithelial cells and can act as an autocrine growth factor for immortalized and neoplastic prostatic epithelial cells. It can also promote stromal proliferation, although only at higher concentrations. Expression of FGF17 per epithelial cell was increased 2-fold in BPH. CONCLUSIONS FGF17 is expressed by normal, hyperplastic, and neoplastic prostatic epithelial cells and can promote epithelial proliferation in an autocrine manner. FGF17 expression is increased 2-fold in BPH and may contribute to the increased epithelial proliferation seen in this disease. © 2004 Wiley-Liss, Inc. [source]

Epithelial stem cell-related alterations in Trichinella spiralis -infected small intestine

CELL PROLIFERATION, Issue 3 2009
R. Walsh
Objectives:, Infection of mice with the parasite Trichinella spiralis leads to small intestinal inflammation, characterized by changes in mucosal architecture and subpopulations of epithelial cells. This model has been used to explore changes in the epithelial proliferative cell population and expression of transforming growth factor-beta (TGF-,). Materials and methods:, Histochemical and immunohistochemical studies were undertaken in duodenal samples. Location and number of Ki-67-positive cells were assessed using Score and Wincrypts program. Changes in mRNA transcripts were studied by real-time RT-PCR. Results:,T. spiralis infection induced an increase in total number of proliferative (Ki-67-positive) cells per half crypt on day 2 post-infection. Transcription of Math1, a transcription factor required for secretory cell differentiation in the intestine, was up-regulated on days 6,18 post-infection. At these time points, numbers of Paneth cells at the crypt base were also increased and the epithelial proliferative zone was shifted up the crypt-villus axis. Transcription of TGF-, isoforms within the small intestine was up-regulated on days 6 and 12 post-infection, but anti-TGF-, antibody treatment had no effect on T. spiralis -induced changes in mucosal architecture or increase in Paneth/intermediate cells. Conclusions:,T. spiralis infection promotes an initial increase in small intestinal epithelial proliferation and subsequent cell differentiation along the secretory cell lineage. The resulting increase in numbers of Paneth cells at the crypt base causes the proliferative zone to move up the crypt-villus axis. Further studies are required to determine the significance of an increase in the expression of TGF-, transcripts. [source]

Laminin-2 stimulates the proliferation of epithelial cells in a conjunctival epithelial cell line

CELL PROLIFERATION, Issue 2 2004
J. Dowgiert
To test the hypothesis that LN-2 can additionally modulate epithelial cell biology, an analysis of the role of LN-2 in cell adhesion, activation of signalling intermediates and proliferation was undertaken. A virally transformed human conjunctival epithelial cell line (HC0597) was utilized in this study. Adhesion assays using function-inhibiting antibodies demonstrated that ,3,1 integrin is essential for the rapid attachment of conjunctival epithelial cells to LN-2. Bromodeoxyuridine (BrdU) incorporation analyses revealed that, compared with LN-1 or LN-10, LN-2 significantly promotes epithelial proliferation. Phosphorylation of the signalling intermediates Erk1/2 and Akt-1 was observed within 15 min of cell adhesion to LN-2. Inhibiting ,3,1 integrin function decreased total cellular phosphotyrosine levels, specifically inhibited phosphorylation of Erk1/2 and Akt-1, and dampened the proliferation response of epithelial cells adherent to LN-2. Inhibition of Erk or Akt activation inhibited cell proliferation in a dose-dependent manner. However, the inhibition of Erk resulted in a stronger suppression of proliferation compared with Akt inhibition. From these results, it is concluded that human conjunctival epithelial cells adhere to immobilized LN-2 using ,3,1 integrin. ,3,1 integrin/LN-2 signalling, transduced primarily through an Erk pathway, enhances epithelial cell proliferation. These results demonstrate that LN-2 can impact on epithelial cell biology in addition to nerve and muscle, and provide information regarding the role of this isoform in ocular surface epithelial cells. [source]

Neurokinin-1 receptor activation induces reactive oxygen species and epithelial damage in allergic airway inflammation

Is there a special relationship between CD30-positive lymphoproliferative disorders and epidermal proliferation?

JOURNAL OF CUTANEOUS PATHOLOGY, Issue 6 2000
Yvana P. Cespedes
The relationship between CD30+ lymphoma and epithelial proliferations is not well defined. CD30+ lymphoma and lymphomatoid papulos (LyP) share immunohistochemical epitopes and some other features. A single case of LyP associated with multiple keratoacanthomas (KAs) was recently reported. We report two cases of atypical lymphocytic proliferation with features of CD30+ lymphoma and LyP intimately associated to KA and squamous cell carcinoma (SCC), KA type. This similar combination of an epidermal tumor and apparent involvement with atypical lymphocytic infiltrates raises the possibility of an association between the two entities. We speculate that the association may be more than expected to occur by chance and suggest several mechanisms by which the association may evolve. [source]

Double immunostaining with p63 and high-molecular-weight cytokeratins distinguishes borderline papillary lesions of the breast

PATHOLOGY INTERNATIONAL, Issue 3 2007
Shu Ichihara
Papillary breast lesions remain a source of diagnostic confusion because the full range of epithelial proliferations may arise within, or secondarily involve, papilloma. The expression of p63 and high-molecular-weight cytokeratins (HMWCK) was studied simultaneously in 33 papillary lesions including intraductal papilloma (IP, n = 10), atypical papilloma (AP, n = 8) and intraductal papillary carcinoma (IPC, n = 15) by double immunostaining. The myoepithelial cell nuclei were stained dark brown whereas the cytoplasms of usual ductal hyperplasia (UDH) and myoepithelium were stained purple. The myoepithelial layer was recognized as a dark brown dotted line at the epithelial stromal junction in all IP (10/10), most AP (7/8) and some IPC (7/15), suggesting that the retained myoepithelial layer in the papillary processes does not necessarily guarantee benignity. However, the malignant epithelial cells in AP and IPC were typically recognized as monotonous populations unstained with either chromogen. These monotonous cells contrasted with the proliferating cells of UDH in papilloma, which had intense purple cytoplasm in a mosaic-like fashion. The present data suggest that the double immunostaining with the two popular antibodies p63 and HMWCK is a useful tool for reproducible classification of papillary breast lesions. [source]