scholarly journals Increased Cell Proliferation in ChronicHelicobacter pyloriPositive Gastritis and Gastric Carcinoma – Correlation between Immuno-Histochemistry and Tv Image Cytometry

2000 ◽  
Vol 20 (2-3) ◽  
pp. 131-139 ◽  
Author(s):  
Erika Szaleczky ◽  
László Prónai ◽  
Béla Molnár ◽  
Lajos Berczi ◽  
János Fehér ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Epithelial Cell ◽  
Gastric Carcinoma ◽  
Chronic Gastritis ◽  
Image Cytometry ◽  
S Phase ◽  
Epithelial Cell Proliferation ◽  
Cell Proliferation Activity ◽  
Proliferation Activity ◽  
H Pylori

Backgound: Epithelial cell proliferation activity has been reported both to be unaltered and increased inHelicobacter pylori(H. pylori) associated chronic gastritis. The proliferation rate decreased followingH. pylorieradication, but results are controversial whether this change is dependent on the success of eradication. We compared the cell proliferation activity ofH. pyloripositive and negative gastric epithelial biopsies in chronic gastritis with and without intestinal metaplasia (IM) and gastric cancer by the expression of proliferation cell nuclear antigen (PCNA) and Tv image cytometry, and assessed the effect ofH. pylorieradication on the cell proliferation rate in the gastric epithelium.Methods: Brush smears and antral biopsies were taken from 70 patients (42 men, 28 women, mean age 58 ± 15 y.o.) on routine endoscopy. Patients were divided into four groups according to the histology; normal epithelia (n=10), chronic gastritis without IM (n=24), chronic gastritis with IM (n=20), and gastric carcinoma (n=16). Thirty‐three patients wereH. pyloripositive, and success of eradication was controlled in 24 cases. Cell proliferation was measured by immunohistochemistry using PCNA labeling index (LI) and by Tv image cytometry evaluating 12 morpho‐ and densitometric parameters of each nuclei and 6 additional parameters of each smear.Results: PCNA LI, DNA index and S + G2 ratio were all higher in chronic gastritis than in the normal epithelium, and were further increased in carcinoma. The lower PCNA LI observed in chronic gastritis with IM corresponds to the lower S phase ratio determined by Tv image analysis. InH. pyloripositive cases, the proliferation activity was 69.3 ± 13.05% prior to the eradication and it decreased to 55.8 ± 23.31% after the successful eradication therapy. When immunohistochemistry was compared with Tv image cytometry, PCNA LI significantly correlated with the percentage of cells in G1 phase (r=−0.415) and S phase (r=0.385), Integrated Optical Density mean (r=0.598), density maximum (r=0.608), surface (r=0.670), layers (r=0.638), diameter minimum (r=0.619), diameter maximum (r=0.730) and perimeter (r=0.501), respectively (p< 0.05).Conclusions: Epithelial cell turnover is increased in chronic gastritis with or without IM, and in gastric carcinoma. The lower PCNA LI observed in chronic gastritis with IM corresponds to the lower S phase ratio determined by Tv image analysis. Cell proliferation decreases after successfulH. pylorieradication. Both methods proved to be reliable for the determination of epithelial cell proliferation.

scholarly journals KMT2D deficiency disturbs the proliferation and cell cycle activity of dental epithelial cell line (LS8) partially via Wnt signaling

2021 ◽  
Author(s):  
Liping Pang ◽  
Hua Tian ◽  
Xuejun Gao ◽  
Weiping Wang ◽  
Xiaoyan Wang ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Cell Proliferation ◽  
Epithelial Cell ◽  
Wnt Signaling ◽  
Cell Line ◽  
Tooth Development ◽  
Epithelial Cell Line ◽  
Cell Proliferation Activity ◽  
Proliferation Activity

KMT2D, as one of the key histone methyltransferases responsible for histone 3 lysine 4 methylation (H3K4me), has been proved to be the main pathogenic gene of Kabuki syndrome disease. Kabuki patients with KMT2D mutation frequently present various dental abnormalities, including abnormal tooth number and crown morphology. However, the exact function of KMT2D in tooth development remains unclear. In this report, we systematically elucidate the expression pattern of KMT2D in early tooth development and outline the molecular mechanism of KMT2D in dental epithelial cell line. KMT2D and H3K4me mainly expressed in enamel organ and Kmt2d knockdown led to the reduction of cell proliferation activity and cell cycling activity in dental epithelial cell line (LS8). RNA-seq and KEGG enrichment analysis screened out several important pathways that affected by Kmt2d knockdown including Wnt signaling. Consistently, Top/Fop assay confirmed the reduction of Wnt signaling activity in Kmt2d knockdown cells. Nuclear translocation of β-catenin was significantly reduced by Kmt2d knockdown, while lithium chloride (LiCl) partially reversed this phenomenon. Moreover, LiCl partially reversed the decrease of cell proliferation activity and G1 arrest, and the downregulation of Wnt-related genes in Kmt2d knockdown cells. In summary, this study uncovered a pivotal role of histone methyltransferase KMT2D in dental epithelium proliferation and cell cycle homeostasis partially through regulating Wnt/β-catenin signaling. The findings are important for understanding the role of KMT2D and histone methylation in tooth development.

Expression of p21WAF1/CIP1 and p53 proteins in gastric carcinoma: its relationships with cell proliferation activity and prognosis

2001 ◽  
Vol 170 (2) ◽  
pp. 183-189 ◽  
Author(s):  
Xiu Ping Liu ◽  
Kureo Tsushimi ◽  
Mutsuo Tsushimi ◽  
Shigeto Kawauchi ◽  
Atsunori Oga ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Gastric Carcinoma ◽  
Cell Proliferation Activity ◽  
Proliferation Activity

scholarly journals Transforming growth factor beta 1 inhibition of p34cdc2 phosphorylation and histone H1 kinase activity is associated with G1/S-phase growth arrest.

1991 ◽  
Vol 11 (3) ◽  
pp. 1185-1194 ◽  
Author(s):  
P H Howe ◽  
G Draetta ◽  
E B Leof
Keyword(s):  
Cell Proliferation ◽  
Growth Factor ◽  
Epithelial Cell ◽  
Transforming Growth Factor Beta ◽  
Kinase Activity ◽  
Transforming Growth Factor ◽  
S Phase ◽  
Epithelial Cell Proliferation ◽  
Tgf Beta ◽  
Growth Factor Beta

Transforming growth factor beta 1 (TGF beta 1) is a potent inhibitor of epithelial cell proliferation. We present data which indicate that epithelial cell proliferation is inhibited when TGF beta 1 is added throughout the prereplicative G1 phase. Cultures become reversibly blocked in late G1 at the G1/S-phase boundary. The inhibitory effects of TGF beta 1 on cell growth occur in the presence of the RNA synthesis inhibitor 5,6-dichloro-1-beta-D-ribofuranosylbenzimidazole. Associated with this inhibitory effect is a decrease in the phosphorylation and histone H1 kinase activity of the p34cdc2 protein kinase. These data suggest that TGF beta 1 growth inhibition in epithelial cells involves the regulation of p34cdc2 activity at the G1/S transition.

Transforming growth factor beta 1 inhibition of p34cdc2 phosphorylation and histone H1 kinase activity is associated with G1/S-phase growth arrest

1991 ◽  
Vol 11 (3) ◽  
pp. 1185-1194
Author(s):  
P H Howe ◽  
G Draetta ◽  
E B Leof
Keyword(s):  
Cell Proliferation ◽  
Growth Factor ◽  
Epithelial Cell ◽  
Transforming Growth Factor Beta ◽  
Kinase Activity ◽  
Transforming Growth Factor ◽  
S Phase ◽  
Epithelial Cell Proliferation ◽  
Tgf Beta ◽  
Growth Factor Beta

Transforming growth factor beta 1 (TGF beta 1) is a potent inhibitor of epithelial cell proliferation. We present data which indicate that epithelial cell proliferation is inhibited when TGF beta 1 is added throughout the prereplicative G1 phase. Cultures become reversibly blocked in late G1 at the G1/S-phase boundary. The inhibitory effects of TGF beta 1 on cell growth occur in the presence of the RNA synthesis inhibitor 5,6-dichloro-1-beta-D-ribofuranosylbenzimidazole. Associated with this inhibitory effect is a decrease in the phosphorylation and histone H1 kinase activity of the p34cdc2 protein kinase. These data suggest that TGF beta 1 growth inhibition in epithelial cells involves the regulation of p34cdc2 activity at the G1/S transition.

scholarly journals Helicobacter pylori gastritis and epithelial cell proliferation in patients with reflux oesophagitis after treatment with lansoprazole

Gut ◽  
1997 ◽  
Vol 41 (6) ◽  
pp. 740-747 ◽  
Author(s):  
A E Berstad ◽  
J G Hatlebakk ◽  
H Maartmann-Moe ◽  
A Berstad ◽  
P Brandtzaeg
Keyword(s):  
Cell Proliferation ◽  
Helicobacter Pylori ◽  
Epithelial Cell ◽  
Reflux Oesophagitis ◽  
Gastric Body ◽  
Epithelial Cell Proliferation ◽  
Ki 67 ◽  
Before And After ◽  
H Pylori ◽  
Reflux Œsophagitis

Background—Helicobacter pylorigastritis may spread proximally in the stomach during profound acid inhibition.Aims—To examine histological gastric body changes and epithelial cell proliferation before and after treatment with lansoprazole.Patients and methods—Patients diagnosed as having reflux oesophagitis grade 1 or 2 were enrolled and treated for 12 weeks with lansoprazole (30 mg every morning). After 12 weeks, 103 of the 118 patients appeared endoscopically healed and were asymptomatic; they then received maintenance treatment with 15 or 30 mg lansoprazole daily. Biopsy specimens obtained from similar sites before and after treatment, were available from 90 patients after a median of 64 weeks (range 15–73 weeks). Epithelial cell proliferation was determined by the number of Ki-67 antigen positive cells per gland.Results—Of these 90 patients, 44 (49%) were found to be infected with H pylori. Their median inflammation score had increased from grade 1 before to grade 2 after treatment (p<0.0001). Initially, the number of Ki-67 antigen positive cells per gland was significantly higher in the H pyloriinfected than in the uninfected group and increased further after treatment (p<0.0001). In uninfected patients, no significant change in inflammation or proliferation occurred during treatment.Conclusions—A marked increase in body gastritis was observed in H pylori infected individuals during long term treatment with the proton pump inhibitor lansoprazole. Epithelial cell proliferation and atrophy also increased in infected but not in uninfected patients.

scholarly journals Enhanced intestinal epithelial cell proliferation in diabetic rats correlates with β-catenin accumulation

2015 ◽  
Vol 226 (3) ◽  
pp. 135-143 ◽  
Author(s):  
Tatiana Dorfman ◽  
Yulia Pollak ◽  
Rima Sohotnik ◽  
Arnold G Coran ◽  
Jacob Bejar ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Epithelial Cell ◽  
Real Time ◽  
Real Time Pcr ◽  
Intestinal Epithelial Cell ◽  
Diabetic Rats ◽  
Male Rats ◽  
Intestinal Cell ◽  
Intestinal Epithelial ◽  
Epithelial Cell Proliferation

The Wnt/β-catenin signaling cascade is implicated in the control of stem cell activity, cell proliferation, and cell survival of the gastrointestinal epithelium. Recent evidence indicates that the Wnt/β-catenin pathway is activated under diabetic conditions. The purpose of this study was to evaluate the role of Wnt/β-catenin signaling during diabetes-induced enteropathy in a rat model. Male rats were divided into three groups: control rats received injections of vehicle; diabetic rats received injections of one dose of streptozotocin (STZ); and diabetic–insulin rats received injections of STZ and were treated with insulin given subcutaneously at a dose of 1 U/kg twice daily. Rats were killed on day 7. Wnt/β-catenin-related genes and expression of proteins was determined using real-time PCR, western blotting, and immunohistochemistry. Among 13 genes identified by real-time PCR, seven genes were upregulated in diabetic rats compared with control animals including the target genes c-Myc and Tcf4. Diabetic rats also showed a significant increase in β-catenin protein compared with control animals. Treatment of diabetic rats attenuated the stimulating effect of diabetes on intestinal cell proliferation and Wnt/β-catenin signaling. In conclusion, enhanced intestinal epithelial cell proliferation in diabetic rats correlates with β-catenin accumulation.

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