Epithelial cell proliferation activity of the biliary ductal system with congenital biliary malformations

1999 ◽  
Vol 6 (3) ◽  
pp. 294-302 ◽  
Author(s):  
Hideki Fujii ◽  
Yang Yang ◽  
Ruifang Tang ◽  
Kazuyosi Kunitomo ◽  
Jun Itakura ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Epithelial Cell ◽  
Epithelial Cell Proliferation ◽  
Ductal System ◽  
Cell Proliferation Activity ◽  
Proliferation Activity

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.

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.

scholarly journals Deaf-1 regulates epithelial cell proliferation and side-branching in the mammary gland

2008 ◽  
Vol 8 (1) ◽  
pp. 94 ◽  
Author(s):  
Holly E Barker ◽  
Gordon K Smyth ◽  
James Wettenhall ◽  
Teresa A Ward ◽  
Mary L Bath ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Mammary Gland ◽  
Epithelial Cell ◽  
Epithelial Cell Proliferation

Cyclin D1 expression in astrocytomas is associated with cell proliferation activity and patient prognosis

1999 ◽  
Vol 188 (3) ◽  
pp. 289-293 ◽  
Author(s):  
Satu-Leena Sallinen ◽  
Pauli K. Sallinen ◽  
Juha T. Kononen ◽  
Kirsi M. Syrj�koski ◽  
Nina N. Nupponen ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Cyclin D1 ◽  
Cell Proliferation Activity ◽  
Proliferation Activity ◽  
Patient Prognosis

scholarly journals c-Src inactivation reduces renal epithelial cell-matrix adhesion, proliferation, and cyst formation

2011 ◽  
Vol 301 (2) ◽  
pp. C522-C529 ◽  
Author(s):  
Justine Elliott ◽  
Nadezhda N. Zheleznova ◽  
Patricia D. Wilson
Keyword(s):  
Cell Proliferation ◽  
Epithelial Cell ◽  
Epithelial Cells ◽  
Collecting Duct ◽  
Specific Inhibitor ◽  
Cell Phenotype ◽  
Epithelial Cell Proliferation ◽  
Matrix Adhesion ◽  
Cyst Lining

c-Src is a non-receptor tyrosine kinase whose activity is induced by phosphorylation at Y418 and translocation from the cytoplasm to the cell membrane. Increased activity of c-Src has been associated with cell proliferation, matrix adhesion, motility, and apoptosis in tumors. Immunohistochemistry suggested that activated (pY418)-Src activity is increased in cyst-lining autosomal dominant polycystic kidney disease (ADPKD) epithelial cells in human and mouse ADPKD. Western blot analysis showed that SKI-606 (Wyeth) is a specific inhibitor of pY418-Src without demonstrable effects on epidermal growth factor receptor or ErbB2 activity in renal epithelia. In vitro studies on mouse inner medullary collecting duct (mIMCD) cells and human ADPKD cyst-lining epithelial cells showed that SKI-606 inhibited epithelial cell proliferation over a 24-h time frame. In addition, SKI-606 treatment caused a striking statistically significant decrease in adhesion of mIMCD and human ADPKD to extracellular collagen matrix. Retained viability of unattached cells was consistent with a primary effect on epithelial cell anchorage dependence mediated by the loss of extracellular matrix (ECM)-attachment due to α2β1-integrin function. SKI-606-mediated attenuation of the human ADPKD hyperproliferative and hyper-ECM-adhesive epithelial cell phenotype in vitro was paralleled by retardation of the renal cystic phenotype of Pkd1 orthologous ADPKD heterozygous mice in vivo. This suggests that SKI-606 has dual effects on cystic epithelial cell proliferation and ECM adhesion and may have therapeutic potential for ADPKD patients.

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