ABSTRACT
The aim of the present study was to investigate the changes in mitotic reorientation and relative differential gene expression in rat prostate epithelial cells following long-term exposure to testosterone propionate (TP). Sprague-Dawley rats were randomly divided into two groups as follows: TP group, which received 3.7 mg/kg/day TP for 30 days (n=10); and control group, in which rats were injected with olive oil (n=10). Microscopic analysis of the prostate tissue was performed by immunohistochemical analysis and hematoxylin and eosin staining. Differential gene expression analysis was performed via gene microarray, and a total of five genes (Dkk3, Ran, Fas, Tgm4 and Wnt2) were selected and their expression levels were verified using reverse transcription-polymerase chain reaction. For rats treated with TP, mitosis was significantly reoriented, becoming parallel to the basement membrane. By contrast, in the control group cells mitotic orientation remained perpendicular to the basement membrane. Genes such as Ran and Tgm4 in the androgen receptor (AR) signaling pathway and Wnt2 in the Wnt signaling pathway, were upregulated following treatment with TP. Conversely, the Dkk3 and Fas genes were downregulated following treatment with TP. In conclusion, mitotic orientation of prostate epithelial cells was altered following long-term administration of TP. Wnt and AR signaling pathways influenced cell proliferation and may have participated in the mitotic orientation change.
ABSTRACT
A clinical requirement exists for early biomarkers that can predict the severity of acute pancreatitis (AP). In order to determine whether E-cadherin is associated with the severity of AP, a pancreatitic rat model was established and the expression levels of E-cadherin were detected. A study population of 24 Sprague Dawley rats was administered intraperitoneal injections of various concentrations of L-arginine in order to induce pancreatitis. Rats were assigned to the severe acute pancreatitis (SAP) or mild acute pancreatitis (MAP) group based on the results of histological evaluations and the serum levels of amylase. An additional 8 rats received intraperitoneal injections of NaCl solution, as a control group. For each group, the serum concentrations of soluble E-cadherin and the expression levels of E-cadherin protein in the pancreatic tissue were detected. The results indicated that the rat model of pancreatitis was successfully established. Rats in the high concentration L-arginine treatment group, which exhibited a higher pancreatitis pathology score and level of serum amylase, were assigned to the SAP group. Low concentration L-arginine group rats were assigned to the MAP group. The pathology scores and levels of serum amylase in the SAP and MAP group rats were higher compared with the control group rats. The levels of serum E-cadherin were the most elevated in the SAP group. Statistically significant differences were detected in the SAP and MAP groups compared with the control group, and in the SAP group compared with the MAP group (P<0.05). Furthermore, the levels of E-cadherin protein in the pancreatic tissue were elevated in the SAP group compared with the MAP and control groups. In conclusion, the present study demonstrated that E-cadherin was overexpressed in SAP rats, and the overexpression of E-cadherin may be associated with the severity of AP.
