Cultured rat epididymal tissue explants formed >90% pure, adherent growing epithelial cell monolayers. Despite their flattened and apparently androgen receptor-negative phenotype, these cells for a short period kept characteristics of the epididymal duct epithelium, i.e., expression of the tissue-specific marker CD52 and responsiveness of its mRNA toward temperature elevation and androgen withdrawal. When cells were grown on permeable supports at 33 degrees C, androgen supplementation or withdrawal specifically modulated the levels as well as the length of the CD52 mRNA. Elevation of the culture temperature to a quasi abdominal milieu of 37 degrees C selectively reduced the CD52 mRNA levels under all culture conditions. This reduction was not affected by the presence of androgens and was not accompanied by changes in length, suggesting that the modulation of CD52 mRNA in epididymal cells by androgens and by temperature is synergic, but may involve different molecular mechanisms. CD52 mRNA levels, however, were not stable in the primary cultures but decreased rapidly to undetectable levels after 4-5 days at all culture conditions. GAPDH mRNA levels, on the other hand, were stable throughout the culture period.

Download full-text PDF

Source
http://dx.doi.org/10.1002/(SICI)1098-2795(200005)56:1<26::AID-MRD4>3.0.CO;2-KDOI Listing

Publication Analysis

Top Keywords

cd52 mrna
20
mrna levels
12
androgens temperature
8
culture conditions
8
cd52
6
mrna
6
levels
5
mrna modulated
4
modulated androgens
4
temperature
4

Similar Publications

(1) BACKGROUND: Hashimoto's thyroiditis (HT) can cause angiogenesis in the thyroid gland. However, the molecular mechanism of endothelial cells and angiogenesis related genes (ARGs) has not been extensively studied in HT. (2) METHODS: The HRA001684, GSE29315 and GSE163203 datasets were included in this study.

View Article and Find Full Text PDF

The immune-modulating protein CD52 attenuates lymphocyte function and is associated with autoimmune disorders, for example, multiple sclerosis (MS). CD52 represents a therapeutic target in MS and chronic lymphocytic leukemia (CLL). Its expression has prognostic and predictive value in CLL and is prognostic in breast cancer.

View Article and Find Full Text PDF

Background: Chinese hamster ovary (CHO) cells are the most predominantly utilized host for the production of monoclonal antibodies (mAbs) and other complex glycoproteins. A major challenge in the process of CHO cell culture is the occurrence of cell death following different stressful conditions, which hinders the production yield. Engineering genes involved in pathways related to cell death is a remarkable strategy to delay apoptosis, improve cell viability and enhance productivity.

View Article and Find Full Text PDF
Article Synopsis
  • - Uterine endometrial cancer (EC) is increasingly prevalent, and traditional hormone therapy using progesterone is effective for initial treatment, but many patients develop resistance over time, leading to poor outcomes for PR-negative tumors.
  • - Histone deacetylase inhibitors (HDACi), like entinostat and romidepsin, have shown promise in reversing the downregulation of progesterone receptors (PR) in EC cells, enhancing their responsiveness to progestin therapy, and demonstrating tumor growth inhibition in models.
  • - A clinical trial supported by these findings indicated that while entinostat combined with MPA (a progestin) reduced tumor proliferation markers, romidepsin significantly improved treatment effectiveness and up
View Article and Find Full Text PDF

Objective: To identify tumor microenvironment (TME)- related genes associated with the occurrence of invasive breast cancer as potential prognostic biomarkers and therapeutic targets.

Methods: RNA transcriptome data and clinically relevant data were retrieved from TCGA database, and the StromalScore and ImmuneScore were calculated using the ESTIMATE algorithm. The differentially expressed genes (DEGs) were screened by taking the intersection.

View Article and Find Full Text PDF

Want AI Summaries of new PubMed Abstracts delivered to your In-box?

Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!