Does 5-bromo-2'-deoxyuridine (BrdU) disrupt cell proliferation and neuronal maturation in the adult rat hippocampus in vivo?

Behav Brain Res

Department of Psychology, University of North Carolina, 601 South College Road, Wilmington, NC 28403-5612, United States.

Published: May 2009

5-Bromo-2'-deoxyuridine (BrdU) is frequently used as a mitotic marker in studies of cell proliferation. Recent studies have reported cytotoxic effects of BrdU on neural progenitor cells in embryonic and neonatal brains in vivo and in adult tissue studied in vitro. The present study was conducted to assess whether BrdU interferes with cell proliferation and neuronal maturation in the rat adult hippocampus in vivo. BrdU effects across a wide range of doses (40-480 mg/kg) on cell proliferation and the population of immature neurons in the adult hippocampus were investigated using immunohistochemical labeling methods for the cell cycle marker Ki67 and a marker for immature neurons, doublecortin. BrdU did not influence cell proliferation in the dentate gyrus or the population of immature neurons observed in the adult hippocampus relative to those observed in saline treated controls. Thus, in contrast with reports of deleterious effects of BrdU in embryonic and neonatal tissue and adult tissue studied in vitro, BrdU does not appear to have cytotoxic effects on proliferating hippocampal cells or immature neurons in vivo in rats.

Download full-text PDF

Source
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4154233PMC
http://dx.doi.org/10.1016/j.bbr.2008.11.050DOI Listing

Publication Analysis

Top Keywords

cell proliferation
20
immature neurons
16
adult hippocampus
12
5-bromo-2'-deoxyuridine brdu
8
proliferation neuronal
8
neuronal maturation
8
cytotoxic effects
8
effects brdu
8
embryonic neonatal
8
adult tissue
8

Similar Publications

The mammalian Hippo kinases, MST1 and MST2, regulate organ development and suppress tumor formation by balancing cell proliferation and death. In macrophages, inflammasomes detect molecular patterns from invading pathogens or damaged host cells and trigger programmed cell death. In addition to lytic pyroptosis, the signatures associated with apoptosis are induced by inflammasome activation, but how the inflammasomes coordinate different cell death processes remains unclear.

View Article and Find Full Text PDF

Cardiovascular and cardiometabolic diseases are leading causes of morbidity and mortality worldwide, driven in part by chronic inflammation. Emerging research suggests that the bone marrow microenvironment, or marrow niche, plays a critical role in both immune system regulation and disease progression. The bone marrow niche is essential for maintaining hematopoietic stem cells (HSCs) and orchestrating hematopoiesis.

View Article and Find Full Text PDF

Background: Hypoxia in tumor cells is linked to increased drug resistance and more aggressive behavior. In pancreatic cancer, the tumor microenvironment is notably hypoxic and exhibits strong immunosuppressive properties. Given that immunotherapy is now approved for pancreatic cancer treatment, further understanding of how pancreatic tumor cell hypoxia influences T-cell cytotoxicityis essential.

View Article and Find Full Text PDF

Background: Previously, we demonstrated that changes in circulating tumor DNA (ctDNA) are promising biomarkers for early response prediction (ERP) to immune checkpoint inhibitors (ICI) in metastatic urothelial cancer (mUC). In this study, we investigated the value of whole blood immunotranscriptomics for ERP-ICI and integrated both biomarkers into a multimodal model to boost accuracy.

Methods: Blood samples of 93 patients were collected at baseline and after 2-6 weeks of ICI for ctDNA (N=88) and immunotranscriptome (N=79) analyses.

View Article and Find Full Text PDF

Targeting oncogene-induced cellular plasticity for tumor therapy.

Adv Biotechnol (Singap)

July 2024

MOE Key Laboratory of Gene Function and Regulation, State Key Laboratory of Biocontrol, School of Life Sciences, Sun Yat-sen University, Guangzhou, 510275, Guangdong, China.

Cellular plasticity, the remarkable adaptability of cancer cells to survive under various stress conditions, is a fundamental hallmark that significantly contributes to treatment resistance, tumor metastasis, and disease recurrence. Oncogenes, the driver genes that promote uncontrolled cell proliferation, have long been recognized as key drivers of cellular transformation and tumorigenesis. Paradoxically, accumulating evidence demonstrates that targeting certain oncogenes to inhibit tumor cell proliferation can unexpectedly induce processes like epithelial-to-mesenchymal transition (EMT), conferring enhanced invasive and metastatic capabilities.

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!