Identification and characterisation of functional bombesin receptors in human astrocytes.

Eur J Pharmacol

Pfizer Global Research and Development, Cambridge Laboratories, Cambridge University Forvie Site, Robinson Way, Cambridge CB2 2QB, UK.

Published: March 2002

Reverse transcription polymerase chain reaction (RT-PCR) demonstrated the presence of bombesin BB2 receptor mRNA but not bombesin BB1 receptor or bombesin BB3 receptor mRNA in cultured human astrocytes. Neuromedin C hyperpolarised human astrocytes in whole-cell current and voltage clamp recordings and increased the intracellular free Ca(2+) ion concentration ([Ca(2+)](i)) in single astrocytes. Treatment with neuromedin C caused larger and more frequent increases in [Ca(2+)](i) than those triggered by neuromedin B, with 96% and 78% of cells responding, respectively. The stimulatory effects of neuromedin C were inhibited significantly by treatment with U73122 or the bombesin BB2 receptor antagonist [D-Phe(6), des-Met(14)]bombesin-(6-14) ethylester. A Fluorometric Imaging Plate Reader (FLIPR) was used to measure [Ca(2+)](i) in cell populations. Neuromedin C was approximately 50-fold more potent than neuromedin B in elevating [Ca(2+)](i) in astrocytes and Chinese hamster ovary (CHO) cells expressing human bombesin BB2 receptors (hBB2-CHO). However, in CHO cells expressing the bombesin BB1 receptor hBB1-CHO, neuromedin B was 32-fold more potent than neuromedin C. [D-Phe(6), des-Met(14)]bombesin-(6-14) ethylester was a partial agonist in hBB1-CHO cells (E(max)=55%) but was a noncompetitive antagonist in both hBB2-CHO cells and astrocytes. These studies report the first identification of functional bombesin receptors on cultured human astrocytes and have demonstrated that the bombesin BB2 receptor contributes significantly to astrocyte physiology.

Download full-text PDF

Source
http://dx.doi.org/10.1016/s0014-2999(02)01268-2DOI Listing

Publication Analysis

Top Keywords

human astrocytes
16
bombesin bb2
16
bb2 receptor
12
bombesin
9
functional bombesin
8
bombesin receptors
8
receptor mrna
8
bombesin bb1
8
bb1 receptor
8
cultured human
8

Similar Publications

Neurodegenerative diseases are characterized by progressive loss of neurons and persistent inflammation. Neurons are terminally differentiated cells, and lost neurons cannot be replaced since neurogenesis is restricted to only two neurogenic niches in the adult brain, whose neurogenic potential decreases with age. In this regard, the astrocytes reprogramming into neurons may represent a promising strategy for restoring the lost neurons and rebuilding neural circuits.

View Article and Find Full Text PDF

Neuroinflammatory Loop in Schizophrenia, Is There a Relationship with Symptoms or Cognition Decline?

Int J Mol Sci

January 2025

Departamento de Ciencias Biológicas y Químicas, Facultad De Medicina y Ciencia, Universidad San Sebastián, Sede Tres Pascualas Lientur 1457, Concepción 4080871, Chile.

Schizophrenia (SZ), a complex psychiatric disorder of neurodevelopment, is characterised by a range of symptoms, including hallucinations, delusions, social isolation and cognitive deterioration. One of the hypotheses that underlie SZ is related to inflammatory events which could be partly responsible for symptoms. However, it is unknown how inflammatory molecules can contribute to cognitive decline in SZ.

View Article and Find Full Text PDF

Traumatic brain injuries (TBIs) are a leading cause of mortality and morbidity, particularly in forensic settings where determining the cause of death and timing of injury is critical. Glial fibrillary acidic protein (GFAP), a biomarker specific to astrocytes, has emerged as a valuable tool in post-mortem analyses of TBI. A PRISMA-based literature search included studies examining GFAP in human post-mortem samples such as brain tissue, cerebrospinal fluid (CSF), serum, and urine.

View Article and Find Full Text PDF

Alzheimer's disease (AD), the most prevalent form of dementia in the elderly, involves critical changes such as reduced aerobic glycolysis in astrocytes and increased neuronal apoptosis, both of which are significant in the disease's pathology. In our study, astrocytes treated with amyloid β1-42 (Aβ) to simulate AD conditions exhibited upregulated expressions of small ubiquitin-like modifier (SUMO)-specific protease 1 (SENP1) and Pumilio RNA Binding Family Member 2 (PUM2), alongside decreased levels of Nuclear factor erythroid 2-related factor 2 (NRF2). SENP1 is notably the most upregulated SUMOylation enzyme in Aβ-exposed astrocytes.

View Article and Find Full Text PDF

F-53B disrupts energy metabolism by inhibiting the V-ATPase-AMPK axis in neuronal cells.

J Hazard Mater

January 2025

Key Laboratory for Prevention and Control of Emerging Infectious Diseases and Public Health Security, the Xinjiang Production and Construction Corps, School of Medicine, Shihezi University, Shihezi, PR China; Key Laboratory of Xinjiang Endemic and Ethnic Diseases (Ministry of Education), School of Medicine, Shihezi University, Shihezi, Xinjiang, PR China; NHC Key Laboratory of Prevention and Treatment of Central Asia High Incidence Diseases (First Affiliated Hospital, School of Medicine, Shihezi University), PR China. Electronic address:

6:2 chloro-polyfluorooctane ether sulfonate (F-53B) is considered neurotoxic, but its mechanisms remain unclear. This study aimed to investigate the toxic effects of F-53B on neuronal cells, focusing on the role of the V-ATPase-AMPK axis in the mechanism of abnormal energy metabolism. Mouse astrocytes (C8-D1A) and human neuroblastoma cells (SH-SY5Y) exposed to F-53B were used as in vitro models.

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!