Neuroglobin (Ngb), a recently discovered intracellular respiratory globin in neurons, may play a crucial role in oxygen homeostasis in the brain. We report preliminary findings indicating the presence of functional neuroglobin in primary cultures of cerebral cortical astrocytes. Reverse transcription real-time polymerase chain reaction (RRT-PCR) and immunostaining confirmed such presence in cultured astrocytes isolated from newborn mouse brain. Ngb antisense treatment increased apoptosis in ischemic astrocytes. The discovery of Ngb in astrocytes may provide some insight into how oxygen homeostasis is regulated in the brain.
Download full-text PDF |
Source |
|---|---|
| http://dx.doi.org/10.1002/glia.20147 | DOI Listing |
Publication Analysis
Top Keywords
Similar Publications
Mitochondrial fatty acid oxidase CPT1A ameliorates postoperative cognitive dysfunction by regulating astrocyte ferroptosis.
Brain Res
December 2024
Department of Urology Surgery, People's Hospital of Shenzhen, Shenzhen City, Guangdong Province, China.
Article Synopsis
- Postoperative cognitive dysfunction (POCD) is a complication related to surgery involving cognitive decline, potentially influenced by neuroinflammation, ferroptosis, and mitochondrial fatty acid metabolism, particularly via the protein Carnitine palmitoyl transferase 1a (CPT1A).
- The study used SVG P12 astrocytes to explore how CPT1A affects mitochondrial function, inflammation, and neuron damage by overexpressing or knocking down CPT1A and assessing the resulting changes in cellular conditions.
- Results showed that higher levels of CPT1A improved mitochondrial function and reduced oxidative stress and inflammation in astrocytes, which benefitted neuron health, while these effects depended on functional mitochondrial respiration, as demonstrated when treatments disrupted this process.
Elevated Astrocytic NFAT5 of the hippocampus increases epilepsy susceptibility in hypoxic-ischemic mice.
Epilepsia
December 2024
Department of Physiology, School of Basic Medical Sciences, Wuhan University, Wuhan, China.
Objective: Hypoxic-ischemic brain damage (HIBD) is a leading cause of neonatal mortality, resulting in brain injury and persistent seizures that can last into the late neonatal period and beyond. Effective treatments and interventions for infants affected by hypoxia-ischemia remain lacking. Clinical investigations have indicated an elevation of nuclear factor of activated T cells 5 (NFAT5) in whole blood from umbilical cords of severely affected HIBD infants with epilepsy.
View Article and Find Full Text PDFDevelopment of a multi-scale nanofiber scaffold platform for structurally and functionally replicated artificial perforating arteries.
Bioprocess Biosyst Eng
December 2024
Department of Biological Engineering, Inha University, 100 Inha-Ro, Nam-Gu, Incheon, 22212, Republic of Korea.
Experimental models for exploring abnormal brain blood vessels, including ischemic stroke, are crucial in neuroscience; recently, significant attention has been paid to artificial tissues through tissue engineering. Nanofibers, although commonly used as tissue engineering scaffolds, undergo structural deformations easily, making it challenging to create uniform tissue, especially for the smallest-diameter ones such as perforating arteries. This study focused on the development of a platform capable of reconstructing structurally and functionally replicated perforating arteries.
View Article and Find Full Text PDFCarboxylated Zn-phthalocyanine attenuates brain Aβ in AD model mouse.
Brain Res
December 2024
Department of Neurology, Faculty of Medicine, Shimane University, 89-1 Enya-Cho, Izumo 693-8501, Japan; Department of Laboratory Medicine, Faculty of Medicine, Shimane University, Izumo 693-8501, Japan. Electronic address:
The deposition of aggregated amyloid β (Aβ) is considered as a key factor for Alzheimer's Disease (AD). Previously, we demonstrated that a carboxylated Zn-phthalocyanine (ZnPc) inhibits Aβ fibril formation, consequently protects neurons in culture. This study evaluated the effects of ZnPc on pathological changes in an AD mouse model (J20).
View Article and Find Full Text PDFMicroglial cell proliferation is regulated, in part, by reactive astrocyte ETB signaling after ischemic stroke.
Exp Neurol
December 2024
Department of Medicine, Cardiovascular Research Institute, University of Vermont, Colchester, VT 05446, USA; Department of Neurological Sciences and Neuroscience Graduate Program, University of Vermont, Burlington, VT 05401, USA. Electronic address:
Reciprocal communication between reactive astrocytes and microglial cells provides local, coordinated control over critical processes such as neuroinflammation, neuroprotection, and scar formation after CNS injury, but is poorly understood. The vasoactive peptide hormone endothelin (ET) is released and/or secreted by endothelial cells, microglial cells and astrocytes early after ischemic stroke and other forms of brain injury. To better understand glial cell communication after stroke, we sought to identify paracrine effectors produced and secreted downstream of astroglial endothelin receptor B (ETB) signaling.
View Article and Find Full Text PDFWant 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!