Aims: This study immunohistochemically examined the orbitofrontal cortex for three possible candidates in hypoxic/ischemic signaling: the cytokine transforming growth factor-β, the glucose transporter-1 and the neuron-specific oxygen-binding protein neuroglobin.
Methods: Post-mortem tissue from 20 depressed and 20 non-depressed individuals was obtained and the expression of the three proteins was analyzed using image analysis software.
Results: No significant changes were found in transforming growth factor-β or neuroglobin in the orbitofrontal cortex between depressed and non-depressed individuals. There was, however, a trend towards a reduction in glucose transporter-1 in the depressed group.
Conclusions: This study does not clearly support the hypothesis that hypoxic/ischemic processes are behind the pathological deficits in the frontal-subcortical circuitry associated with depression and therefore does not provide evidence to support the 'vascular depression' hypothesis.
Download full-text PDF |
Source |
|---|---|
| http://dx.doi.org/10.1111/j.1440-1819.2010.02176.x | DOI Listing |
Publication Analysis
Top Keywords
Similar Publications
Glucose transporter 1 in vascular smooth muscle cells is dispensable for abdominal aortic aneurysm induced by angiotensin II.
JVS Vasc Sci
December 2024
Department of Cardiovascular Science, Lewis Katz School of Medicine at Temple University, Philadelphia, PA.
Treatment with an inhibitor of glucose use via glucose transporters (GLUT) has been shown to attenuate experimental abdominal aortic aneurysm (AAA) development in mice. Vascular smooth muscle cell (VSMC) signaling seems to be essential for angiotensin II (Ang II)-induced AAA in mice. Accordingly, we have tested a hypothesis that VSMC silencing of the major GLUT, GLUT1, prevents AAA development and rupture in mice treated with Ang II plus β-aminopropionitrile.
View Article and Find Full Text PDFGlucose Transporter 1 Deficiency Impairs Glucose Metabolism and Barrier Induction in Human Induced Pluripotent Stem Cell-Derived Astrocytes.
J Cell Physiol
January 2025
Department of Pharmaceutical Sciences and Center for Blood-Brain Barrier Research, Jerry H. Hodge School of Pharmacy, Texas Tech University Health Sciences Center, Amarillo, Texas, USA.
Glucose is a major source of energy for the brain. At the blood-brain barrier (BBB), glucose uptake is facilitated by glucose transporter 1 (GLUT1). GLUT1 Deficiency Syndrome (GLUT1DS), a haploinsufficiency affecting SLC2A1, reduces glucose brain uptake.
View Article and Find Full Text PDF[Casticin inhibits proliferation of non-small cell lung cancer cells by regulating glucose metabolism through suppression of HIF-1α].
Zhongguo Zhong Yao Za Zhi
December 2024
Department of Thoracic Surgery, Shaanxi Provincial Cancer Hospital Xi'an 710061, China.
The study investigated the effect of casticin on the proliferation of non-small cell lung cancer(NSCLC) H322 cells and explored its molecular mechanism. Firstly, the cell counting kit-8(CCK-8) assay, colony formation assay, and EdU assay were used to detect the effect of casticin on the proliferation capacity of H322 cells under different concentrations and treatment durations. Then, glucose uptake, lactate production, extracellular pH, and oxygen consumption of H322 cells were measured before and after casticin treatment to analyze its impact on glycolysis in NSCLC H322 cells.
View Article and Find Full Text PDFSUMOylated GLUT1 inhibited the glycometabolism disorder in chondroctyes during osteoarthritis.
Glycoconj J
January 2025
Department of Orthopaedics, Nanchang People's Hospital (The Third Hospital of Nanchang), Nanchang City, Jiangxi Province, China.
Reduction of glucose transporter 1 (GLUT1), even deletion, may results in cartilage fibrosis and osteoarthritis. This study aims to investigate the SUMOylation of GLUT1 in osteoarthritis through small ubiquitin-like modifier 1(SUMO1), and explore the role of SUMOylated GLUT1 in glycometabolism, proliferation and apoptosis in chondrocytes. Human chondrocytes were incubated with 10 ng/mL of IL-1β to mimic osteoarthritis in vitro.
View Article and Find Full Text PDFSENP1 inhibits aerobic glycolysis in Aβ-incubated astrocytes by promoting PUM2 deSUMOylation.
Cell Biol Toxicol
January 2025
Department of Neurology, The Fourth Affiliated Hospital of China Medical University, Shenyang, China.
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 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!