Background: Angiogenesis is crucial in neuroprotection of secondary thalamic injury after cortical infarction. The p75 neurotrophin receptor (p75) plays a key role in activating angiogenesis. However, the effects of p75 on angiogenesis in the thalamus after cortical infarction are largely unknown. Herein we investigate whether p75 facilitates angiogenesis to attenuate secondary thalamic damage via activating hypoxia-inducible factor 1α (HIF-1α)/vascular endothelial growth factor (VEGF) pathway mediated by Von Hippel-Lindau (VHL) after distal middle cerebral artery occlusion (dMCAO).
Methods: The male rat model of dMCAO was established. The effects of p75 on the angiogenesis was evaluated using RNA-sequencing, immunohistochemistry, western blot, quantitative real-time polymerase chain reaction, magnetic resonance imaging, behavior tests, viral and pharmacological interventions.
Results: We found that the p75 and vessel density were decreased in ipsilateral thalamus after dMCAO. The p75-VHL interaction was reduced, which promoted the ubiquitination degradation of HIF-1α and reduced VEGF expression after dMCAO. Notably, p75 overexpression restrained the ubiquitination degradation of HIF-1α by inhibiting VHL-HIF-1α interaction, further promoted angiogenesis, increased cerebral blood flow of ipsilateral thalamus and improved neurological function after dMCAO.
Conclusion: For the first time, we highlighted that the enhancement of p75-VHL interaction promoted angiogenesis in attenuating secondary thalamic damage after dMCAO.
Download full-text PDF |
Source |
|---|---|
| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC11284236 | PMC |
| http://dx.doi.org/10.1111/cns.14875 | DOI Listing |
Publication Analysis
Top Keywords
Similar Publications
Traumatic brain injury (TBI) is a leading cause of mortality and disability worldwide and can lead to secondary sequelae such as increased seizure susceptibility. Emerging work suggests that the thalamus, the relay center of the brain that undergoes secondary damage after cortical TBI, is involved with heightened seizure risks after TBI. TBI also induces the recruitment of peripheral immune cells, including T cells, to the site(s) of injury, but it is unclear how these cells impact neurological sequelae post-TBI.
View Article and Find Full Text PDFBackground: Converging evidence from clinical neuroimaging and animal models has strongly implicated dysfunction of thalamocortical circuits in the pathophysiology of schizophrenia. Preclinical models of genetic risk for schizophrenia have shown reduced synaptic transmission from auditory thalamus to primary auditory cortex, which may represent a correlate of auditory disturbances such as hallucinations. Human neuroimaging studies, however, have found a generalized increase in resting state functional connectivity (RSFC) between whole thalamus and sensorimotor cortex in people with schizophrenia (PSZ).
View Article and Find Full Text PDFDifferential neurogenic patterns underlie the formation of primary and secondary areas in the developing somatosensory cortex.
Cereb Cortex
January 2025
Department of Biology, Faculty of Education and Integrated Arts and Sciences, Waseda University, 2-2 Wakamatsu-cho, Shinjuku-ku, 162-8480, Tokyo, Japan.
Article Synopsis
- The cerebral cortex has organized areas that are connected by axons, but how neurogenesis (the development of new neurons) is coordinated between these areas isn’t well understood.
- The somatosensory cortex is important for processing touch and receives sensory information through the thalamus to its primary and secondary areas.
- Our study found that neuron production in the secondary somatosensory cortex (S2) happens before the primary somatosensory cortex (S1) and ends sooner, with a decrease in upper-layer neurons in S2 due to a change at the surface layer, suggesting a specific mechanism that organizes the development of these cortical areas.
Secondary analysis reveals gut microbiota differences in patients with Parkinson's disease and/or cognitive impairment.
Microbiome Res Rep
August 2024
Department of neurology, Weihai Municipal Hospital, Cheeloo College of Medicine, Shandong University, Weihai 264200, Shandong, China.
Parkinson's disease (PD) is a neurodegenerative disorder, and the main clinical characteristics are bradykinesia and muscle stiffness. Cognitive impairment (CI) is a prevalent non-motor manifestation observed in individuals with PD. According to disease severity, it can be divided into PD with mild cognitive impairment (MCI) and PD dementia.
View Article and Find Full Text PDFSpectral and coupling characteristics of somatosensory cortex and centromedian thalamus differentiate between pre- and inter-ictal 5-9 Hz oscillations in a genetic rat model of absence epilepsy.
Neurobiol Dis
December 2024
Institute of Physiology I, Münster University, Münster, Germany. Electronic address:
Spike-wave-discharges (SWD) are the electrophysiological hallmark of absence epilepsy. SWD are generated in the thalamo-cortical network and a seizure onset zone was identified in the somatosensory cortex (S1). We have shown before that inhibition of the centromedian thalamic nucleus (CM) in GAERS rats resulted in a selective suppression of the spike component while rhythmic cortical 5-9 Hz oscillations remained present.
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!