We reported previously that astroglia cultured from aquaporin-4-deficient (AQP4-/-) mice migrate more slowly in vitro than those from wild-type (AQP4+/+) mice (J. Cell Sci. 2005;118, 5691-5698). Here, we investigate the migration of fluorescently labeled AQP4+/+ and AQP4-/- astroglia after implantation into mouse brains in which directional movement was stimulated by a planar stab wound 3 mm away from the axis of the injection needle. Two days after cell injection we determined the location, elongation ratio, and orientation of labeled cells. Migration of AQP4+/+ but not AQP4-/- cells toward the stab was greater than away from the stab. AQP4+/+ astroglia moved on average 1.5 mm toward the stab compared with 0.6 mm for AQP4-/- cells. More than 25% of the migrating AQP4+/+ cells but <3% of AQP4-/- cells appeared elongated (axial ratio>2.5). In transwell assays, AQP4+/+ astroglia migrated faster than AQP4-/- cells in a manner dependent on pore size. At 8 h, approximately 50% of AQP4+/+ cells migrated through 8-microm diameter pores, whereas equivalent migration of AQP4-/- cells was found for 12-microm diameter pores. These results provide in vivo evidence for AQP4-dependent astroglial migration and suggest that modulation of AQP4 expression or function might alter glial scarring.

Download full-text PDF

Source
http://dx.doi.org/10.1096/fj.06-6848comDOI Listing

Publication Analysis

Top Keywords

aqp4-/- cells
16
cells
8
aqp4+/+ aqp4-/-
8
aqp4+/+ astroglia
8
aqp4+/+ cells
8
diameter pores
8
aqp4+/+
7
aqp4-/-
6
migration
5
greatly impaired
4

Similar Publications

NOTCH3 Mutation Causes Glymphatic Impairment and Promotes Brain Senescence in CADASIL.

CNS Neurosci Ther

January 2025

Department of Neurology, Mental and Neurological Disease Research Center, The Third Affiliated Hospital of Sun Yat-Sen University, Guangzhou, China.

Aims: The aim of this study is to investigate the role of glymphatic function of cerebral autosomal dominant arteriopathy, subcortical infarcts, and leukoencephalopathy (CADASIL), the most common monogenic small vessel disease caused by NOTCH3 mutation, and to explore potential therapeutic strategies to improve glymphatic function.

Methods: We assessed glymphatic influx and efflux function in CADASIL mouse models (Notch3) and correlated these findings with brain atrophy in CADASIL patients. We also investigated the underlying mechanisms of glymphatic impairment, focusing the expression of AQP4 in astrocytic endfeet.

View Article and Find Full Text PDF

Background/objective: The Rs1 exon-1-del rat (Rs1KO) XLRS model shows normal retinal development until postnatal day 12 (P12) when small cystic spaces start to form in the inner nuclear layer. These spaces enlarge rapidly, peak at P15, and then collapse by P19.

Methods: We explored the possible involvement of Kir4.

View Article and Find Full Text PDF
Article Synopsis
  • Astrocytes help clear proteins and waste in the brain using aquaporin-4 (AQP4), which can be disrupted in stress-related disorders.
  • Dexamethasone (Dexa), a glucocorticoid used to model stress, was found to reduce the activity of AQP4 and its associated proteins in astrocytes, leading to impaired protein clearance.
  • The study suggests that blocking adenosine A receptors (AR) can restore AQP4 function and clearance, indicating a potential therapeutic strategy to address neurological disorders linked to stress and protein accumulation.
View Article and Find Full Text PDF

Unveiling the shared genes between systemic sclerosis and lung cancer.

Front Med (Lausanne)

December 2024

Department of Rheumatology and Immunology, The Affiliated Huai'an Hospital of Xuzhou Medical University, The Second People's Hospital of Huai'an, Huai'an, China.

The risk of lung cancer is significantly increased in patients with systemic sclerosis (SSc), yet the specific genes underlying this association remain unexplored. Our study aims to identify genes shared by SSc and lung cancer. We identified differentially expressed genes (DEGs) from SSc and lung adenocarcinoma (LUAD) datasets (SSc: GSE95065, LUAD: GSE136043) in the GEO database.

View Article and Find Full Text PDF

Immune cell infiltration and modulation of the blood-brain barrier in a guinea pig model of tuberculosis: Observations without evidence of bacterial dissemination to the brain.

PLoS One

December 2024

Department of Environmental and Radiological Health Sciences, College of Veterinary Medicine and Biomedical Sciences, Colorado State University, Fort Collins, Colorado, United States of America.

Tuberculosis (TB), caused by Mycobacterium tuberculosis (Mtb) infection, is a chronic inflammatory disease. Although typically associated with inflammation of the lungs and other peripheral tissues, increasing evidence has uncovered neurological consequences attributable to Mtb infection. These include deficits in memory and cognition, increased risk for neurodegenerative disease, and progressive neuropathology.

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!