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.
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http://dx.doi.org/10.1096/fj.06-6848com | DOI Listing |
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.
Genes (Basel)
December 2024
Department of Ophthalmology, Eye Center, UC Davis School of Medicine, University of California Davis, Sacramento, CA 95817, USA.
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.
J Neurochem
January 2025
FMUC-Faculty of Medicine, University of Coimbra, Coimbra, Portugal.
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 PDFPLoS 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.
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