Aquaporin-4 deletion in mice reduces brain edema after acute water intoxication and ischemic stroke

By G. Manley, M. Fujimura, T. Ma, N. Noshita, F. Filiz, A. Bollen, Pak H. Chan, A. Verkman. Nature Medicine, 2000

1,548 citations recorded by the source corpus.

Subfields: Molecular Biology, Pulmonary and Respiratory Medicine

View Paper: https://www.semanticscholar.org/paper/951f2e07c5dfb4623eaa7aa0b7db4f30bfaf845e

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Citations in the corpus

Aquaporin water channels in the nervous system (2013, positive): “There is less brain oedema in Aqp4 knockout than in wild-type mice after focal cerebral ischaemia, water intoxication 72,79 or bacterial meningitis 70 .”
Astrocytes: biology and pathology (2009, background): “Although excess uptake of water through AQP4 on astrocyte endfeet can lead to cytotoxic edema [135, 157, 264], the loss of astrocytes or the failure of astrocyte AQP4 channels can also lead to vasogenic edema or accumulation of extracellular fluid [33, 157, 177, 264].”
Astrocytes and Brain Injury (2003, background): “Mice with genetic knockout of AQP4 show less astrocyte swelling, reduced brain edema, and better neurologic outcome after focal ischemia (Manley et al., 2000), supporting a causative role for astrocyte AQP function in these processes.”
The perivascular astroglial sheath provides a complete covering of the brain microvessels: An electron microscopic 3D reconstruction (2010, background): “Targeted disruption of the AQP4 gene similarly reduces the extent of brain edema (Manley et al., 2000).”
Aquaporin Water Channels (2004, result): “Geoff Manley and colleagues independently established the same conclusions with AQP4-null mice (Manley et al., 2000).”
Tight junctions of the blood-brain barrier: development, composition and regulation. (2002, background): “The role of OAP/AQP4 for the water homeostasis of the brain and the maintenance of the blood–brain barrier has been shown in different approaches (Manley et al., 2000; Frigeri et al., 2001; Ke et al., 2001).”
Pattern-specific loss of aquaporin-4 immunoreactivity distinguishes neuromyelitis optica from multiple sclerosis. (2007, background): “Experimental rodent models of ischaemia, trauma and hyponatraemia implicate AQP4 in the development of brain oedema regardless of cause (Manley et al., 2000; Taniguchi et al., 2000; Saadoun et al., 2002; Vajda et al., 2002; Warth et al., 2005).”
Physiological roles of aquaporin-4 in brain. (2013, background): “Taken together with the large number of studies on edema development (4, 7, 19, 81, 99, 140, 176, 192), the studies on saline infusion and postnatal water resorption suggest that AQP4 can become rate limiting for efflux as well as influx of water across the blood-brain interface.”
More than just water channels: unexpected cellular roles of aquaporins (2005, background): “Although AQP4-null mice show no overt neurological abnormalities, they have remarkably reduced brain swelling after cytotoxic edema produced by acute water intoxication and ischemic stroke (Manley et al., 2000).”
Stem cell-related "self-renewal" signature and high epidermal growth factor receptor expression associated with resistance to concomitant chemoradiotherapy in glioblastoma. (2008, background): “AQP4 has been associated with brain tumor related edema.(23) Aquaporins require activation of mitogen-activated protein kinase signaling that may be mediated by EGFR activation.”
The blood–brain barrier in systemic infection and inflammation (2021, background): “In these situations, aquaporin-4 has the opposite effect to the healthy state, mediating influx of water into astrocytes, since its knockout [171, 172] or pharmacological relocalization away from the cell membrane [173] improved or prevented edema.”
Impairment of Glymphatic Pathway Function Promotes Tau Pathology after Traumatic Brain Injury (2014, background): “Although studies focusing on ischemic injury demonstrated an overall protective effect of Aqp4 gene deletion on lesion development (Manley et al., 2000), more recent work in TBI models has not observed any difference in lesion volume after TBI between wild-type and Aqp4 / mice (Lu et al., 2011).”