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Selective knockout of astrocytic Na⁺ /H⁺ exchanger isoform 1 reduces astrogliosis, BBB damage, infarction, and improves neurological function after ischemic stroke.

ABSTRACT: Stimulation of Na⁺ /H⁺ exchanger isoform 1 (NHE1) in astrocytes causes ionic dysregulation under ischemic conditions. In this study, we created a Nhe1^flox/flox (Nhe1^f/f ) mouse line with exon 5 of Nhe1 flanked with two loxP sites and selective ablation of Nhe1 in astrocytes was achieved by crossing Nhe1^f/f mice with Gfap-Cre^ERT2 Cre-recombinase mice. Gfap-Cre^ERT2+/- ;Nhe1^f/f mice at postnatal day 60-90 were treated with either corn oil or tamoxifen (Tam, 75 mg/kg/day, i.p.) for 5 days. After 30 days post-injection, mice underwent transient middle cerebral artery occlusion (tMCAO) to induce ischemic stroke. Compared with the oil-vehicle group (control), Tam-treated Gfap-Cre^ERT2+/- ;Nhe1^f/

SUBMITTER: Begum G

PROVIDER: S-EPMC5705024 | biostudies-literature | 2018 Jan

REPOSITORIES: biostudies-literature

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Selective knockout of astrocytic Na⁺ /H⁺ exchanger isoform 1 reduces astrogliosis, BBB damage, infarction, and improves neurological function after ischemic stroke.

OmicsDI is part of the ELIXIR infrastructure

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Dataset Information

Selective knockout of astrocytic Na+ /H+ exchanger isoform 1 reduces astrogliosis, BBB damage, infarction, and improves neurological function after ischemic stroke.

OmicsDI is part of the ELIXIR infrastructure

Tweets

Selective knockout of astrocytic Na⁺ /H⁺ exchanger isoform 1 reduces astrogliosis, BBB damage, infarction, and improves neurological function after ischemic stroke.