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Repression of adenosine triphosphate-binding cassette transporter ABCG2 by estrogen increases intracellular glutathione in brain endothelial cells following ischemic reperfusion injury.
Shin, Jin A; Jeong, Sae Im; Kim, Hye Won; Jang, Gyeonghui; Ryu, Dong-Ryeol; Ahn, Young-Ho; Choi, Ji Ha; Choi, Youn-Hee; Park, Eun-Mi.
Afiliação
  • Shin JA; Department of Pharmacology, Tissue Injury Defense Research Center, College of Medicine, Ewha Womans University, Seoul, Republic of Korea.
  • Jeong SI; Department of Pharmacology, Tissue Injury Defense Research Center, School of Medicine, Ewha Womans University, Seoul, Republic of Korea.
  • Kim HW; Department of Pharmacology, Tissue Injury Defense Research Center, College of Medicine, Ewha Womans University, Seoul, Republic of Korea.
  • Jang G; Department of Pharmacology, Tissue Injury Defense Research Center, College of Medicine, Ewha Womans University, Seoul, Republic of Korea.
  • Ryu DR; Department of Internal Medicine, Tissue Injury Defense Research Center, College of Medicine, Ewha Womans University, Seoul, Republic of Korea.
  • Ahn YH; Department of Molecular Medicine, Tissue Injury Defense Research Center, College of Medicine, Ewha Womans University, Seoul, Republic of Korea.
  • Choi JH; Department of Pharmacology, Tissue Injury Defense Research Center, College of Medicine, Ewha Womans University, Seoul, Republic of Korea.
  • Choi YH; Department of Physiology, Tissue Injury Defense Research Center, College of Medicine, Ewha Womans University, Seoul, Republic of Korea.
  • Park EM; Department of Pharmacology, Tissue Injury Defense Research Center, College of Medicine, Ewha Womans University, Seoul, Republic of Korea. Electronic address: empark@ewha.ac.kr.
Neurobiol Aging ; 66: 138-148, 2018 06.
Article em En | MEDLINE | ID: mdl-29574357
ABSTRACT
The adenosine triphosphate-binding cassette efflux transporter ABCG2, which is located in the blood-brain barrier limits the entry of endogenous compounds and xenobiotics into the brain, and its expression and activity are regulated by estrogen. This study was aimed to define the role of ABCG2 in estrogen-mediated neuroprotection against ischemic injury. ABCG2 protein levels before and after ischemic stroke were increased in the brain of female mice by ovariectomy, which were reversed by estrogen replacement. In brain endothelial cell line bEnd.3, estrogen reduced the basal ABCG2 protein level and efflux activity and protected cells from ischemic injury without inducing ABCG2 expression. When bEnd.3 cells were transfected with ABCG2 small interfering RNA, ischemia-induced cell death was reduced, and the intracellular concentration of glutathione, an antioxidant that is transported by ABCG2, was increased. In addition, after ischemic stroke in ovariectomized mice, estrogen prevented the reduction of intracellular glutathione level in brain microvessels. These data suggested that the suppression of ABCG2 by estrogen is involved in neuroprotection against ischemic injury by increasing intracellular glutathione, and that the modulation of ABCG2 activity offers a therapeutic target for brain diseases in estrogen-deficient aged women.
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Texto completo: 1 Coleções: 01-internacional Base de dados: MEDLINE Assunto principal: Encéfalo / Traumatismo por Reperfusão / Células Endoteliais / Estrogênios / Membro 2 da Subfamília G de Transportadores de Cassetes de Ligação de ATP / Glutationa Limite: Animals Idioma: En Revista: Neurobiol Aging Ano de publicação: 2018 Tipo de documento: Article

Texto completo: 1 Coleções: 01-internacional Base de dados: MEDLINE Assunto principal: Encéfalo / Traumatismo por Reperfusão / Células Endoteliais / Estrogênios / Membro 2 da Subfamília G de Transportadores de Cassetes de Ligação de ATP / Glutationa Limite: Animals Idioma: En Revista: Neurobiol Aging Ano de publicação: 2018 Tipo de documento: Article
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