Estrogen protects renal endothelial barrier function from ischemia-reperfusion in vitro and in vivo

Michael P. Hutchens, Tetsuhiro Fujiyoshi, Radko Komers, Paco S. Herson, Sharon Anderson

研究成果: ジャーナルへの寄稿記事

49 引用 (Scopus)

抄録

Emerging evidence suggests that renal endothelial function may be altered in ischemia-reperfusion injury. Acute kidney injury is sexually dimorphic, and estrogen protects renal tubular function after experimental ischemic injury. This study tested the hypothesis that during ischemia-reperfusion, estrogen alters glomerular endothelial function to prevent hyperpermeability. Glomerular endothelial cells were exposed to 8-h oxygen-glucose deprivation (OGD) followed by 4- and 8-h reoxygen-ation-glucose repletion. After 4-h reoxygenation-glucose repletion, transendothelial permeability to Ficoll-70 was reduced, and transen-dothelial resistance increased, by 17(3-estradiol vs. vehicle treatment during OGD (OGD-vehicle: 91.0 ± 11.8%, OGD-estrogen: 102.6 ± 10.8%, P < 0.05). This effect was reversed by coadministration of G protein-coupled receptor 30 (GPR30) antagonist G15 with 17(3-estra-diol (OGD-estrogen-G15: 89.5 ± 6.9, P < 0.05 compared with 17(3-estradiol). To provide preliminary confirmation of this result in vivo, Ficoll-70 was administered to mice 24 h after cardiac arrest and cardiopulmonary resuscitation (CA/CPR). Blood urea nitrogen (BUN) and serum creatinine (SCr) in these mice were elevated within 12 h following CA/CPR and reduced at 24 h by pretreatment with 17(3-estradiol (BUN/SCr 17(3-estradiol: 34 ± 19/0.2 ±0.1 vehicle: 92 ± 49/0.5 ± 0.3, n = 8-12, P < 0.05). Glomerular sieving of Ficoll 70 was increased by CA/CPR within 2 h of injury and 17(3-estradiol treatment (0; 17(3-estradiol: 0.74 ± 0.26 vs. vehicle: 1.05 ± 0.53, n = 14-15, P < 0.05). These results suggest that estrogen reduces post-ischemic glomerular endothelial hyperpermeability at least in part through GPR30 and that estrogen may regulate post CA/CPR glomerular permeability in a similar fashion in vivo.

元の言語英語
ジャーナルAmerican Journal of Physiology - Renal Physiology
303
発行部数3
DOI
出版物ステータス出版済み - 8 1 2012

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Reperfusion
Estrogens
Ischemia
Estradiol
Kidney
Glucose
Cardiopulmonary Resuscitation
Heart Arrest
Ficoll
Oxygen
Blood Urea Nitrogen
G-Protein-Coupled Receptors
Permeability
Creatinine
Wounds and Injuries
In Vitro Techniques
Reperfusion Injury
Serum
Acute Kidney Injury
Endothelial Cells

All Science Journal Classification (ASJC) codes

  • Physiology
  • Urology

これを引用

Estrogen protects renal endothelial barrier function from ischemia-reperfusion in vitro and in vivo. / Hutchens, Michael P.; Fujiyoshi, Tetsuhiro; Komers, Radko; Herson, Paco S.; Anderson, Sharon.

:: American Journal of Physiology - Renal Physiology, 巻 303, 番号 3, 01.08.2012.

研究成果: ジャーナルへの寄稿記事

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title = "Estrogen protects renal endothelial barrier function from ischemia-reperfusion in vitro and in vivo",
abstract = "Emerging evidence suggests that renal endothelial function may be altered in ischemia-reperfusion injury. Acute kidney injury is sexually dimorphic, and estrogen protects renal tubular function after experimental ischemic injury. This study tested the hypothesis that during ischemia-reperfusion, estrogen alters glomerular endothelial function to prevent hyperpermeability. Glomerular endothelial cells were exposed to 8-h oxygen-glucose deprivation (OGD) followed by 4- and 8-h reoxygen-ation-glucose repletion. After 4-h reoxygenation-glucose repletion, transendothelial permeability to Ficoll-70 was reduced, and transen-dothelial resistance increased, by 17(3-estradiol vs. vehicle treatment during OGD (OGD-vehicle: 91.0 ± 11.8{\%}, OGD-estrogen: 102.6 ± 10.8{\%}, P < 0.05). This effect was reversed by coadministration of G protein-coupled receptor 30 (GPR30) antagonist G15 with 17(3-estra-diol (OGD-estrogen-G15: 89.5 ± 6.9, P < 0.05 compared with 17(3-estradiol). To provide preliminary confirmation of this result in vivo, Ficoll-70 was administered to mice 24 h after cardiac arrest and cardiopulmonary resuscitation (CA/CPR). Blood urea nitrogen (BUN) and serum creatinine (SCr) in these mice were elevated within 12 h following CA/CPR and reduced at 24 h by pretreatment with 17(3-estradiol (BUN/SCr 17(3-estradiol: 34 ± 19/0.2 ±0.1 vehicle: 92 ± 49/0.5 ± 0.3, n = 8-12, P < 0.05). Glomerular sieving of Ficoll 70 was increased by CA/CPR within 2 h of injury and 17(3-estradiol treatment (0; 17(3-estradiol: 0.74 ± 0.26 vs. vehicle: 1.05 ± 0.53, n = 14-15, P < 0.05). These results suggest that estrogen reduces post-ischemic glomerular endothelial hyperpermeability at least in part through GPR30 and that estrogen may regulate post CA/CPR glomerular permeability in a similar fashion in vivo.",
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AU - Herson, Paco S.

AU - Anderson, Sharon

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N2 - Emerging evidence suggests that renal endothelial function may be altered in ischemia-reperfusion injury. Acute kidney injury is sexually dimorphic, and estrogen protects renal tubular function after experimental ischemic injury. This study tested the hypothesis that during ischemia-reperfusion, estrogen alters glomerular endothelial function to prevent hyperpermeability. Glomerular endothelial cells were exposed to 8-h oxygen-glucose deprivation (OGD) followed by 4- and 8-h reoxygen-ation-glucose repletion. After 4-h reoxygenation-glucose repletion, transendothelial permeability to Ficoll-70 was reduced, and transen-dothelial resistance increased, by 17(3-estradiol vs. vehicle treatment during OGD (OGD-vehicle: 91.0 ± 11.8%, OGD-estrogen: 102.6 ± 10.8%, P < 0.05). This effect was reversed by coadministration of G protein-coupled receptor 30 (GPR30) antagonist G15 with 17(3-estra-diol (OGD-estrogen-G15: 89.5 ± 6.9, P < 0.05 compared with 17(3-estradiol). To provide preliminary confirmation of this result in vivo, Ficoll-70 was administered to mice 24 h after cardiac arrest and cardiopulmonary resuscitation (CA/CPR). Blood urea nitrogen (BUN) and serum creatinine (SCr) in these mice were elevated within 12 h following CA/CPR and reduced at 24 h by pretreatment with 17(3-estradiol (BUN/SCr 17(3-estradiol: 34 ± 19/0.2 ±0.1 vehicle: 92 ± 49/0.5 ± 0.3, n = 8-12, P < 0.05). Glomerular sieving of Ficoll 70 was increased by CA/CPR within 2 h of injury and 17(3-estradiol treatment (0; 17(3-estradiol: 0.74 ± 0.26 vs. vehicle: 1.05 ± 0.53, n = 14-15, P < 0.05). These results suggest that estrogen reduces post-ischemic glomerular endothelial hyperpermeability at least in part through GPR30 and that estrogen may regulate post CA/CPR glomerular permeability in a similar fashion in vivo.

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