17β-Estradiol Inhibits MMP-9 and SUR1/TrpM4 Expression and Activation and Thereby Attenuates BSCB Disruption/Hemorrhage After Spinal Cord Injury in Male Rats

Blood-spinal cord barrier (BSCB) disruption and progressive hemorrhage after spinal cord injury (SCI) lead to secondary injury and the subsequent apoptosis and/or necrosis of neuron and glia, causing permanent neurological deficits. In this study, we examined the effect of 17β-estradiol (E2) on BSCB...

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Veröffentlicht in:Endocrinology (Philadelphia) 2015-05, Vol.156 (5), p.1838-1850
Hauptverfasser: Lee, Jee Y, Choi, Hae Y, Na, Won H, Ju, Bong G, Yune, Tae Y
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creator Lee, Jee Y
Choi, Hae Y
Na, Won H
Ju, Bong G
Yune, Tae Y
description Blood-spinal cord barrier (BSCB) disruption and progressive hemorrhage after spinal cord injury (SCI) lead to secondary injury and the subsequent apoptosis and/or necrosis of neuron and glia, causing permanent neurological deficits. In this study, we examined the effect of 17β-estradiol (E2) on BSCB breakdown and hemorrhage as well as subsequent inflammation after SCI. After a moderate contusion injury at the 9th thoracic segment of spinal cord, E2 (300 μg/kg) was administered by iv injection immediately after SCI, and the same dose of E2 was then administered 6 and 24 hours after injury. Our data show that E2 attenuated BSCB permeability and hemorrhage and reduced the infiltration of neutrophils and macorphages after SCI. Consistent with this finding, the expression of inflammatory mediators was significantly reduced by E2. Furthermore, E2 treatment significantly inhibited the expression of sulfonylurea receptor 1 and transient receptor potential melastatin 4 after injury, which are known to mediate hemorrhage at an early stage after SCI. Moreover, the expression and activation of matrix metalloprotease-9 after injury, which is known to disrupt BSCB, and the degradation of tight junction proteins, such as zona occludens-1 and occludin, were significantly inhibited by E2 treatment. Furthermore, the protective effects of E2 on BSCB disruption and functional improvement were abolished by an estrogen receptor antagonist, ICI 182780 (3 mg/kg). Thus, our study provides evidence that the neuroprotective effect of E2 after SCI is, in part, mediated by inhibiting BSCB disruption and hemorrhage through the down-regulation of sulfonylurea receptor 1/transient receptor potential melastatin 4 and matrix metalloprotease-9, which is dependent on estrogen receptor.
doi_str_mv 10.1210/en.2014-1832
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source Oxford University Press Journals All Titles (1996-Current); MEDLINE; EZB-FREE-00999 freely available EZB journals; Alma/SFX Local Collection; Journals@Ovid Complete
subjects 17β-Estradiol
Animals
Apoptosis
Blood-Brain Barrier - drug effects
Blood-Brain Barrier - metabolism
Capillary Permeability - drug effects
Disruption
Down-regulation
Down-Regulation - drug effects
Estradiol - analogs & derivatives
Estradiol - pharmacology
Estrogen Receptor Antagonists - pharmacology
Estrogen receptors
Estrogens
Fulvestrant
Gelatinase B
Hemorrhage
Hemorrhage - metabolism
Leukocytes (neutrophilic)
Male
Matrix metalloproteinase
Matrix Metalloproteinase 9 - drug effects
Matrix Metalloproteinase 9 - metabolism
Necrosis
Neurological diseases
Neuronal-glial interactions
Neuroprotection
Rats
Rats, Sprague-Dawley
Receptors
Sex hormones
Spinal cord injuries
Spinal Cord Injuries - metabolism
Sulfonylurea
Sulfonylurea Receptors - drug effects
Sulfonylurea Receptors - metabolism
Thorax
Transient receptor potential proteins
TRPM Cation Channels - drug effects
TRPM Cation Channels - metabolism
title 17β-Estradiol Inhibits MMP-9 and SUR1/TrpM4 Expression and Activation and Thereby Attenuates BSCB Disruption/Hemorrhage After Spinal Cord Injury in Male Rats
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