RGD Reference Report - 17ß-estradiol inhibits MMP-9 and SUR1/TrpM4 expression and activation and thereby attenuates BSCB disruption/hemorrhage after spinal cord injury in male rats. - Rat Genome Database

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17ß-estradiol inhibits MMP-9 and SUR1/TrpM4 expression and activation and thereby attenuates BSCB disruption/hemorrhage after spinal cord injury in male rats.

Authors: Lee, Jee Y  Choi, Hae Y  Na, Won H  Ju, Bong G  Yune, Tae Y 
Citation: Lee JY, etal., Endocrinology. 2015 May;156(5):1838-50. doi: 10.1210/en.2014-1832. Epub 2015 Mar 12.
RGD ID: 12791993
Pubmed: PMID:25763638   (View Abstract at PubMed)
DOI: DOI:10.1210/en.2014-1832   (Journal Full-text)

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 17ß-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.

RGD Manual Disease Annotations    Click to see Annotation Detail View

Objects Annotated

Genes (Rattus norvegicus)
Abcc8  (ATP binding cassette subfamily C member 8)
Mmp9  (matrix metallopeptidase 9)
Trpm4  (transient receptor potential cation channel, subfamily M, member 4)

Genes (Mus musculus)
Abcc8  (ATP-binding cassette, sub-family C member 8)
Mmp9  (matrix metallopeptidase 9)
Trpm4  (transient receptor potential cation channel, subfamily M, member 4)

Genes (Homo sapiens)
ABCC8  (ATP binding cassette subfamily C member 8)
MMP9  (matrix metallopeptidase 9)
TRPM4  (transient receptor potential cation channel subfamily M member 4)


Additional Information