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Ovariectomy decreases expression of transcription factors for mitochondrial biogenesis in mouse cerebrovascular endothelial cells
Author(s) -
Kemper Martin F,
Duckles Sue,
Krause Diana
Publication year - 2011
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.25.1_supplement.lb361
Subject(s) - tfam , mitochondrial biogenesis , estrogen , enos , biology , endothelial stem cell , nrf1 , ovariectomized rat , microbiology and biotechnology , endocrinology , mitochondrion , medicine , mitophagy , apoptosis , in vitro , nitric oxide , biochemistry , nitric oxide synthase , autophagy
Estrogen has protective effects on the cerebrovasculature in physiological as well as pathological states such as stroke. However teasing out effects on individual cell types remains elusive. Thus we adapted Dynabeads (Invitrogen) technology using PECAM1 antibodies to isolate brain vascular endothelial cells. We used appropriate cellular markers to demonstrate enrichment of brain endothelial cells as well as decreased presence of other cell types. We developed a method to correct for variations in endothelial enrichment among different preparations. We found that the level of eNOS mRNA is two‐fold higher in endothelial cells from intact females compared to ovariectomized mice. This agrees with our previous observation of higher eNOS in brain vessels from estrogen‐exposed mice. We also evaluated levels of mitochondrial transcription factors in brain endothelial cells. We observed 61% and 38% higher mRNA levels of NRF1 and TFAM, respectively, in endothelial cells from intact females relative to ovariectomized mice. These two factors are essential in maintenance of respiration as well as mitochondrial biogenesis. The findings extend our previous observations that estrogen impacts cerebrovascular mitochondria. This is the first time that female reproductive competency has been shown to influence endothelial cell master regulators of mitochondrial function.