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Mitochondrial fission blocker protects brain endothelial cells but not neurons following oxygen‐glucose deprivation (OGD)
Author(s) -
Wappler Edina A,
Katz Paige S,
Katakam Prasad V.G.,
Busija David W
Publication year - 2012
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.26.1_supplement.711.15
Subject(s) - mitochondrial fission , viability assay , apoptosis , endothelial stem cell , pharmacology , biology , dnm1l , microbiology and biotechnology , reactive oxygen species , mitochondrion , biochemistry , in vitro
The aim of our study was to investigate the effect of mitochondrial fission blocker Mdivi‐1 on cell survival following OGD in neurons and cerebral vascular endothelial cells. Primary rat cortical neurons were isolated from E18 Sprague Dawley fetuses, while primary rat brain endothelial cells (RBEC) were isolated from 2 week old pups. We also used a human brain endothelial cell (HBEC) line in this study. In the confluent cultures, cell viability was measured following 1, 2, and 3 hour of OGD in HBEC, RBEC, and neuronal cells, respectively, which was followed by 24 hour reoxygenation in each case. Each group had a normoxic control with the same treatment as the OGD plates. Cells were exposed to Mdivi‐1 (2.5 μM‐ 250 μM), an inhibitor of the mitochondrial fission protein, dynamin‐related peptide 1 (Drp1), during the OGD. Mdivi‐1 treatment improved cell viability following OGD by 15–45% in HBEC, and 15% in RBEC compared to untreated cells exposed to OGD. However, Mdivi‐1 failed to change the cell viability in the neurons exposed to OGD. In conclusion, the mitochondrial fission blocker Mdivi‐1, is protective against OGD in endothelial cells from both rat and human, but not in rat neurons.