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Overpressure‐induced brain injury at the cellular level
Author(s) -
Leung Lai Yee,
VandeVord Pamela
Publication year - 2009
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.23.1_supplement.307.1
Subject(s) - apoptosis , traumatic brain injury , andrology , overpressure , medicine , neuron , chemistry , biology , microbiology and biotechnology , anesthesia , neuroscience , biochemistry , physics , psychiatry , thermodynamics
Veterans returning from wars exposed to blast with no visible wounds were diagnosed with mild traumatic brain injury (Warden 2006). Animal studies revealed the effects of primary blast wave on central nervous system. These studies mainly focused on systemic effect (Kaur et al 1995‐97; Cernak et al 2001). The molecular mechanism of blast wave‐induced brain injury is still unclear. We conducted a series of in vitro experiments to examine the cellular responses of astrocytes and neurons after exposing to overpressure (OP). A barochamber was designed and fabricated to generate a pressure with magnitude ranged from 17 to 58 psi and duration of 10 msec. Individual cell types were cultured on Petri dish, sealed and then exposed to OP. Viability assays and total RNA extraction for quantitative real‐time PCR were carried out at 24, 48 and 72 hours. Results of astrocytic response were published, which showed that astrocytes survived the OP and became reactive (VandeVord et al 2008). In rat cortical neuron cultures, Bcl‐2/BAX expression ratios were less than 1 (indicating apoptosis) in all groups except controls at 24 hour post‐exposure, followed by a significant increase (ratios>1, indicating survival) at 48 hour. The expression level of apoptosis‐related gene Caspase‐8 reached the peak at 72 hour. Neurons exhibited both apoptotic and survival processes after OP insult. Grant Funding Source VA RR&D Career Development Award