Loss of Ref-1 protein expression precedes DNA fragmentation in apoptotic neurons.
Ref-1 is a bifunctional protein that has been implicated in the transcriptional regulation of AP-1 elements and in DNA repair. To investigate whether Ref-1 is involved in programmed cell death its expression was measured in the 21-day-old rat brain at various time-points following a moderate unilateral hypoxic-ischemic (HI) insult. The CA1 pyramidal cells, which are selectively vulnerable to HI injury, showed a significant decrease in Ref-1 immunoreactivity 48 h-7 days post-insult. This loss of Ref-1 immunoreactivity may contribute to a decrease in endogenous repair activity and the development of apoptosis in the CA1 pyramidal cells.
Walton
M
M
Department of Pharmacology and Clinical Pharmacology, Faculty of Medicine and Health Science, University of Aukland, New Zealand.
Lawlor
P
P
Sirimanne
E
E
Williams
C
C
Gluckman
P
P
Dragunow
M
M
D000818:Animals; D017209:Apoptosis; D019757:Carbon-Oxygen Lyases; D053938:DNA Fragmentation / Q000235:genetics*; D043603:DNA-(Apurinic or Apyrimidinic Site) Lyase; D007150:Immunohistochemistry; D009474:Neurons / Q000378:metabolism*; D009687:Nuclear Proteins / Q000378:metabolism*; D051381:Rats; D017208:Rats, Wistar
D009687:Nuclear Proteins; D019757:Carbon-Oxygen Lyases; C470319:Apex1 protein, rat; D043603:DNA-(Apurinic or Apyrimidinic Site) Lyase