Abstract
Recent experiments suggest that apoptotic mechanisms are involved in neuronal cell death after ischemic injury. Although the exact mechanism that triggers activation of apoptotic machinery remains uncertain, in vitro studies revealed that forced expression of cell cycle-related proteins induced apoptosis. Thus, aberrant expression of such proteins might be related to ischemic neuronal death. In the present experiment, we investigated expression of cell cycle-related proteins, i.e., cyclin B1, cyclin D1, cdk4, and PCNA, in rat brain after transient MCA occlusion, and compared the temporal profile of the results with that of TUNEL study, which detects double strand breaks in DNA. There were no immunoreactivities for cyclin B1, cyclin D1, and PCNA in the brain with and without ischemia. As for cdk4, however, it became present at 1 and 3 days of reperfusion after 2 h of ischemia. On the other hand, TUNEL positive cells appeared as early as 3 h of reperfusion, which peaked at 1 and 3 days. These results indicate that aberrant expression of cdk4, but not cyclin B1, cyclin D1 or PCNA, actually takes place in the brain after MCA occlusion, but this is not the causative mechanism of apoptotic cell death in the brain with ischemia.
| Original language | English |
|---|---|
| Pages (from-to) | 695-698 |
| Number of pages | 4 |
| Journal | Neurological Research |
| Volume | 21 |
| Issue number | 7 |
| Publication status | Published - Oct 1999 |
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Keywords
- Apoptosis
- Brain
- Cell cycle
- Cyclin
- Cyclin dependent kinase
- Infarct
ASJC Scopus subject areas
- Clinical Neurology
- Neuroscience(all)
Cite this
DNA fragmentation precedes aberrant expression of cell cycle-related protein in rat brain after MCA occlusion. / Hayashi, Takeshi; Sakurai, Masahiro; Abe, Koji; Itoyama, Yasuto.
In: Neurological Research, Vol. 21, No. 7, 10.1999, p. 695-698.Research output: Contribution to journal › Article
}
TY - JOUR
T1 - DNA fragmentation precedes aberrant expression of cell cycle-related protein in rat brain after MCA occlusion
AU - Hayashi, Takeshi
AU - Sakurai, Masahiro
AU - Abe, Koji
AU - Itoyama, Yasuto
PY - 1999/10
Y1 - 1999/10
N2 - Recent experiments suggest that apoptotic mechanisms are involved in neuronal cell death after ischemic injury. Although the exact mechanism that triggers activation of apoptotic machinery remains uncertain, in vitro studies revealed that forced expression of cell cycle-related proteins induced apoptosis. Thus, aberrant expression of such proteins might be related to ischemic neuronal death. In the present experiment, we investigated expression of cell cycle-related proteins, i.e., cyclin B1, cyclin D1, cdk4, and PCNA, in rat brain after transient MCA occlusion, and compared the temporal profile of the results with that of TUNEL study, which detects double strand breaks in DNA. There were no immunoreactivities for cyclin B1, cyclin D1, and PCNA in the brain with and without ischemia. As for cdk4, however, it became present at 1 and 3 days of reperfusion after 2 h of ischemia. On the other hand, TUNEL positive cells appeared as early as 3 h of reperfusion, which peaked at 1 and 3 days. These results indicate that aberrant expression of cdk4, but not cyclin B1, cyclin D1 or PCNA, actually takes place in the brain after MCA occlusion, but this is not the causative mechanism of apoptotic cell death in the brain with ischemia.
AB - Recent experiments suggest that apoptotic mechanisms are involved in neuronal cell death after ischemic injury. Although the exact mechanism that triggers activation of apoptotic machinery remains uncertain, in vitro studies revealed that forced expression of cell cycle-related proteins induced apoptosis. Thus, aberrant expression of such proteins might be related to ischemic neuronal death. In the present experiment, we investigated expression of cell cycle-related proteins, i.e., cyclin B1, cyclin D1, cdk4, and PCNA, in rat brain after transient MCA occlusion, and compared the temporal profile of the results with that of TUNEL study, which detects double strand breaks in DNA. There were no immunoreactivities for cyclin B1, cyclin D1, and PCNA in the brain with and without ischemia. As for cdk4, however, it became present at 1 and 3 days of reperfusion after 2 h of ischemia. On the other hand, TUNEL positive cells appeared as early as 3 h of reperfusion, which peaked at 1 and 3 days. These results indicate that aberrant expression of cdk4, but not cyclin B1, cyclin D1 or PCNA, actually takes place in the brain after MCA occlusion, but this is not the causative mechanism of apoptotic cell death in the brain with ischemia.
KW - Apoptosis
KW - Brain
KW - Cell cycle
KW - Cyclin
KW - Cyclin dependent kinase
KW - Infarct
UR - http://www.scopus.com/inward/record.url?scp=0032736977&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=0032736977&partnerID=8YFLogxK
M3 - Article
C2 - 10555194
AN - SCOPUS:0032736977
VL - 21
SP - 695
EP - 698
JO - Neurological Research
JF - Neurological Research
SN - 0161-6412
IS - 7
ER -