Abstract
It is now understood that the mechanisms leading to neuronal cell death after cerebral ischemia are highly complex. A well established fact in this field is that neurons continue to die over days and months after ischemia, and that reperfusion following cerebral ischemia contributes substantially to ischemic injury. It is now well accepted that central to ischemic/reperfusion- induced injury is what occurs to mitochondria hours to days following the ischemic insult. For many years, it has been established that reactive oxygen species (ROS) and reactive nitrogen species (RNS) promote lipid, protein, and DNA oxidation that affects normal cell physiology and eventually leads to neuronal demise. In addition to oxidation of neuronal molecules by ROS and RNS, a novel pathway for molecular modifications has risen from the concept that ROS can activate specific signal transduction pathways that, depending on the insult degree, can lead to either normal plasticity or pathology. Two examples of these pathways could explain why lethal ischemic insults lead to the translocation of protein kinase Cδ (δPKC), which plays a role in apoptosis after cerebral ischemia, or why sublethal ischemic insults, such as in ischemic preconditioning, lead to the translocation of εPKC, which plays a pivotal role in neuroprotection. A better understanding of the mechanisms by which ROS and/or RNS modulate key protein kinases that are involved in signaling pathways that lead to cell death and survival after cerebral ischemia will help devise novel therapeutic strategies.
| Original language | English |
|---|---|
| Pages (from-to) | 1150-1157 |
| Number of pages | 8 |
| Journal | Antioxidants and Redox Signaling |
| Volume | 7 |
| Issue number | 9-10 |
| DOIs | |
| State | Published - Sep 1 2005 |
Fingerprint
ASJC Scopus subject areas
- Biochemistry
Cite this
Role of reactive oxygen species and protein kinase C in ischemic tolerance in the brain. / Perez-Pinzon, Miguel; Dave, Kunjan R; Raval, Ami.
In: Antioxidants and Redox Signaling, Vol. 7, No. 9-10, 01.09.2005, p. 1150-1157.Research output: Contribution to journal › Article
}
TY - JOUR
T1 - Role of reactive oxygen species and protein kinase C in ischemic tolerance in the brain
AU - Perez-Pinzon, Miguel
AU - Dave, Kunjan R
AU - Raval, Ami
PY - 2005/9/1
Y1 - 2005/9/1
N2 - It is now understood that the mechanisms leading to neuronal cell death after cerebral ischemia are highly complex. A well established fact in this field is that neurons continue to die over days and months after ischemia, and that reperfusion following cerebral ischemia contributes substantially to ischemic injury. It is now well accepted that central to ischemic/reperfusion- induced injury is what occurs to mitochondria hours to days following the ischemic insult. For many years, it has been established that reactive oxygen species (ROS) and reactive nitrogen species (RNS) promote lipid, protein, and DNA oxidation that affects normal cell physiology and eventually leads to neuronal demise. In addition to oxidation of neuronal molecules by ROS and RNS, a novel pathway for molecular modifications has risen from the concept that ROS can activate specific signal transduction pathways that, depending on the insult degree, can lead to either normal plasticity or pathology. Two examples of these pathways could explain why lethal ischemic insults lead to the translocation of protein kinase Cδ (δPKC), which plays a role in apoptosis after cerebral ischemia, or why sublethal ischemic insults, such as in ischemic preconditioning, lead to the translocation of εPKC, which plays a pivotal role in neuroprotection. A better understanding of the mechanisms by which ROS and/or RNS modulate key protein kinases that are involved in signaling pathways that lead to cell death and survival after cerebral ischemia will help devise novel therapeutic strategies.
AB - It is now understood that the mechanisms leading to neuronal cell death after cerebral ischemia are highly complex. A well established fact in this field is that neurons continue to die over days and months after ischemia, and that reperfusion following cerebral ischemia contributes substantially to ischemic injury. It is now well accepted that central to ischemic/reperfusion- induced injury is what occurs to mitochondria hours to days following the ischemic insult. For many years, it has been established that reactive oxygen species (ROS) and reactive nitrogen species (RNS) promote lipid, protein, and DNA oxidation that affects normal cell physiology and eventually leads to neuronal demise. In addition to oxidation of neuronal molecules by ROS and RNS, a novel pathway for molecular modifications has risen from the concept that ROS can activate specific signal transduction pathways that, depending on the insult degree, can lead to either normal plasticity or pathology. Two examples of these pathways could explain why lethal ischemic insults lead to the translocation of protein kinase Cδ (δPKC), which plays a role in apoptosis after cerebral ischemia, or why sublethal ischemic insults, such as in ischemic preconditioning, lead to the translocation of εPKC, which plays a pivotal role in neuroprotection. A better understanding of the mechanisms by which ROS and/or RNS modulate key protein kinases that are involved in signaling pathways that lead to cell death and survival after cerebral ischemia will help devise novel therapeutic strategies.
UR - http://www.scopus.com/inward/record.url?scp=24144455328&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=24144455328&partnerID=8YFLogxK
U2 - 10.1089/ars.2005.7.1150
DO - 10.1089/ars.2005.7.1150
M3 - Article
VL - 7
SP - 1150
EP - 1157
JO - Antioxidants and Redox Signaling
JF - Antioxidants and Redox Signaling
SN - 1523-0864
IS - 9-10
ER -