Expression of connexin 43 gap junctions and hemichannels following cerebral ischemia in near-term fetal sheep
(2006)Division of Molecular Medicine and Gene Therapy
- Abstract
- Connexins are proteins that make up the gap junctions that directly link the intracellular spaces of neighboring cells. Each gap junction is formed by the joining up or docking of two hemichannels in the cell membranes. It has been proposed that the gap junctions themselves or opening of hemichannels to the extracellular space may allow the spread of cytotoxic signals after injury, leading to progression of cell death. Prolonged, moderate cerebral hypothermia is consistently protective after cerebral ischemia, however, it is unknown whether this therapy affects the expression of gap junctions and their hemichannels. We therefore investigated the time course of expression of connexin 43 gap junctions and hemichannels in white matter after a... (More)
- Connexins are proteins that make up the gap junctions that directly link the intracellular spaces of neighboring cells. Each gap junction is formed by the joining up or docking of two hemichannels in the cell membranes. It has been proposed that the gap junctions themselves or opening of hemichannels to the extracellular space may allow the spread of cytotoxic signals after injury, leading to progression of cell death. Prolonged, moderate cerebral hypothermia is consistently protective after cerebral ischemia, however, it is unknown whether this therapy affects the expression of gap junctions and their hemichannels. We therefore investigated the time course of expression of connexin 43 gap junctions and hemichannels in white matter after a 30 min episode of cerebral ischemia in term-equivalent fetal sheep. We compared the effect of treatment with brain cooling started 2h after the ischemic insult and continued until 72h, which is known to be protective, with cooling delayed until 6h after ischemia, which has been reported not to reduce white matter injury. Quantification of immunoreactivity was performed with confocal microscopy. The preliminary results indicate that ischemia was associated with a transient increase in both Cx43 and hemichannel expression, maximal at 24h and resolving by 5 days after ischemia. Intriguingly, hemichannel expression was greater after 5 days in animals that had been cooled from 6h post-insult than those in which cooling was initiated at 2h after the start of ischemia, suggesting that late cooling may not be advantageous, but in fact lead to delayed induction of connexin expression once the cooling is removed (Less)
Please use this url to cite or link to this publication:
http://lup.lub.lu.se/student-papers/record/8996693
- author
- Hawranek, Carolina
- supervisor
- organization
- year
- 2006
- type
- H2 - Master's Degree (Two Years)
- subject
- keywords
- Connexin 43, connexin 43 hemichannels, ischemic brain damage, apoptosis, astrocytic network, cell death spread, brain cooling, hypothermia
- language
- English
- id
- 8996693
- date added to LUP
- 2019-10-16 15:05:42
- date last changed
- 2019-10-16 15:05:42
@misc{8996693,
abstract = {{Connexins are proteins that make up the gap junctions that directly link the intracellular spaces of neighboring cells. Each gap junction is formed by the joining up or docking of two hemichannels in the cell membranes. It has been proposed that the gap junctions themselves or opening of hemichannels to the extracellular space may allow the spread of cytotoxic signals after injury, leading to progression of cell death. Prolonged, moderate cerebral hypothermia is consistently protective after cerebral ischemia, however, it is unknown whether this therapy affects the expression of gap junctions and their hemichannels. We therefore investigated the time course of expression of connexin 43 gap junctions and hemichannels in white matter after a 30 min episode of cerebral ischemia in term-equivalent fetal sheep. We compared the effect of treatment with brain cooling started 2h after the ischemic insult and continued until 72h, which is known to be protective, with cooling delayed until 6h after ischemia, which has been reported not to reduce white matter injury. Quantification of immunoreactivity was performed with confocal microscopy. The preliminary results indicate that ischemia was associated with a transient increase in both Cx43 and hemichannel expression, maximal at 24h and resolving by 5 days after ischemia. Intriguingly, hemichannel expression was greater after 5 days in animals that had been cooled from 6h post-insult than those in which cooling was initiated at 2h after the start of ischemia, suggesting that late cooling may not be advantageous, but in fact lead to delayed induction of connexin expression once the cooling is removed}},
author = {{Hawranek, Carolina}},
language = {{eng}},
note = {{Student Paper}},
title = {{Expression of connexin 43 gap junctions and hemichannels following cerebral ischemia in near-term fetal sheep}},
year = {{2006}},
}