Cited by 93Cell death mechanisms and regulationAcute Ischemic Stroke ManagementNeurological Disorders and Treatments

Apoptosis in Focal Cerebral Ischemia

Chopp, Michael, Li, Y.·1996·Mechanisms of Secondary Brain Damage in Cerebral Ischemia and Trauma

Abstract

An ischemic insult to the brain evokes cell damage which may progress to cell death. We invariably associated cell death with necrosis. Necrosis exhibits well defined morphological characteristics, and the biochemical and biophysical processes associated with necrosis have been identified. However, another form of cell death exists, apoptosis. Apoptosis plays an important role in the early development of tissues. Cells undergoing apoptosis exhibit very different morphological characteristics and temporal profiles of change from cells undergoing necrosis. Apoptosis has been identified with the internucleosomal fragmentation of DNA. More importantly, apoptosis has been associated with a process of programmed cell death, in which a genetic program is activated which results in the death of the cell. In this presentation, we will review our data on the morphological, biochemical and molecular evidence of apoptosis in the rodent (rat, mouse) brain after middle cerebral artery occlusion. Emphasis will be placed on describing the temporal profile and the anatomical distribution of cells undergoing apoptosis as functions of duration of MCA occlusion and reperfusion after MCA occlusion. This possible contribution of selective genes in promoting and/or inhibiting apoptosis will also be discussed.

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Crossref · 10.1007/978-3-7091-9465-2_4

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42 of 42 references verified0 citation errors · 0 not checkable

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  • Up to 95% of apoptotic cells after focal cerebral ischemia are neurons.

    “Up to 95% of apoptotic cells are neurons [2].”

    From MicroRNA‐21 protects neurons from ischemic death (2010) · cites this paper as [2]

  • Apoptosis reaches its peak level 1 to 2 days after stroke.

    “Apoptosis reaches its peak level 1 to 2 days after stroke [2].”

    From MicroRNA‐21 protects neurons from ischemic death (2010) · cites this paper as [2]

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Authors
Chopp, M., & Li, Y.
Affiliations
  • Henry Ford Health (US)
  • Oakland University (US)
Venue
Mechanisms of Secondary Brain Damage in Cerebral Ischemia and Trauma
Published
1996
Volume
66
Pages
21-26
OpenAlex
W32230716
Cited by
93
References
42
Citations by year
2023: 2 · 2021: 1 · 2020: 1 · 2018: 1 · 2017: 1 · 2016: 2 · 2015: 1 · 2014: 3 · 2013: 5 · 2012: 2
FWCI
8.03
Type
book chapter
Language
it
Open access
closed
Locations
  • Springer eBooks (publishedVersion)
  • PubMed (publishedVersion)
Topics
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Cell death mechanisms and regulation
  • Health Sciences › Medicine › Epidemiology › Acute Ischemic Stroke Management
  • Life Sciences › Neuroscience › Neurology › Neurological Disorders and Treatments
Keywords
apoptosis, focal cerebral ischemia, middle cerebral artery occlusion, programmed cell death, necrosis, internucleosomal DNA fragmentation, reperfusion, ischemic cell death, apoptosis-related genes, rat brain, mouse brain
MeSH terms
Animals, Brain, Brain Damage, Chronic, Brain Mapping, Brain Ischemia, Apoptosis, Mice, Rats, DNA Fragmentation

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