Evidence for hypoxia‐induced, programmed cell death of cultured neurons

Evidence for hypoxia‐induced, programmed cell death of cultured neurons Apoptosis, a form of cell death (“programmed” cell death) in which the nucleus and cytoplasm shrink and often fragment, serves to eliminate excessive or unwanted cells during remodeling of embryonic tissues, during organ involution, and in tumor regression. In acute pathological states, such as ischemia, the cells tend to swell and lyse—a process called necrosis. We hypothesize that the delayed neural death clinically associated with hypoxia may, in part, represent apoptosis. A tissue culture model of 24 hours of hypoxia was employed using sympathetic neurons. Pretreatment with an endonuclease inhibitor (aurintricarboxylic acid) decreased cell death by 53%, depolarizing conditions (55 mM potassium chloride) decreased cell death by 33%, and an RNA synthesis inhibitor (actinomycin D) by 26% (all have been shown to prevent apoptosis). Pretreatment with antisense c‐myc had no effect. Fluorescent staining with propidium iodide (a DNA marker) demonstrated chromatin condensation and agarose gel electrophoresis demonstrated a DNA “ladder.” These data suggest that apoptosis may play a role in hypoxic cell death and that in this paradigm, expression of c‐myc is unnecessary. This would suggest a new approach to our understanding of hypoxia and open new strategies to lessen neuronal damage secondary to this process. http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png Annals of Neurology Wiley

Evidence for hypoxia‐induced, programmed cell death of cultured neurons

Loading next page...
 
/lp/wiley/evidence-for-hypoxia-induced-programmed-cell-death-of-cultured-neurons-lNUl6u8klK
Publisher
Wiley
Copyright
Copyright © 1994 American Neurological Association
ISSN
0364-5134
eISSN
1531-8249
D.O.I.
10.1002/ana.410360610
Publisher site
See Article on Publisher Site

Abstract

Apoptosis, a form of cell death (“programmed” cell death) in which the nucleus and cytoplasm shrink and often fragment, serves to eliminate excessive or unwanted cells during remodeling of embryonic tissues, during organ involution, and in tumor regression. In acute pathological states, such as ischemia, the cells tend to swell and lyse—a process called necrosis. We hypothesize that the delayed neural death clinically associated with hypoxia may, in part, represent apoptosis. A tissue culture model of 24 hours of hypoxia was employed using sympathetic neurons. Pretreatment with an endonuclease inhibitor (aurintricarboxylic acid) decreased cell death by 53%, depolarizing conditions (55 mM potassium chloride) decreased cell death by 33%, and an RNA synthesis inhibitor (actinomycin D) by 26% (all have been shown to prevent apoptosis). Pretreatment with antisense c‐myc had no effect. Fluorescent staining with propidium iodide (a DNA marker) demonstrated chromatin condensation and agarose gel electrophoresis demonstrated a DNA “ladder.” These data suggest that apoptosis may play a role in hypoxic cell death and that in this paradigm, expression of c‐myc is unnecessary. This would suggest a new approach to our understanding of hypoxia and open new strategies to lessen neuronal damage secondary to this process.

Journal

Annals of NeurologyWiley

Published: Dec 1, 1994

References

  • Glutamate neurotoxicity in cortical cell culture
    Choi, Choi; Maulucci‐Gedde, Maulucci‐Gedde; Kriegstein, Kriegstein
  • Inhibitors of protein synthesis and RNA synthesis prevent neuronal death caused by nerve growth factor deprivation
    Martin, Martin; Schmidt, Schmidt; DiStefano, DiStefano
  • Expression of c‐fos and c‐jun family genes after focal ischemia
    An, An; Lin, Lin; Liu, Liu
  • Oxidative stress induces apoptosis in embryonic cortical neurons
    Ratan, Ratan; Murphy, Murphy; Barabim, Barabim

You’re reading a free preview. Subscribe to read the entire article.


DeepDyve is your
personal research library

It’s your single place to instantly
discover and read the research
that matters to you.

Enjoy affordable access to
over 18 million articles from more than
15,000 peer-reviewed journals.

All for just $49/month

Explore the DeepDyve Library

Search

Query the DeepDyve database, plus search all of PubMed and Google Scholar seamlessly

Organize

Save any article or search result from DeepDyve, PubMed, and Google Scholar... all in one place.

Access

Get unlimited, online access to over 18 million full-text articles from more than 15,000 scientific journals.

Your journals are on DeepDyve

Read from thousands of the leading scholarly journals from SpringerNature, Elsevier, Wiley-Blackwell, Oxford University Press and more.

All the latest content is available, no embargo periods.

See the journals in your area

DeepDyve

Freelancer

DeepDyve

Pro

Price

FREE

$49/month
$360/year

Save searches from
Google Scholar,
PubMed

Create folders to
organize your research

Export folders, citations

Read DeepDyve articles

Abstract access only

Unlimited access to over
18 million full-text articles

Print

20 pages / month

PDF Discount

20% off