|
|
 Previous Article | Table of Contents | Next Article 
The acid deoxyribonuclease of neutrophils: a possible participant in
apoptosis-associated genome destruction
RA Gottlieb, HA Giesing, RL Engler and BM Babior
Department of Molecular and Experimental Medicine, Scripps Research
Institute, La Jolla, CA 92037, USA.
Human neutrophils are terminally differentiated cells that spontaneously
undergo apoptosis in tissue culture. Apoptosis in these cells can be
delayed by culture in the presence of granulocyte colony- stimulating
factor or other inflammatory mediators. Neutrophils were found to contain
an acid endonuclease that appeared to be responsible for the
internucleosomal DNA cleavage that accompanies apoptosis. As measured by a
plasmid nicking assay, this endonuclease had a molecular weight (M(r)) of
35,000, a pH optimum of 5.5, and a threshold for activity of pH 6.6 to 6.8.
It was weakly inhibited by divalent cations (Ca2+, Mg2+, and Zn2+) and more
strongly inhibited by aurintricarboxylic acid and N-bromosuccinimide. DNA
from neutrophils treated with nigericin in buffers of defined pH displayed
nucleosomal ladders whose prominence varied with pH in a manner that
paralleled the pH dependence of the plasmid cleavage assays, consistent
with internucleosomal DNA cleavage by the acid endonuclease. We have
previously shown that neutrophils undergo acidification to a pH value as
low as 6.0 during apoptosis; we suggest that this endonuclease may be
responsible for the DNA cleavage seen in apoptotic neutrophils.
Volume 86,
Issue 6,
pp. 2414-2418,
09/15/1995
Copyright © 1995 by The American Society of Hematology
 CiteULike  Connotea  Del.icio.us  Digg  Reddit  Technorati What's this?
This article has been cited by other articles:
|
|
|
|
 
C.-Y. Xiao, M. Chen, Z. Zsengeller, H. Li, L. Kiss, M. Kollai, and C. Szabo
Poly(ADP-Ribose) Polymerase Promotes Cardiac Remodeling, Contractile Failure, and Translocation of Apoptosis-Inducing Factor in a Murine Experimental Model of Aortic Banding and Heart Failure
J. Pharmacol. Exp. Ther.,
March 1, 2005;
312(3):
891 - 898.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
R. Benson, C Dive, and A. Watson
Cytoplasmic acidification is not an effector mechanism of VP16 or DEX-induced apoptosis in CEM T leukaemia cells
J. Cell Sci.,
January 6, 1999;
112(11):
1755 - 1760.
[Abstract]
[PDF]
|
|
|
|
|
|
|
A. Urbano, R. McCaffrey, and F. Foss
Isolation and Characterization of NUC70, a Cytoplasmic, Hematopoietic Apoptotic Endonuclease
J. Biol. Chem.,
December 25, 1998;
273(52):
34820 - 34827.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
P.-F. Li, R. Dietz, and R. von Harsdorf
Differential Effect of Hydrogen Peroxide and Superoxide Anion on Apoptosis and Proliferation of Vascular Smooth Muscle Cells
Circulation,
November 18, 1997;
96(10):
3602 - 3609.
[Abstract]
[Full Text]
|
|
|
|
|
|
|
I. Furlong, R Ascaso, A Lopez Rivas, and M. Collins
Intracellular acidification induces apoptosis by stimulating ICE-like protease activity
J. Cell Sci.,
January 3, 1997;
110(5):
653 - 661.
[Abstract]
[PDF]
|
|
|
|
|
|
|
H. Fliss and D. Gattinger
Apoptosis in Ischemic and Reperfused Rat Myocardium
Circ. Res.,
November 1, 1996;
79(5):
949 - 956.
[Abstract]
[Full Text]
|
|
|
|
|
|
|
G. W. Meisenholder, S. J. Martin, D. R. Green, J. Nordberg, B. M. Babior, and R. A. Gottlieb
Events in Apoptosis. ACIDIFICATION IS DOWNSTREAM OF PROTEASE ACTIVATION AND BCL-2 PROTECTION
J. Biol. Chem.,
July 5, 1996;
271(27):
16260 - 16262.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
R. C. Elble and B. U. Pauli
Tumor Suppression by a Proapoptotic Calcium-activated Chloride Channel in Mammary Epithelium
J. Biol. Chem.,
October 26, 2001;
276(44):
40510 - 40517.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
